Timothy Hughes
Adelaide Medical School
Faculty of Health and Medical Sciences
Eligible to supervise Masters and PhD - email supervisor to discuss availability.
Professor Timothy P. Hughes, MD, FRACP, FRCPA, MBBS, FAAHMS - TITLEHOLDER.
Professor Timothy Hughes is Precision Medicine Theme Leader at SAHMRI
Professor Timothy Hughes is the Precision Medicine Theme Leader at SAHMRI; Beat Cancer Professor at the University of Adelaide and Consultant Haematologist at the RAH. He is also Chair of the International Chronic Myeloid Leukemia Foundation (iCMLf); an inaugural Fellow of the Australian Academy of Health and Medical Sciences (AAHMS)
Professor Hughes had a significant leadership role in the establishment of the molecular response criteria and kinase domain mutation screening guidelines that are used world-wide to monitor response and resistance in chronic myeloid leukaemia (CML). He has been a principal investigator on many of the key Global and Australian CML trials that have shaped the way tyrosine-kinase inhibitors (TKI's) are selected and sequenced. He has been a leader in the area of treatment-free remission (TFR) and influential in the recent recommendations to make TFR a mainstream goal of therapy. He has published over 300 papers with over 54,000 citations.
In recognition of his outstanding contributions to the field, Professor Hughes was awarded an L3 Investigator Grant from the NHMRC (2022-2026) for his project "A curative approach for chronic myeloid leukaemia".
Chronic Myeloid Leukaemia (CML) - Precision Medicine Theme, SAHMRI
Lead: Professor Tim Hughes.
Brief description of research area.
The treatment of chronic myeloid leukaemia (CML) has been one of the most remarkable cancer success stories this century, heralding the widespread application of small molecules to target oncogenic kinases. Insights from CML research in this era have provided guidance for the targeted therapy programs in many other cancers. The improvement in 10-year survival for CML patients from 20% in the 1990s to over 80% today has been achieved with the clinical application of tyrosine kinase inhibitor (TKI) therapy targeting BcrAbl. Despite the improvements in outcomes achieved with TKI therapy, major challenges still confront the CML clinician. Transformation to blast crisis is still seen in -10%, similar numbers are resistant to all TKls and only -50% overall achieve deep molecular responses (DMR). Furtherme>re most CML patients will remain dependent on TKI therapy for life with current approaches. As well as the massive cost burden, this longterm dependence on TKI therapy often leads to impaired quality of life and, in some cases, significant organ damage. Pioneering work from the Bordeaux and Adelaide trial groups has shown that around half of the patients who achieve stable DMR can cease TKI therapy without evidence of molecular relapse, even with long-term follow-up ( defined as achieving treatment-free remission -TFR). By contrast the other half have molecular evidence of recurrence, usually within 6 months of stopping, and have to restart TKI therapy. We have made excellent progress in understanding some of the key drivers of DMR and TFR and are already translating some of these findings into clinical trials to expand opportunity for these optimal outcomes. This emerging knowledge will provide urgently needed criterio for safe TKI cessation and guide the design of future trials to maximise TFR with consequent major benefits for many CML patients. CML is projected to become the most prevalent leukaemia by 2040, so for f'he thousands of CML patients in Australia who are facing lifelong dependence on expensive and debilitating therapy, support for this work is critical.
Research Project 1 – Dr Ilaria Pagani
Title: Identifying and exploiting metabolic dependencies for improved therapeutic outcomes in chronic myeloid leukaemia.
While the treatment of BCR-ABL1 driven chronic myeloid leukaemia (CML) with tyrosine kinase inhibitors (TKI) has been a success story of modern medicine, not all patients respond optimally, with a small but significant minority progressing to fatal blast crisis.
The inability of TKIs to eradicate leukaemic stem and progenitor cells (LSPC) provides a potential pool for subsequent relapse. This is exemplified by the dependence of most CML patients on lifelong TKI treatment, even in patients who achieve molecular responses. Universally, the presence of an activated tyrosine kinase drives metabolic changes, and the perturbation of these metabolic pathways provides potential avenues for exploration of therapeutic interventions. Targeting metabolic pathways may potentiate the effect of TKI therapies particularly in the LSPC compartment.
The aim of the project will be to investigate the metabolic pathways that exists within normal haematopoietic cells (important knowledge to avoid toxicity), and in LSPC including cases sensitive and resistant to TKIs to enable a clear understanding of whether the metabolome of LSPC can be targeted to sensitise this pool to TKI therapy.
This novel and innovative approach will likely provide a combinational treatment strategy with greater efficacy than current approaches, specifically in CML blast crisis.
Project available for: Honours / Mphil / PhD
Location: SAHMRI
Research project start: Semester 1
Special requirements: Police Clearance
Research Project 2 – Dr Ilaria Pagani
Title: Monitoring of minimal residual disease on chronic myeloid leukaemia patients in a setting of treatment free remission.
For patients who have achieved deep molecular responses and have minimal residual disease after treatment, the new goal for clinicians today is to identify candidate patients that can safely cease TKI therapy achieving treatment free remission (TFR). It is estimated that approximately 50% of CML patients may be eligible to stop TKIs, however half of them experience molecular relapse, usually within 6 months, and have to restart therapy. CML is projected to become the most prevalent leukaemia by 2040, therefore is critical to maximise the number of patients achieving TFR. However, unravelling the critical mediators of TFR is a major challenge.
The aim of the project will be to characterise the residual leukaemia population in TFR patients, and understand why some patients relapse and others don’t. One possible line of inquiry involves identifying the lineage of residual CML cells, through a highly sensitive DNA approach. This will involve a characterization of the genomic breakpoint and the development of a patient-specific assay to monitor residual leukaemia on sorted cell populations.
Project available for: Honours / Mphil / PhD
Location: SAHMRI
Research project start: Semester 1
Special requirements: Police Clearance
Research Project 3 - Dr David Yeung, Dr Liu Lu and Dr Ilaria Pagani
Title: Investigating the efficacy of a combination of TKI and a novel allosteric inhibitor asciminib in chronic myeloid leukaemia.
Clinical trials for the treatment of CML are currently underway using asciminib (ABL001), an allosteric inhibitor, alone and in combination with ATP-competitive tyrosine kinase inhibitors (TKIs: imatinib, nilotinib or dasatinib), to inhibit the constitutively active tyrosine kinase Bcr-Abl. The aims of this project are:
- Investigation of the synergistic effect of the combination of TKI and asciminib.
- Understand the signalling pathway changes in BCR-ABL+ cell lines and CML patient cells when combination therapy is given.
- Generation of resistant cell lines in the laboratory setting. This provides a useful tool for predicting and studying patient responses in vivo.
Understanding how these drugs work in synergy will enhance our ability to predict whether patients are likely to respond to combination therapy, and clarify ways to maximise synergism between these agents. In this project, BCR-ABL1+ cell lines will be exposed long term to gradually increasing concentrations of asciminib in combination with TKI. Mechanisms of resistance will be interrogated during resistance development and once overt resistance is observed. We will then examine mechanisms of treatment resistance in vitro, in an attempt to predict emergent disease resistance mechanisms that may arise.
Project available for: Honours / Mphil / PhD
Location: SAHMRI
Research project start: Semester 1
Special requirements: Police Clearance
Research Project 4 - Dr Chung Kok
Title: Developing an artificial intelligence-based algorithm to enable a risk-adapted approach to frontline therapy in chronic myeloid leukaemia (CML).
Chronic myeloid leukaemia (CML) is a model cancer for targeted therapy, driven by an activated mutant kinase. BCR-ABL1 is both necessary and sufficient to cause CML, through the expression of the constitutively active tyrosine kinase Bcr-Abl, targetable using tyrosine kinase inhibitors (TKIs). Despite the excellent progress we have made, major challenges remain. Even with our current choice of 5 TKIs, 15-20% respond poorly to TKI therapy and half of these patients will die from CML-related causes. Approximately 10% patients still fail to respond despite receiving second generation TKIs frontline, which are more potent than the first generation TKI imatinib. This very high-risk (VHR) group would likely be more effectively managed with a “dual targeted” approach from the start of therapy. For this reason, we have focused on developing baseline predictors of treatment failure to first and second generation TKIs, so that subsequent adverse outcomes can be minimized in high-risk cases by using a more intensive approach upfront. However, this approach would not be beneficial for most patients - adding toxicity without clinical benefit in the low-risk (LR) setting. Predictors that are capable of identifying the patients most likely to benefit from the use of a more potent TKI (high-risk (HR)) and the patients who will do poorly with any of the currently available TKIs (VHR) are urgently needed. We have previously published several bioassays that are predictive of response to frontline therapy in CML, however no single assay allows a sufficiently precise classification of patient risk groups to be clinically actionable.
We propose that the most effective approach will be to utilise all of these biomarkers to develop an artificial intelligence (AI) based algorithm to guide front-line therapy. This will enable up-front triaging of CML patients, tailoring therapy to the most appropriate risk-adapted approach. The theme of this proposal, therefore, is maximising the clinical effectiveness of rationally targeted therapies in CML.
HYPOTHESES
High-risk and very high-risk patients can be identified using an artificial-intelligence derived predictive algorithm based on informative biomarkers to
- enable optimal risk-adapted treatment decisions and
- maximise the clinical effectiveness of rationally targeted therapies.
SPECIFIC AIMS
Aim 1. Develop and validate an artificial intelligence (AI) based algorithm by integrating clinical and laboratory information to predict therapy-specific risk of failure in CML
Aim 2. Design interventions in patients identified as very high-risk based on pathways identified as potential actionable targets
Aim 3. Explore the potential use of the AI algorithm in a dynamic setting to enhance clinical utility
Project available for: Honours / Mphil / PhD
Location: SAHMRI
Research project start: Semester 1
Special requirements: Police Clearance
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Appointments
Date Position Institution name 2019 - ongoing Precision Medicine Theme Leader South Australian Health and Medical Research Institute (SAHMRI) 2015 - 2020 Chair SA Comprehensive Cancer Collaborative (SACCC) 2015 - 2018 Cancer Theme Leader South Australian Health and Medical Research Institute 2013 - ongoing Cancer Council Professor SAHMRI 2013 - ongoing Chair International CML Foundation (iCMLf) 2008 - ongoing Co-founder International CML Foundation (iCMLf) 2008 - 2014 Head, Department of Haematology SA Pathology 1993 - ongoing Consultant Haematologist, , Division of Haematology Royal Adelaide Hospital & SA Pathology 1991 - 1993 Post-Doctoral Fellow Howard Hughes Medical Institute, UCLA, California USA 1989 - 1991 Leukaemia Research Fellow Adult Leukaemia Research Centre, Royal Postgraduate Medical School, Hammersmith Hospital, London UK 1987 - 1988 Haematology Registrar Prince Henry Hospital, Sydney -
Awards and Achievements
Date Type Title Institution Name Country Amount 2019 Award Ramaciotti Medal for Excellence in Biomedical Research Ramaciotti Australia - 2018 Achievement Clarivate top 1% of cited scientists in their field internationally Clarivate Australia - 2017 Award GSK Award for Research Excellence, Research Australia Health & Medical Research Awards Research Australia Health & Medical Research Australia - 2017 Award Goldman Prize, International CML Foundation (iCMLf) – outstanding lifetime contribution to the management of CML International CML Foundation (iCMLf) Australia - 2015 Research Award CIC on Top Ranked NHMRC Program Grant assessed in 2013 NHMRC Australia - 2015 Fellowship Inaugural Fellow of the Australian Academy of Health and Medical Sciences (AAHMS) Australian Academy of Health and Medical Sciences (AAHMS) Australia - 2015 Achievement Carl De Gruchy Award, HSANZ for lifetime achievements HSANZ Australia - 2015 Award The World’s Most Influential Scientific Minds 2015, “Clinical Medicine” Thomson Reuters Australia - 2014 Award Top 1% of highly cited Scientists in 2014 Thomson Reuters Australia - 2011 Research Award NHMRC Ten of the Best Research Projects NHMRC Australia - -
Education
Date Institution name Country Title 1993 University of New South Wales Australia Doctor of Medicine 1988 Fellowship of the Royal Australasian College of Physicians Australia FRACP 1988 Fellowship of the Royal College of Pathologists of Australia Australia FRCPA 1981 The University of New South Wales Australia MBBS Hons -
Research Interests
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Journals
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Books
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Book Chapters
Year Citation 2016 Ross, D., & Hughes, T. (2016). Discontinuation of therapy and treatment-free remission in CML. In M. Kizaki (Ed.), Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia (pp. 183-193). Japan: Springer.
DOI Scopus12016 Yeung, D., & Hughes, T. (2016). Chronic Myeloid Leukaemia. In A. V. Hoffbrand, & D. R. Higgs (Eds.), Postgraduate Haematology: Seventh Edition (pp. 419-437). Wiley.
DOI Scopus22011 Hiwase, D. K., & Hughes, T. P. (2011). Therapy of Advanced-Stage and Resistant Chronic Myeloid Leukemia. In Leukemias: Principles and Practice of Therapy (pp. 281-295). Wiley.
DOI2008 Hiwase, D. K., & Hughes, T. (2008). Monitoring response to therapy for patients with chronic myeloid leukemia. In Chronic Myeloproliferative Disorders (pp. 103-117). 2007 Hughes, T., & Branford, S. (2007). Monitoring disease response. In J. Melo, & J. Goldman (Eds.), Myeloproliferative disorders. Hematologic Malignancies (pp. 143-164). Berlin: Springer. -
Conference Papers
Year Citation 2018 Shanmuganathan, N., Branford, S., Yong, A., Hiwase, D., Yeung, D., Ross, D., & Hughes, T. (2018). Predictors of Success in Treatment-Free Remission: A Single Centre Experience. In CLINICAL LYMPHOMA MYELOMA & LEUKEMIA Vol. 18 (pp. S224). CIG MEDIA GROUP, LP.
DOI2018 Mauro, M. J., Lang, F., Kim, D. -W., Cortes, J. E., Hughes, T. P., Hochhaus, A., . . . DeAngelo, D. J. (2018). Clinical Development of Asciminib (ABL001): A Randomized Phase 3 Study of Asciminib vs Bosutinib in Patients with Chronic Myeloid Leukemia (CML). In CLINICAL LYMPHOMA MYELOMA & LEUKEMIA Vol. 18 (pp. S223). CIG MEDIA GROUP, LP.
DOI WoS12018 Cortes, J. E., Hughes, T. P., Geissler, J., Hois, S., Quenet, S., Hourcade-Potelleret, F., . . . Saglio, G. (2018). Asciminib (ABL001) in Combination with Imatinib in Patients with Chronic Myeloid Leukemia in Chronic Phase Who Have Not Achieved a Deep Molecular Response with Long-Term Frontline Imatinib: A Randomized, Open-Label, Multicenter, Phase 2 Study. In CLINICAL LYMPHOMA MYELOMA & LEUKEMIA Vol. 18 (pp. S222-S223). CIG MEDIA GROUP, LP.
DOI WoS12018 Hughes, T. P., Boquimpani, C., Takahashi, N., Benyamini, N., Clementino, N. C. D., Shuvaev, V., . . . Mahon, F. -X. (2018). ENESTop 144-Week Update: Long-Term Treatment-Free Remission (TFR) in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) After Stopping Second-Line Nilotinib. In CLINICAL LYMPHOMA MYELOMA & LEUKEMIA Vol. 18 (pp. S222). CIG MEDIA GROUP, LP.
DOI WoS32018 Yong, A. S., Shanmuganathan, N., & Hughes, T. (2018). Treatment-Free Remission in CML: Selecting the Best Candidates. In CLINICAL LYMPHOMA MYELOMA & LEUKEMIA Vol. 18 (pp. S3-S5). CIG MEDIA GROUP, LP.
DOI2018 Mauro, M. J., Lang, F., Kim, D. -W., Cortes, J. E., Hughes, T. P., Hochhaus, A., . . . Rea, D. (2018). Clinical development of asciminib (ABL001) in chronic myeloid leukemia (CML): A randomized phase 3 study vs. bosutinib.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 36 (pp. 1 page). AMER SOC CLINICAL ONCOLOGY.
DOI2018 Thomson, D., Shahrin, H., Wang, P., Wadham, C., Hughes, T. P., Schreiber, A., & Branford, S. (2018). High Recombination Activating Gene (RAG) Expression and RAG Mediated Recombination Is Associated with Oncogenic Rearrangement Observed with Tyrosine Kinase Inhibitor Resistant CML. In BLOOD Vol. 132 (pp. 4 pages). CA, San Diego: AMER SOC HEMATOLOGY.
DOI WoS12018 Yeung, D. T., Grigg, A. P., Shanmuganathan, N., Cunningham, I., Shortt, J., Rowling, P., . . . Hughes, T. P. (2018). Combination of Nilotinib and Pegylated Interferon Alfa-2b Results in High Molecular Response Rates in Chronic Phase CML: Interim Results of the ALLG CML 11 Pinnacle Study. In BLOOD Vol. 132 (pp. 5 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS52018 Tvorogov, D., Thomas, D., Liau, N. P. D., Dottore, M., Barry, E. F., Lathi, M., . . . Lopez, A. F. (2018). Accumulation of JAK Activation-Loop Phosphorylation Promotes Type I JAK Inhibitor Withdrawal Syndrome in Myelofibrosis. In BLOOD Vol. 132 (pp. 4 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI2018 Rea, D., Lang, F., Kim, D. -W., Cortes, J. E., Hughes, T. P., Minami, H., . . . Mauro, M. J. (2018). Asciminib, a Specific Allosteric BCR-ABL1 Inhibitor, in Patients with Chronic Myeloid Leukemia Carrying the T315I Mutation in a Phase 1 Trial. In BLOOD Vol. 132 (pp. 4 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS42017 Mueller, M., Baccarani, M., Deininger, M. W. N., Guilhot, F., Hochhaus, A., Hughes, T. P., . . . Cortes, J. E. (2017). Impact of early landmark responses with ponatinib on 4-yr outcomes in CP-CML patients (pts) in PACE, a pivotal phase II trial.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 35 (pp. 6 pages). Chicago, IL: AMER SOC CLINICAL ONCOLOGY.
DOI WoS12017 Ross, D. M., Pagani, I. S., Shanmuganathan, N., Seymour, J. F., Mills, A. K., Filshie, R. J., . . . Hughes, T. P. (2017). Long-term Follow-up of the ALLG CML8 TWISTER Study of Treatment-free Remission (TFR) in Patients With Chronic Myeloid Leukemia (CML).. In Blood Vol. 130 (pp. 1597). Atlanta: American Society of Hematology. 2017 Pagani, I., Dang, P., Kommers, I., Goyne, J., Saunders, V., Prime, J., . . . Ross, D. (2017). Comparison of genomic and reverse transcriptase Q-PCR for the monitoring of first-line imatinib treatment: an ALLG CML9 sub-study. In Haematologica. Madrid: Ferrata Storti Foundation. 2016 Pagani, I. S., Kok, C. H., Saunders, V., Goyne, J., McLean, J., VanderHoek, M., . . . Ross, D. M. (2016). The genomic landscape of mitochondrial DNA mutations in chronic myeloid leukaemia.. In European Journal of Human Genetics. Barcelona: Natue Publishing Group. 2016 Mahon, F. -X., Boquimpani, C. M., Takahashi, N., Benyamini, N., Clementino, N. C. D., Shuvaev, V., . . . Hughes, T. P. (2016). Patient-Reported Quality of Life before and after Stopping Treatment in the ENESTop Trial of Treatment-Free Remission for Patients with Chronic Myeloid Leukemia in Chronic Phase. In BLOOD Vol. 128 (pp. 6 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS22016 Hughes, T. P., Boquimpani, C. M., Takahashi, N., Benyamini, N., Clementino, N. C. D., Shuvaev, V., . . . Mahon, F. -X. (2016). Treatment-Free Remission in Patients with Chronic Myeloid Leukemia in Chronic Phase According to Reasons for Switching from Imatinib to Nilotinib: Subgroup Analysis from ENESTop. In BLOOD Vol. 128 (pp. 6 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS52016 Asari, K., Heatley, S. L., Sadras, T., Leclercq, T. M., Fitter, S., Kok, C. H., . . . White, D. L. (2016). <i>In Vitro</i> Modeling of Ph-like ALL Fusions Identifies Novel Kinase-Domain Mutations As Mode of TKI-Resistance Implications for Targeted Therapy. In BLOOD Vol. 128 (pp. 5 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI2016 Jabbour, E. J., Cortes, J. E., Talpaz, M., Baccarani, M., Mauro, M. J., Hochhaus, A., . . . Kantarjian, H. M. (2016). Long-Term Follow-up of the Efficacy and Safety of Ponatinib in Philadelphia Chromosome-Positive Leukemia Patients with the T315I Mutation. In BLOOD Vol. 128 (pp. 7 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI2016 Hiwase, D. K., Tan, P., D'Rozario, J., Taper, J., Powell, A. R., Irving, I., . . . Hughes, T. P. (2016). Efficacy and Safety of Nilotinib 300 Mg Twice Daily (BD) in Patients with CML in Chronic Phase (CML-CP) Who Are Intolerant to Prior BCR-ABL Tyrosine Kinase Inhibitors (TKIs): Results from the Randomized, Phase IIIb ENES Tswift Study. In BLOOD Vol. 128 (pp. 6 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI2016 Shanmuganathan, N., Branford, S., Braley, J., Hiwase, D., Yeung, D. T., Ross, D. M., & Hughes, T. P. (2016). For Patients with Sustained MR4-MR4.5, Less Frequent Molecular Monitoring during the First 12 Months after Tyrosine Kinase Inhibitor Cessation Is Viable for Timely Detection of Loss of MMR. In BLOOD Vol. 128 (pp. 7 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI2016 Yeung, D. T., Osborn, M. P., White, D. L., Branford, S., Gerber, T., Butcher, B., . . . Hughes, T. P. (2016). Upfront Imatinib with Selective Early Switching to Nilotinib Leads to Excellent Achievement of Deep Molecular Response in Chronic Phase CML: 5 Year (Final) Analysis of the TIDEL-II Study. In BLOOD Vol. 128 (pp. 6 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI2016 Hughes, T. P., Goh, Y. -T., Ottmann, O. G., Minami, H., Rea, D., Lang, F., . . . Kim, D. -W. (2016). Expanded Phase 1 Study of ABL001, a Potent, Allosteric Inhibitor of BCR-ABL, Reveals Significant and Durable Responses in Patients with CML-Chronic Phase with Failure of Prior TKI Therapy. In BLOOD Vol. 128 (pp. 6 pages). San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS22016 Pagani, I. S., Kok, C. H., Wang, J., Saunders, V., Goyne, J., McLean, J., . . . Ross, D. M. (2016). MITOCHONDRIAL DNA MUTATIONS IDENTIFY CLONAL HETEROGENEITY IN CHRONIC MYELOID LEUKAEMIA. In HAEMATOLOGICA Vol. 101 (pp. 234). Copenhagen, DENMARK: FERRATA STORTI FOUNDATION. 2016 Lu, L., Saunders, V., Kok, C., Leclercq, T., Hughes, T., & White, D. (2016). MODELLING PONATINIB RESISTANCE IN BCR-ABL1+CELL LINES: IMPLICATIONS FOR PONATINIB THERAPY. In HAEMATOLOGICA Vol. 101 (pp. 182-183). Copenhagen, DENMARK: FERRATA STORTI FOUNDATION. 2015 Pritchard, J., Lustgarten, S., Hodgson, J. G., Baccarani, M., Cortes, J. E., Deininger, M. W., . . . Rivera, V. M. (2015). ANALYSIS OF THE RELATIONSHIP BETWEEN DOSE AND BCR-ABL HALVING TIME IN CP-CML PATIENTS TREATED WITH PONATINIB OR IMATINIB. In HAEMATOLOGICA Vol. 100 (pp. 448-449). Vienna, AUSTRIA: FERRATA STORTI FOUNDATION. 2015 Cortes, J. E., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., Chuah, C., . . . Shah, N. P. (2015). Evaluation of the Benefit/Risk Profile of Ponatinib in CP-CML Patients over Time: 4-Year Follow-up of the Phase 2 PACE Study. In BLOOD Vol. 126 (pp. 4 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Hochhaus, A., Saglio, G., Hughes, T. P., Larson, R. A., Taningco, L., Deng, W., . . . Kantarjian, H. M. (2015). Impact of Treatment with Frontline Nilotinib (NIL) vs Imatinib (IM) on Sustained Deep Molecular Response (MR) in Patients (pts) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP). In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Ottmann, O. G., Alimena, G., DeAngelo, D. J., Goh, Y. -T., Heinrich, M. C., Hochhaus, A., . . . Dong-Wook, K. (2015). ABL001, a Potent, Allosteric Inhibitor of BCR-ABL, Exhibits Safety and Promising Single- Agent Activity in a Phase I Study of Patients with CML with Failure of Prior TKI Therapy. In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS192015 Hughes, T. P., Cervantes, F., Spector, N., Leber, B., Branford, S., Glynos, T. A., . . . Lipton, J. H. (2015). Treatment-Free Remission (TFR) Eligibility in Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) and Residual Disease on Long-Term Imatinib (IM) Who Switched to Second-Line Nilotinib (NIL). In BLOOD Vol. 126 (pp. 4 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Hochhaus, A., Cortes, J. E., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., . . . Kantarjian, H. M. (2015). Efficacy and Safety of Ponatinib in CP-CML Patients By Number of Prior Tyrosine Kinase Inhibitors: 4-Year Follow-up of the Phase 2 PACE Trial. In BLOOD Vol. 126 (pp. 5 pages). Orlando, FL: AMER SOC HEMATOLOGY.
WoS42015 Hughes, T. P., Larson, R. A., Kim, D. W., Issaragrisil, S., le Coutre, P. D., Lobo, C., . . . Kantarjian, H. M. (2015). EFFICACY AND SAFETY OF NILOTINIB VS IMATINIB IN PATIENTS WITH NEWLY DIAGNOSED CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE: 6-YEAR FOLLOW-UP OF ENESTND. In HAEMATOLOGICA Vol. 100 (pp. 61). Vienna, AUSTRIA: FERRATA STORTI FOUNDATION. 2015 Cortes, J. E., Kim, D. G., Pinilla-Ibarz, J., Le Coutre, P. D., Paquette, R., Chuah, C., . . . Kantarjian, H. M. (2015). Efficacy and safety of ponatinib in heavily pretreated leukemia patients in the PACE trial: 3-year results.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 33 (pp. 1 page). Chicago, IL: AMER SOC CLINICAL ONCOLOGY.
DOI2015 Khoury, H. J., Baccarani, M., Guilhot, F., Hochhaus, A., Hughes, T. P., Lipton, J. H., . . . Mauro, M. J. (2015). Elevated blood pressure (BP) and adverse events (AEs) of hypertension (HTN) in ponatinib (PON) leukemia trials.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 33 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS. 2015 Branford, S., Wang, P. P. S., Parker, W. T., Yeung, D., Marum, J. E., Stangl, D., . . . Hughes, T. P. (2015). High Incidence of Mutated Cancer-Associated Genes at Diagnosis in CML Patients with Early Transformation to Blast Crisis. In BLOOD Vol. 126 (pp. 4 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Hughes, T. P., Cervantes, F., Leber, B., Spector, N., Lipton, J. H., Pasquini, R., . . . Branford, S. (2015). ENESTCMR 4-Y RESULTS: PATIENTS (PTS) WITH CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE (CML-CP) AND RESIDUAL DISEASE MORE LIKELY TO ACHIEVE DEEP MOLECULAR RESPONSE FOLLOWING SWITCH TO NILOTINIB (NIL). In HAEMATOLOGICA Vol. 100 (pp. 61-62). Vienna, AUSTRIA: FERRATA STORTI FOUNDATION. 2015 Eadie, L. N., Saunders, V. A., Leclercq, T. M., Branford, S., White, D. L., & Hughes, T. P. (2015). The Allosteric Inhibitor ABL001 Is Susceptible to Resistance in Vitro Mediated By Overexpression of the Drug Efflux Transporters ABCB1 and ABCG2. In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Yeung, D. T., Parker, W. T., Phillis, S., Georgievski, J., Scott, H. S., Hughes, T. P., & Branford, S. (2015). BCR-ABL Assay Sensitivity of MR4.5 Achieved in >90%, and MR5 in >75% of Samples, through mRNA Selection before qRT-PCR. In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Wang, J., Kok, C. H., Leclercq, T. M., Saunders, V. A., D'Andrea, R. J., Hughes, T. P., & White, D. L. (2015). High Peroxisome Proliferator-Activated Receptor-Gamma (PPARγle) Transcriptional Activity Reduces Active Influx of Imatinib and Kinase Inhibition in CML Cells. In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Eadie, L. N., Hughes, T. P., & White, D. L. (2015). The Clinical Significance of Early Imatinib Induced ABCB1 Overexpression in Chronic Phase CML Patients: A TIDEL II Sub-Study. In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS12015 Marum, J. E., Purins, L., Yeung, D. T., Parker, W. T., Price, D. J., Wang, P. P. S., . . . Branford, S. (2015). Germline Genetic Variation of ASXL1 and BIM Predicts Response to Imatinib and Identifies a Subset of High Sokal Risk Patients with the Greatest Risk of Treatment Failure and Disease Progression. In BLOOD Vol. 126 (pp. 4 pages). Orlando, FL: AMER SOC HEMATOLOGY.
DOI2015 Kok, C. H., Leclercq, T. M., Watkins, D., Yeung, D. T., Saunders, V. A., White, D. L., & Hughes, T. P. (2015). A 20 Gene Expression Signature That Predicts Early Molecular Response Failure in Chronic Phase CML Patients Treated with Frontline Imatinib. In BLOOD Vol. 126 (pp. 3 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Hughes, A., Tang, C., Clarson, J., Vidovic, L., Hughes, T. P., & Yong, A. S. (2015). Chronic Myeloid Leukemia Patients with Deep Molecular Responses to Tyrosine Kinase Inhibitors Have Increased Effector Natural Killer and Cytotoxic T Cell Immune Responses to Leukaemia-Associated Antigens and Concomitant Reduced Immune Suppressors. In BLOOD Vol. 126 (pp. 2 pages). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS42015 Nicolini, F. E., Basak, G. W., Kim, D. -W., Olavarria, E., Pinilla-Ibarz, J., Apperley, J. F., . . . Cortes, J. E. (2015). The Impact of Ponatinib Versus Allogeneic Stem Cell Transplant (SCT) on Outcomes in Patients with Chronic Myeloid Leukemia (CML) or Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph plus ALL) with the T315I Mutation. In BLOOD Vol. 126 (pp. 4 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2015 Hughes, T. P., Salvino, M. A., Chuan, O. T., Elhaddad, A., Abdulkadyrov, K., Shortt, J., . . . Lipton, J. H. (2015). Dose-Optimized Nilotinib (NIL) in Patients (Pts) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP): Final Results from ENESTxtnd Study. In BLOOD Vol. 126 (pp. 4 pages). Orlando, FL: AMER SOC HEMATOLOGY. 2014 Hughes, T. P., Munhoz, E. C., Elhaddad, A., Chuan, O. T., Abdulkadyrov, K., Shortt, J., . . . Lipton, J. H. (2014). Efficacy and Safety of Dose-Optimized Nilotinib (NIL) in Patients (Pts) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP): ENESTxtnd Interim Analysis. In BLOOD Vol. 124 (pp. 4 pages). San Francisco, CA: AMER SOC HEMATOLOGY. 2014 Mahon, F. -X., Baccarani, M., Mauro, M. J., Hughes, T. P., Sagilo, G., Savona, M., . . . Hochhaus, A. (2014). Treatment-free remission (TER) following nilotinib (NIL) in patients (pis) with chronic myeloid leukemia in chronic phase (CML-CP): ENESTfreedom, ENESTop, ENESTgoal, and ENESTpath.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 32 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
DOI WoS122014 Larson, R. A., Kim, D. -W., Jootar, S., Pasquini, R., Clark, R. E., Lobo, C., . . . Hughes, T. P. (2014). ENESTnd 5-year (y) update: Long-term outcomes of patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP) treated with frontline nilotinib (NIL) versus imatinib (IM).. In JOURNAL OF CLINICAL ONCOLOGY Vol. 32 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
DOI WoS102014 Hughes, T. P., le Coutre, P. D., Jootar, S., Reiffers, J., Turkina, A. G., Saglio, G., . . . Larson, R. A. (2014). ENESTND 5-YEAR FOLLOW-UP: CONTINUED BENEFIT OF FRONTLINE NILOTINIB (NIL) COMPARED WITH IMATINIB (IM) IN PATIENTS (PTS) WITH CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE (CML-CP). In HAEMATOLOGICA Vol. 99 (pp. 236-237). Milan, ITALY: FERRATA STORTI FOUNDATION.
WoS92014 Spector, N., Clementino, N. C. D., Dorlhiac-Llacer, P. E., Leber, B., Hughes, T. P., Cervantes, F., . . . Lipton, J. H. (2014). Effect of continued imatinib (IM) in pts with detectable BCR-ABL after ≥ 2 years on study on deep molecular responses (MR): 36-month update from ENESTcmr.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 32 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
DOI2014 Lipton, J. H., Chuah, C., Guerci-Bresler, A., Rosti, G., Simpson, D., Lustgarten, S., . . . Deininger, M. W. N. (2014). EPIC: A phase III trial of ponatinib (PON) versus imatinib (IM) in patients (pts) with newly diagnosed CP-CML.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 32 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
DOI WoS22014 Deininger, M. W., Shah, N. P., Cortes, J. E., Kim, D. W., Nicolini, F. E., Talpaz, M., . . . Branford, S. (2014). LONGER-TERM FOLLOW-UP OF THE IMPACT OF BASELINE (BL) MUTATIONS ON PONATINIB RESPONSE AND END OF TREATMENT (EOT) MUTATION ANALYSIS IN PATIENTS (PTS) WITH CHRONIC PHASE CHRONIC MYELOID LEUKEMIA (CP-CML). In HAEMATOLOGICA Vol. 99 (pp. 533). Milan, ITALY: FERRATA STORTI FOUNDATION. 2014 Branford, S., Kamel-Reid, S., Bendit, I., Etienne, G., Guerci-Bresler, A., Hughes, T. P., . . . Cervantes, F. (2014). EARLY MOLECULAR RESPONSE PREDICTS ACHIEVEMENT OF UNDETECTABLE BCR-ABL IN PATIENTS (PTS) WITH CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE (CML-CP) TREATED WITH NILOTINIB: 3-YEAR FOLLOW-UP OF ENESTCMR. In HAEMATOLOGICA Vol. 99 (pp. 532). Milan, ITALY: FERRATA STORTI FOUNDATION.
WoS32014 Larson, R. A., Kim, D. -W., Issaragrilsil, S., le Coutre, P., Dorlhiac Llacer, P. E., Etienne, G., . . . Hughes, T. P. (2014). Efficacy and Safety of Nilotinib (NIL) vs Imatinib (IM) in Patients (pts) With Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP): Long-Term Follow-Up (f/u) of ENESTnd. In BLOOD Vol. 124 (pp. 4 pages). San Francisco, CA: AMER SOC HEMATOLOGY.
DOI WoS22014 Eadie, L. N., Hughes, T. P., & White, D. L. (2014). Increasing expression of the efflux transporter ABCB1 may predispose CML cells to over TKI resistance. In NDLR Abstract Handbook Vol. 122 (pp. 2 pages). Noosa, QLD: AMER SOC HEMATOLOGY.
DOI2014 Hochhaus, A., Pinilla-Ibarz, J., Kim, D. -W., Le Coutre, P. D., Paquette, R., Chuah, C., . . . Cortes, J. E. (2014). Clinical impact of dose modification and dose intensity on response to ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph plus ) leukemias.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 32 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
DOI WoS62014 Mueller, M. C., Baccarani, M., Deininger, M. W., Guilhot, F., Hochhaus, A., Hughes, T. P., . . . Cortes, J. E. (2014). Achieving Early Landmark Response Is Predictive of Outcomes in Heavily Pretreated Patients with Chronic Phase Chronic Myeloid Leukemia (CP-CML) Treated with Ponatinib. In BLOOD Vol. 124 (pp. 4 pages). San Francisco, CA: AMER SOC HEMATOLOGY.
DOI WoS12013 Larson, R. A., Hochhaus, A., Saglio, G., Kim, D. -W., Jootar, S., Le Coutre, P. D., . . . Kantarjian, H. M. (2013). Nilotinib versus imatinib in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd 4-year (y) update. In JOURNAL OF CLINICAL ONCOLOGY Vol. 31 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
WoS122013 Lipton, J. H., Deininger, M. W. N., Lustgarten, S., Turner, C. D., Rivera, V. M., Clackson, T., . . . Haluska, F. G. (2013). EPIC: A phase III randomized, open-label study of ponatinib versus imatinib in adult patients with newly diagnosed chronic myeloid leukemia in chronic phase.. In JOURNAL OF CLINICAL ONCOLOGY Vol. 31 (pp. 1 page). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS. 2013 Saglio, G., Hughes, T. P., Larson, R. A., Issaragrilsil, S., Turkina, A. G., Steegmann, J. L., . . . Hochhaus, A. (2013). Impact of early molecular response to nilotinib (NIL) or imatinib (IM) on the long-term outcomes of newly diagnosed patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP): Landmark analysis of 4-year (y) data from ENESTnd. In JOURNAL OF CLINICAL ONCOLOGY Vol. 31 (pp. 2 pages). Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS. 2012 Kantarjian, H. M., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P., Paquette, R., Chuah, C., . . . Cortes, J. E. (2012). Efficacy and Safety of Ponatinib in Patients with Accelerated Phase or Blast Phase Chronic Myeloid Leukemia (AP-CML or BP-CML) or Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ ALL): 12-Month Follow-up of the PACE Trial. In BLOOD Vol. 120 (pp. 3 pages). GA, Atlanta: AMER SOC HEMATOLOGY. 2012 Mauro, M. J., Cortes, J. E., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P., Paquette, R., . . . Kantarjian, H. M. (2012). Multivariate Analyses of the Clinical and Molecular Parameters Associated with Efficacy and Safety in Patients with Chronic Myeloid Leukemia (CML) and Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph plus ALL) Treated with Ponatinib in the PACE Trial. In BLOOD Vol. 120 (pp. 3 pages). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS52012 Cortes, J. E., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P., Paquette, R., Chuah, C., . . . Kantarjian, H. M. (2012). A Pivotal Phase 2 Trial of Ponatinib in Patients with Chronic Myeloid Leukemia (CML) and Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph plus ALL) Resistant or Intolerant to Dasatinib or Nilotinib, or with the T315I BCR-ABL Mutation: 12-Month Follow-up of the PACE Trial. In BLOOD Vol. 120 (pp. 3 pages). GA, Atlanta: AMER SOC HEMATOLOGY.
DOI WoS222012 Kantarjian, H. M., Kim, D. -W., Issaragrisil, S., Clark, R. E., Reiffers, J., Nicolini, F. E., . . . Larson, R. A. (2012). Enestnd 4-Year (y) Update: Continued Superiority of Nilotinib Vs Imatinib in Patients (pts) with Newly Diagnosed Philadelphia Chromosome-Positive (Ph plus ) Chronic Myeloid Leukemia in Chronic Phase (CML-CP). In BLOOD Vol. 120 (pp. 3 pages). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS152012 Kantarjian, H., Flinn, I. W., Goldberg, S., Bunworasate, U., Zanichelli, M. A., Nakamae, H., . . . Larson, R. A. (2012). Nilotinib versus imatinib in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd 3-year (yr) follow-up (f/u). In JOURNAL OF CLINICAL ONCOLOGY Vol. 30 (pp. 2 pages). Chicago, IL: AMER SOC CLINICAL ONCOLOGY.
WoS22012 Lipton, J. H., Hughes, T. P., Leber, B., De Souza, C., Dorlhiac-Llacer, P. E., Steegmann, J. L., . . . Spector, N. (2012). Switch to nilotinib versus continued imatinib in patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP) with detectable BCR-ABL after 2 or more years on imatinib: ENESTcmr 12-month (mo) follow-up. In JOURNAL OF CLINICAL ONCOLOGY Vol. 30 (pp. 1 page). Chicago, IL: AMER SOC CLINICAL ONCOLOGY.
WoS22012 Kim, D. -W., Cortes, J. E., Pinilla-Ibarz, J., le Coutre, P., Paquette, R., Chuah, C., . . . Kantarjian, H. M. (2012). Efficacy and Safety of Ponatinib According to Prior Approved Tyrosine Kinase Inhibitor (TKI) Therapy in Patients with Chronic Myeloid Leukemia in Chronic Phase (CP-CML): Results From the PACE Trial. In BLOOD Vol. 120 (pp. 3 pages). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS22012 Hochhaus, A., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P., Paquette, R., Chuah, C., . . . Cortes, J. E. (2012). Molecular Responses with Ponatinib in Patients with Philadelphia Chromosome Positive (Ph plus ) Leukemia: Results From the PACE Trial. In BLOOD Vol. 120 (pp. 3 pages). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI2012 Morley, A., Bartley, P., Latham, S., Budgen, B., Ross, D., Hughes, E., . . . Hughes, T. (2012). DNA-qPCR vs RT-qPCR for Monitoring MRD in Chronic Myeloid Leukemia. In JOURNAL OF MOLECULAR DIAGNOSTICS Vol. 14 (pp. 662-663). Long Beach, CA: ELSEVIER SCIENCE INC. 2011 le Coutre, P. D., Giles, F. J., Pinilla-Ibarz, J., Larson, R. A., Gattermann, N., Ottmann, O. G., . . . Kantarjian, H. M. (2011). Nilotinib in Imatinib-Resistant or -Intolerant Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP): 48-Month Follow-up Results of a Phase 2 Study. In BLOOD Vol. 118 (pp. 1610). San Diego, CA: AMER SOC HEMATOLOGY.
WoS12011 Pasquini, R., Cortes, J. E., Kantarjian, H. M., Joske, D., Meillon, L. A., Zernovak, O., . . . Kim, D. -W. (2011). Survey of the Frontline Treatment and Management of Chronic Myeloid Leukemia (CML) in a Real-Word Setting: The 3rd Annual Update of the Worldwide Observational Registry Collecting Longitudinal Data on Management of Chronic Myeloid Leukemia Patients (The WORLD CML Registry). In BLOOD Vol. 118 (pp. 738). San Diego, CA: AMER SOC HEMATOLOGY. 2011 Nieborowska-Skorska, M., Kopinski, P., Ray, R., Hoser, G., Ngaba, D., Flis, S., . . . Skorski, T. (2011). Targeting Rac2-Mitochondrial Respiratory Chain Complex III Signaling to Prevent Genomic Instability in Leukemia Stem and Progenitor Cells. In BLOOD Vol. 118 (pp. 1176-1177). San Diego, CA: AMER SOC HEMATOLOGY. 2011 Parker, W. T., Ho, M., Scott, H. S., Hughes, T. P., & Branford, S. (2011). Multiple Low Level Mutations Identifies Imatinib Resistant CML Patients At Risk of Poor Response to Second-Line Inhibitor Therapy, Irrespective of the Resistance Profile of the Mutations. In BLOOD Vol. 118 (pp. 54). San Diego, CA: AMER SOC HEMATOLOGY.
WoS12011 Watkins, D. B., Kok, C. H., Hughes, T. P., Slader, C., D'Andrea, R., & White, D. L. (2011). Differential Lineage Involvement Between Very Low and Higher OCT-1 Activity Chronic-Phase CML Patients. In BLOOD Vol. 118 (pp. 727). San Diego, CA: AMER SOC HEMATOLOGY. 2011 Hughes, T. P., Lipton, J. H., Leber, B., Spector, N., Cervantes, F., Pasquini, R., . . . Branford, S. (2011). Complete Molecular Response (CMR) Rate with Nilotinib in Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) without CMR, After ≥ 2 Years on Imatinib: Preliminary Results From the Randomized ENESTcmr Trial of Nilotinib 400 Mg Twice Daily (BID) Vs Imatinib. In BLOOD Vol. 118 (pp. 278). San Diego, CA: AMER SOC HEMATOLOGY.
WoS12011 Yeung, D. T., Osborn, M., White, D. L., Branford, S., Kornhauser, M., Slader, C., . . . Hughes, T. P. (2011). Upfront Imatinib Therapy in CML Patients with Rapid Switching to Nilotinib for Failure to Achieve Molecular Targets or Intolerance Achieves High Overall Rates of Molecular Response and a Low Risk of Progression - An Update of the TIDEL-II Trial. In BLOOD Vol. 118 (pp. 208). San Diego, CA: AMER SOC HEMATOLOGY.
WoS12011 White, D. L., Saunders, V. A., Frede, A., GrootObbink, K., Slader, C., Yeung, D. T., . . . Hughes, T. P. (2011). The Strategy of Early Nilotinib Switch Based on Failure to Achieve Optimal Molecular Targets on Imatinib May Not Overcome the Negative Impact of a Low OCT-1 Activity in De-Novo CP-CML Patients. In BLOOD Vol. 118 (pp. 735). San Diego, CA: AMER SOC HEMATOLOGY. 2011 Nievergall, E., White, D. L., Ramshaw, H., Lopez, A. F., Hughes, T. P., & Hiwase, D. K. (2011). Antibody-Targeting of IL-3 Receptor-α Increases the Susceptibility of CD34<SUP>+</SUP> CML Progenitors to Dasatinib-Induced Cell Death. In BLOOD Vol. 118 (pp. 1599). San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS12011 Wang, J., Hughes, T. P., Kok, C. H., Saunders, V. A., Frede, A., GrootObbink, K., . . . White, D. L. (2011). Non-Steroidal Anti-Inflammatory Drugs and Imatinib; Drug Interactions That May Impact Efficacy. In BLOOD Vol. 118 (pp. 1493-1494). San Diego, CA: AMER SOC HEMATOLOGY. 2011 Branford, S., Yeung, D. T., Prime, J., Ross, D., & Hughes, T. P. (2011). Imatinib Dose Interruption in Responding CML Patients Is Associated with Characteristic BCR-ABL Kinetics, Which Could Help to Differentiate Non-Adherence From Drug Resistance. In BLOOD Vol. 118 (pp. 55). San Diego, CA: AMER SOC HEMATOLOGY.
WoS12011 White, D. L., Lu, L., Clackson, T. P., Saunders, V. A., & Hughes, T. P. (2011). ATP Dependent Efflux Transporters ABCB1 and ABCG2 Are Unlikely to Impact the Efficacy, or Mediate Resistance to the Tyrosine Kinase Inhibitor, Ponatinib. In BLOOD Vol. 118 (pp. 1180). San Diego, CA: AMER SOC HEMATOLOGY.
WoS12011 Alexander, W., & Shah, N. (2011). American Society of Hematology, 52nd Annual Meeting and Exposition: Dasatinib (Sprycel) versus imatinib (Gleevec) in newly diagnosed chronic-phase chronic myeloid leukemia: The DASISION trial, 18-month follow-up. In P and T Vol. 36 (pp. 100).
Scopus32010 White, E., Matejtschuk, P., Rigsby, P., Gabert, J., Wang, Y., Branford, S., . . . Cross, N. (2010). ESTABLISHMENT OF THE 1ST WORLD HEALTH ORGANIZATION INTERNATIONAL GENETIC REFERENCE PANEL FOR QUANTITATION OF BCR-ABL MRNA. In HAEMATOLOGICA Vol. 95 (pp. 84-85). Barcelona, SPAIN: FERRATA STORTI FOUNDATION. 2010 White, D. L., Saunders, V., Frede, A., GrootObbink, K., Slader, C., Yeung, D. T., . . . Hughes, T. (2010). Early Switching From Imatinib to Nilotinib In CML Patients Failing to Achieve Early Molecular Targets May Not Be An Effective Approach In Patients with Very Low OCT-1 Activity: A TIDEL II Sub-Study. In BLOOD Vol. 116 (pp. 160-161). Orlando, FL: AMER SOC HEMATOLOGY. 2010 Yeung, D. T., Osborn, M., White, D. L., Branford, S., Haswell, L., Slader, C., . . . Hughes, T. (2010). Selective Escalation of Imatinib Therapy and Early Switching to Nilotinib In De Novo Chronic Phase CML Patients: Interim Results From the TIDEL-II Trial. In BLOOD Vol. 116 (pp. 96). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS102010 White, D. L., Saunders, V., Andrew, M., Rofe, A., Slader, C., Yeung, D. T., . . . Hughes, T. (2010). Imatinib PK: Observations From the TIDEL II Study.. In BLOOD Vol. 116 (pp. 943). Orlando, FL: AMER SOC HEMATOLOGY. 2010 Parker, W., Ho, M., Lawrence, R., Irwin, D., Scott, H., Hughes, T., & Branford, S. (2010). Detection of low level nilotinib or dasatinib resistant BCR-ABL mutations by mass spectrometry in CML patients who fail Imatinib is highly predivtive of their subsequent clonal expansion when treated with the drug for which their mutation confers resistance. In Proceedings of 2010 american society of hematology meeting Vol. 116 (pp. 0 pages). Florida, USA: AMER SOC HEMATOLOGY. 2010 Prime, H., Romeo, G., Phillis, S., Field, C., Jamison, B., Prime, J., . . . Branford, S. (2010). Contrasting response of patients with chronic myeloid leukaemia (CML) and the highly imatinib resistant L248V mutation that may be related to an increased propensity of some patients to form an associated deletion mutant with increased imatinib sensitivity. In Proceedings of Haematology association of australasia annual meeting (pp. 0 pages). Auckland, New Zealand. 2010 Branford, S., Goh, H., Izzo, B., Beppu, L., Ortmann, C., Duniec, K., . . . Hughes, T. (2010). A Review of Mutation Analysis In the TOPS Trial of Standard Dose Versus High Dose IM In CML Suggests That Refinements to the ELN Recommendations for Mutation Screening May Be Appropriate. In Proceedings of 52nd American Society of Hematology Meeting (ASH), as published in Blood Vol. 116 (pp. 389-390). Washington, DC: American Society of Hematology.
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WoS32010 Saglio, G., Larson, R. A., Hughes, T. P., Issaragrisil, S., Turkina, A. G., Marin, D., . . . Hochhaus, A. (2010). Efficacy and Safety of Nilotinib In Chronic Phase (CP) Chrome Myeloid Leukemia (CML) Patients (Pts) with Type 2 Diabetes In the ENESTnd Trial. In BLOOD Vol. 116 (pp. 1405-1406). Orlando, FL: AMER SOC HEMATOLOGY.
WoS42010 Larson, R. A., Hochhaus, A., Saglio, G., Rosti, G., Lopez, J. L., Stenke, L., . . . Kantarjian, H. M. (2010). Cardiac Safety Profile of Imatinib and Nilotinib In Patients (pts) with Newly Diagnosed Chronic Myeloid Leukemia In Chronic Phase (CML-CP): Results From ENESTnd.. In BLOOD Vol. 116 (pp. 944-945). Orlando, FL: AMER SOC HEMATOLOGY.
WoS12010 Hochhaus, A., Saglio, G., Larson, R. A., Kim, D. -W., Flinn, I. W., Goh, Y. -T., . . . Hughes, T. P. (2010). Nilotinib Lowers the Incidence of BCR-ABL Mutations and Improves the Molecular Response Kinetics Compared with Imatinib in Patients (Pts) with Newly Diagnosed Chronic Myeloid Leukemia (CML). In BLOOD Vol. 116 (pp. 1406-1407). Orlando, FL: AMER SOC HEMATOLOGY.
WoS12010 Soverini, S., Angelini, S., Turrini, E., Burnett, M., Ravegnini, G., Thornquist, M., . . . Martinelli, G. (2010). Specific Drug Transporter Genotypes Are Significantly Associated with Increased Rates of Major and Complete Molecular Responses In Newly Diagnosed Chronic Myeloid Leukemia Patients Treated with Imatinib - A TOPS Correlative Substudy. In BLOOD Vol. 116 (pp. 293-294). Orlando, FL: AMER SOC HEMATOLOGY. 2010 Hughes, T. P., Hochhaus, A., Saglio, G., Kim, D. -W., Jootar, S., le Coutre, P. D., . . . Kantarjian, H. M. (2010). ENESTnd Update: Continued Superiority of Nilotinib Versus Imatinib In Patients with Newly Diagnosed Chronic Myeloid Leukemia In Chronic Phase (CML-CP). In BLOOD Vol. 116 (pp. 94-95). Orlando, FL: AMER SOC HEMATOLOGY.
WoS52010 Morley, A., Bartley, P., Ross, D., Latham, S., Budgen, B., Hughes, E., . . . Hughes, T. (2010). Monitoring of CML by DNA qPCR. In JOURNAL OF MOLECULAR DIAGNOSTICS Vol. 12 (pp. 868). San Jose, CA: AMER SOC INVESTIGATIVE PATHOLOGY, INC. 2010 Martinelli, G., Hochhaus, A., Radich, J., Soverini, S., Branford, S., Erben, P., . . . Kim, D. (2010). DETECTION OF NEW MUTATIONS IN NILOTINIB-TREATED PATIENTS WITH IMATINIB-RESISTANT CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE. In HAEMATOLOGICA Vol. 95 (pp. 62). Barcelona, SPAIN: FERRATA STORTI FOUNDATION. 2010 Saglio, S., Hughes, T., Kim, D., Hanfstein, B., Gottardi, E., Branford, S., . . . Martinelli, G. (2010). RESPONSE TO NILOTINIB IN PATIENTS WITH IMATINIB-RESISTANT OR -INTOLERANT CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE (CML-CP) WITH DIFFERENT BCR-ABL TRANSCRIPT TYPES. In HAEMATOLOGICA Vol. 95 (pp. 342-343). FERRATA STORTI FOUNDATION. 2010 Stein, A., Shou, Y., Bottino, D., Chia, Y., Woodman, R., Martinelli, G., . . . Radich, J. (2010). RAPID INITIAL DECLINE IN BCR-ABL LEVELS IS ASSOCIATED WITH SUPERIOR RESPONSES IN IMATINIB-RESISTANT OR -INTOLERANT CHRONIC MYELOID LEUKEMIA PATIENTS IN CHRONIC PHASE (CML-CP) TREATED WITH NILOTINIB. In HAEMATOLOGICA Vol. 95 (pp. 56). Barcelona, SPAIN: FERRATA STORTI FOUNDATION. 2010 Tang, C., Schafranek, L., Watkins, D., Parker, W. T., Prime, J., White, D. L., & Hughes, T. (2010). Modelling of TKI Resistance In CML Cell Lines: Kinase Domain Mutations Usually Arise In the Setting of BCR-ABL Overexpression. In BLOOD Vol. 116 (pp. 1385). Orlando, FL: AMER SOC HEMATOLOGY. 2010 Hiwase, D. K., Engler, J., Saunders, V., White, D. L., & Hughes, T. (2010). In Contrast to Imatinib, Dasatinib Intracellular Concentration In CML-CD34<SUP>+</SUP> Progenitors Is Not Significantly Different Than That Observed In CD34<SUP>-</SUP> Mature Cells.. In BLOOD Vol. 116 (pp. 517). Orlando, FL: AMER SOC HEMATOLOGY. 2010 Hiwase, D. K., Eadie, L., Saunders, V., Hughes, T., & White, D. L. (2010). Proton Pump Inhibitors Augment Nilotinib and Dasatinib Mediated Bcr-Abl Kinase Inhibition.. In BLOOD Vol. 116 (pp. 1626-1627). Orlando, FL: AMER SOC HEMATOLOGY.
WoS12010 Hughes, T., Kim, D., Martinelli, G., Branford, S., Mueller, M., Beppu, L., . . . Hochhaus, A. (2010). EARLY MOLECULAR RESPONSE TO NILOTINIB IN PATIENTS WHO FAILED IMATINIB IS ASSOCIATED WITH A HIGHER PROBABILITY OF CYTOGENETIC RESPONSE IN CHRONIC MYELOID LEUKEMIA (CML). In HAEMATOLOGICA Vol. 95 (pp. 54). Barcelona, SPAIN: FERRATA STORTI FOUNDATION.
WoS12010 Kim, D., Kim, S., Goh, H., Pane, F., Hughes, T., Radich, J., . . . Kim, D. (2010). BCR-ABL MUTATION ANALYSIS USING BOTH ASO-PCR AND DIRECT SEQUENCING IN NEW CHRONIC PHASE CHRONIC MYELOID LEUKEMIA PATIENTS WITH SUBOPTIMAL RESPONSE OR TREATMENT FAILURE FROM IMATINIB TREATMENT. In HAEMATOLOGICA Vol. 95 (pp. 344-345). FERRATA STORTI FOUNDATION. 2009 Saglio, G., Hochhaus, A., Martinelli, G., Gottardi, E., Soverini, S., Branford, S., . . . Kim, D. (2009). DYNAMICS OF CYTOGENETIC AND MOLECULAR RESPONSE TO NILOTINIB IS SIMILAR IN IMATINIB-RESISTANT CHRONIC MYELOID LEUKEMIA PATIENTS IN CHRONIC PHASE (CML-CP) WITH AND WITHOUT BCR-ABL MUTATIONS EXCEPT E255K/V, Y253H, AND F359C/V. In HAEMATOLOGICA Vol. 94 (pp. 261). Berlin, GERMANY: FERRATA STORTI FOUNDATION. 2009 White, D. L., Saunders, V. A., Frede, A., Dang, P., Zrim, S., Osborn, M. P., . . . Hughes, T. (2009). The Functional Activity of the OCT-1 Protein Is Predictive of Molecular Response and Survival in CP-CML Patients Treated with Imatinib: A 5 Year Update of the TIDEL Trial. In BLOOD Vol. 114 (pp. 209-210). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Osborn, M. P., White, D. L., Saunders, V. A., Cambareri, B., Branford, S., Menelaou, A., . . . Hughes, T. P. (2009). Early Dose-Escalation in Chronic Myeloid Leukaemia Patients with Low Plasma Imatinib Levels Leads to Equivalent BCR-ABL Values and Drug Levels at 6 Months to Those with Optimal Drug Levels: First Analysis From the TIDEL II Trial of De-Novo Patients Treated with 600mg Imatinib.. In BLOOD Vol. 114 (pp. 465). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Martinelli, G., Kim, D. W., Saglio, G., Branford, S., Erben, P., Gottardi, E., . . . Radich, J. (2009). RESPONSE TO NILOTINIB IS SIMILAR IN IMATINIB-RESISTANT CHRONIC MYELOID LEUKEMIA PATIENTS IN ACCELERATED PHASE (CML-AP) WITH AND WITHOUT BCR-ABL MUTATIONS EXCEPT E25SK/V, Y253H, AND F359C/V. In HAEMATOLOGICA-THE HEMATOLOGY JOURNAL Vol. 94 (pp. 258-259). Berlin, GERMANY: FERRATA STORTI FOUNDATION.
WoS12009 Deininger, M., O'Brien, S. G., Guilhot, F., Goldman, J. M., Hochhaus, A., Hughes, T. P., . . . Druker, B. J. (2009). International Randomized Study of Interferon Vs STI571 (IRIS) 8-Year Follow up: Sustained Survival and Low Risk for Progression or Events in Patients with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Treated with Imatinib.. In BLOOD Vol. 114 (pp. 462). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS702009 Larson, R. A., Chia, Y. L., Granvil, C., Guilhot, F., Druker, B. J., O'Brien, S. G., . . . Wang, Y. (2009). Steady-State Imatinib Trough Levels as Well as Dose Interruptions Are Associated with Clinical Response (CCyR and MMR) and Adverse Events (AEs) in Patients with Chronic Myeloid Leukemia (CML) Receiving IM as Frontline Therapy. In BLOOD Vol. 114 (pp. 872). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS22009 Soverini, S., Angelini, S., Turrini, E., Pane, F., Quarantelli, F., Hughes, T. P., . . . Martinelli, G. (2009). Association Between Imatinib (IM) Transporters and Metabolizing Enzymes Genotype and Response in Newly Diagnosed Chronic Myeloid Leukemia (CML) Patients (Pts) Is Influenced by Ethnicity. In BLOOD Vol. 114 (pp. 1271). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Radich, J. P., Martinelli, G., Hochhaus, A., Gottardi, E., Soverini, S., Branford, S., . . . Saglio, G. (2009). Response and Outcomes to Nilotinib at 24 Months in Imatinib-Resistant Chronic Myeloid Leukemia Patients in Chronic Phase (CML-CP) and Accelerated Phase (CML-AP) with and without BCR-ABL Mutations.. In BLOOD Vol. 114 (pp. 464-465). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS12009 Kantarjian, H. M., Giles, F. J., Bhalla, K. N., Pinilla-Ibarz, J., Larson, R. A., Gattermann, N., . . . le Coutre, P. D. (2009). Update On Imatinib-Resistant Chronic Myeloid Leukemia Patients in Chronic Phase (CML-CP) On Nilotinib Therapy at 24 Months: Clinical Response, Safety, and Long-Term Outcomes.. In BLOOD Vol. 114 (pp. 464). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS142009 Branford, S., Kim, D. -W., Soverini, S., Gottardi, E., Beppu, L., Mueller, M. C., . . . Hochhaus, A. (2009). Molecular Response at 3 Months On Nilotinib Therapy Predicts Response and Long-Term Outcomes in Patients with Imatinib-Resistant or -Intolerant Chronic Myeloid Leukemia in Chronic Phase (CML-CP). In BLOOD Vol. 114 (pp. 1275-1276). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS12009 Branford, S., Hochhaus, A., Mueller, M., Bahceci, E., Ploughman, L., Mukhopadhyay, J., & Hughes, T. (2009). Analysis of Molecular Data and the Emergence of Mutations for Chronic-Phase Chronic Myelogenous Leukemia (CML-CP) Patients Treated with Dasatinib After Imatinib Failure.. In BLOOD Vol. 114 (pp. 1270-1271). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Hughes, T. (2009). Reduction of bcr-abl transcript levels with imatinib (Gleevec) in chronic myeloid leukemia (Chronic Phase). In P and T Vol. 34 (pp. 96-97). 2009 Kim, D. -W., Granvil, C., Demirhan, E., Reynolds, J., Jin, Y., Wang, Y., . . . Guilhot, F. (2009). Comparison of Steady-State Imatinib (IM) Trough Levels, Clinical Response, and Safety Between Caucasian and Asian Patients with Chronic Lyeloid Leukemia in Chronic Phase (CML-CP) Treated with 400mg and 800mg Daily Doses of IM in the Tyrosine Kinase Inhibitor Optimization and Selectivity (TOPS) Study.. In BLOOD Vol. 114 (pp. 462-463). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS12009 Baccarani, M., Druker, B. J., Cortes-Franco, J., Hughes, T. P., Kim, D. -W., Pane, F., . . . Guilhot, F. (2009). 24 Months Update of the TOPS Study: a Phase III, Randomized, Open-Label Study of 400mg/d (SD-IM) Versus 800mg/d (HD-IM) of Imatinib Mesylate (IM) in Patients (Pts) with Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP). In BLOOD Vol. 114 (pp. 142-143). New Orleans, LA: AMER SOC HEMATOLOGY.
WoS122009 Hiwase, D. K., White, D. L., Powell, J. A., Saunders, V. A., Zrim, S., Frede, A., . . . Hughes, T. (2009). Blocking of Cytokine Survival Signals along with Intense Bcr-Abl Kinase Inhibition May Eradicate CML Progenitor Cells. In BLOOD Vol. 114 (pp. 1258-1259). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Osborn, M. P., Branford, S., White, D. L., Seymour, J. F., Columbus, R., Taylor, K., . . . Hughes, T. P. (2009). Maintaining Imatinib ≥600 Mg Daily in the First 12 Months of Chronic Phase CML Treatment Is Associated with Superior Event-Free Survival at 5 Years.. In BLOOD Vol. 114 (pp. 461-462). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Esposito, N., Quintarelli, C., Colavita, I., Izzo, B., Peluso, A. L., Ruoppolo, M., . . . Pane, F. (2009). Reduced Expression Level of SHP1 Gives An Additive Survival Advantage to the Ph plus Cells of Chronic Myeloid Leukemia (CML) Patients and Provides a Novel Pretreatment Predictor of Major Molecular Response Achievement in CML Patients. In BLOOD Vol. 114 (pp. 871-872). New Orleans, LA: AMER SOC HEMATOLOGY. 2009 Engler, J. R., Frede, A., Saunders, V. A., Zannettino, A. C. W., White, D. L., & Hughes, T. P. (2009). OCT-1 Activity in CML CD34+Cells Is Not Predictive of Molecular Response to Imatinib Treatment in CP-CML Patients, Despite the Strong Predictive Value of MNC OCT-1 Activity. In BLOOD Vol. 114 (pp. 861). New Orleans, LA: AMER SOC HEMATOLOGY. 2008 Engler, J. R., Frede, A., Zannettino, A. C. W., White, D. L., & Hughes, T. P. (2008). Reduced Activity of the OCT-1 Protein in Primitive CML Cells: A Likely Determinant of Stem Cell Resistance in Imatinib Treated CML Patients. In BLOOD Vol. 112 (pp. 80). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS22008 Hiwase, D. K., White, D. L., Saunders, V. A., Melo, J. V., Kumar, S., & Hughes, T. P. (2008). Short-Term Intense Bcr-Abl Kinase Inhibition Is Adequate to Trigger Cell Death in CML Cell Lines but Not in CML-CD34+Cells Unless They Are Growth Factor Deprived. In BLOOD Vol. 112 (pp. 397). San Francisco, CA: AMER SOC HEMATOLOGY. 2008 Esposito, N., Colavita, I., Quarantelli, F., Izzo, B., Luciano, L., Del Vecchio, L., . . . Pane, F. (2008). A decreased Level of Shp1 provides an additive survival advantage to the Ph plus Cells of CML Patients and may account for Resistance to Imatinib Treatment. In BLOOD Vol. 112 (pp. 1093). San Francisco, CA: AMER SOC HEMATOLOGY. 2008 White, D., Dang, P., Obbink, K. G., Frede, A., Kok, C., Hughes, T. P., & D'Andrea, R. (2008). Enhancing the Functional Activity of the OCT-1 Influx Pump May Overcome the Negative Impact of Low OCT-1 Activity in Imatinib Treated CML Patients. In BLOOD Vol. 112 (pp. 268-269). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS12008 Cross, C., Hochhaus, A., Mueller, M., Saglio, G., Branford, S., Hughes, T., . . . White, H. (2008). DEVELOPMENT OF PROTOTYPE REFERENCE MATERIALS FOR BCR-ABL QUANTITATIVE RT-PCR. In HAEMATOLOGICA Vol. 93 (pp. 54). Copenhagen, DENMARK: FERRATA STORTI FOUNDATION. 2008 Cortes, J., Baccarani, M., Guilhot, F., Druker, B. J., Branford, S., Kim, D. -W., . . . Hughes, T. P. (2008). A Phase III, Randomized. Open-Label Study of 400 Mg Versus 800 Mg of Imatinib Mesylate (1M) in Patients (pts) with Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Using Molecular Endpoints: 1-Year Results of TOPS (Tyrosine Kinase Inhibitor Optimization and Selectivity) Study. In BLOOD Vol. 112 (pp. 130-131). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS142008 White, D., Saunders, V., Quinn, S., & Hughes, T. (2008). PATIENT-SPECIFIC IC50 ASSAYS IN IMATINIB-RESISTANT CIVIL PATIENTS ARE HIGHLY VARIABLE AND MAY BE CLINICALLY RELEVANT. In HAEMATOLOGICA-THE HEMATOLOGY JOURNAL Vol. 93 (pp. 41). Copenhagen, DENMARK: FERRATA STORTI FOUNDATION. 2008 Cortes, J. G., Baccarani, M., Guilhot, F., Druker, B. J., Yu, R., Rudoltz, M., . . . Hughes, T. (2008). FIRST REPORT OF THE TOPS STUDY: A RANDOMIZED PHASE III TRIAL OF 400MG VS 800MG IMATINIB IN PATIENTS WITH NEWLY DIAGNOSED, PREVIOUSLY UNTREATED CML IN CHRONIC PHASE USING MOLECULAR ENDPOINTS. In HAEMATOLOGICA-THE HEMATOLOGY JOURNAL Vol. 93 (pp. 160). Copenhagen, DENMARK: FERRATA STORTI FOUNDATION.
WoS62008 Mullighan, C. G., Radtke, I., Zhang, J., Phillips, L. A., Su, X., Ma, J., . . . Downing, J. R. (2008). Genome-Wide Analysis of Genetic Alterations in Chronic Myelogenous Leukemia. In BLOOD Vol. 112 (pp. 397-398). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS62008 Vandyke, K., Dewar, A., Diamond, P., Fitter, S., Farrugia, A. N., To, L. B., . . . Zannettino, A. C. W. (2008). Dasatinib (Sprycel™) Inhibits Oteoclast Activity <i>in Vitro</i> and <i>in Vivo</i> Via a C-Fms-Dependent and C-Src-Independent Mechanism. In BLOOD Vol. 112 (pp. 1102-1103). San Francisco, CA: AMER SOC HEMATOLOGY. 2008 Morley, A. A., Bartley, P., Ross, D. M., Latham, S., Martin-Harris, H., Budgen, B., . . . Hughes, T. (2008). DNA-Based Monitoring of Minimal Residual Disease(MRD) in Chronic Myeloid Leukemia(CML). In BLOOD Vol. 112 (pp. 406). San Francisco, CA: AMER SOC HEMATOLOGY. 2008 Shah, N. P., Kantarjian, H. M., Kim, D. W., Réa, D., Dorlhiac-Llacer, P. E., Milone, J. H., . . . Hochhaus, A. (2008). Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia. In Journal of Clinical Oncology Vol. 26 (pp. 3204-3212). Vienna, AUSTRIA: AMER SOC CLINICAL ONCOLOGY.
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WoS1302008 Mueller, M. C., Cortes, J., Kim, D. -W., Druker, B. J., Erben, P., Pasquini, R., . . . Hochhaus, A. (2008). Dasatinib Efficacy in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) and Pre-Existing BCR-ABL Mutations. In BLOOD Vol. 112 (pp. 171-172). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS52008 Hochhaus, A., Mueller, M. C., Radich, J., Branford, S., Hanfstein, B., Rousselot, P., . . . Hughes, T. P. (2008). Dasatinib-Associated Major Molecular Responses Are Rapidly Achieved in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Following Resistance, Suboptimal Response, or Intolerance on Imatinib. In BLOOD Vol. 112 (pp. 400). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS42008 Esposito, N., Quarantelli, F., Luciano, L., Izzo, B., Peluso, A. L., Picardi, M., . . . Pane, F. (2008). The Expression of shp-1 and SHP-2: A Novel Powerful Predictor of Major Molecular Response (MMR) Achievement in Chronic Myeloid Leukemia Gleevec-Treated Patients Enrolled into the TOPS Clinical Trial. In BLOOD Vol. 112 (pp. 404). San Francisco, CA: AMER SOC HEMATOLOGY. 2008 Hughes, T. P., Hochhaus, A., Branford, S., Mueller, M. C., Foroni, L., Druker, B. J., . . . Goldman, J. M. (2008). Reduction of BCR-ABL Transcript Levels at 6, 12, and 18 Months (mo) Correlates with Long-Term Outcomes on Imatinib (IM) at 72 Mo: An Analysis from the International Randomized Study of Interferon versus STI571 (IRIS) in Patients (pts) with Chronic Phase Chronic Myeloid Leukemia (CML-CP). In BLOOD Vol. 112 (pp. 129-130). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS102008 Guilhot, F., Hughes, T. P., Cortes, J., Wang, Y., Hayes, M., Gichangi, A., . . . Baccarani, M. (2008). Imatinib (IM) Pharmacokinetic (PK) Exposure and Its Correlation with Clinical Outcome in Patients with Chronic-Phase Chronic Myeloid Leukemia (CML-CP) for 400 Mg and 800 Mg Daily Doses (Tyrosine Kinase Dose Optimization Study [TOPS]). In BLOOD Vol. 112 (pp. 170-171). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS42008 Hochhaus, A., Kim, D. -W., Martinelli, G., Hughes, T. P., Soverini, S., Branford, S., . . . Radich, J. P. (2008). Nilotinib Efficacy According to Baseline BCR-ABL Mutations in Patients with Imatinib-Resistant Chronic Myeloid Leukemia in Chronic Phase (CML-CP). In BLOOD Vol. 112 (pp. 1103-1104). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS22008 Branford, S., Lawrence, R., Grigg, A., Seymour, J. F., Schwarerl, A., Arthur, C., . . . Hughes, T. (2008). Long Term Follow up of Patients with CML in Chronic Phase Treated with First-Line Imatinib Suggests That Earlier Achievement of a Major Molecular Response Leads to Greater Stability of Response. In BLOOD Vol. 112 (pp. 735-736). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS32008 Branford, S., Lawrence, R., Fletcher, L., Field, C., Rudzki, Z., & Hughes, T. (2008). The Initial Molecular Response of Chronic Phase CML Patients Treated with Second Generation ABL Inhibitor Therapy after Imatinib Failure Can Predict Inadequate Response and Provide Indications for Rational Mutation Screening. In BLOOD Vol. 112 (pp. 128). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS22008 White, D. L., Saunders, V. A., Kalebic, T., & Hughes, T. P. (2008). The IC50 Assay Is Predictive of Molecular Response, and Indicative of Optimal Dose in De-Novo CML Patients. In BLOOD Vol. 112 (pp. 405). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS12008 White, D. L., Saunders, V. A., Dang, P., Frede, A., Eadie, L., Soverini, S., . . . Hughes, T. (2008). CML Patients with Low OCT-1 Activity Achieve Better Molecular Responses on High Dose Imatinib Than on Standard Dose. Those with High OCT-1 Activity Have Excellent Responses on Either Dose: A TOPS Correlative Study. In BLOOD Vol. 112 (pp. 1093-1094). San Francisco, CA: AMER SOC HEMATOLOGY.
WoS32008 Radich, J., Kim, D. -W., Martinelli, G., Soverini, S., Branford, S., Mueller, M., . . . Saglio, G. (2008). RESPONSE TO NILOTINIB IN CHRONIC MYELOGENOUS LEUKEMIA PATIENTS IN CHRONIC PHASE (CML-CP) ACCORDING TO BCR-ABL MUTATIONS AT BASELINE. In HAEMATOLOGICA Vol. 93 (pp. 55). Copenhagen, DENMARK: FERRATA STORTI FOUNDATION.
WoS32007 Branford, S., Fletcher, L., Cross, N. C. P., Hochhaus, A., Mueller, M. C., Kim, D. -W., . . . Hughes, T. (2007). Validation of the international scale for measurement of BCR-ABL by RQ-PCR based on deriving laboratory-specific conversion factors. In BLOOD Vol. 110 (pp. 307A). Atlanta, GA: AMER SOC HEMATOLOGY.
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WoS12007 Toplin, J., Fuller, C., Fletcher, L., Wong, S., Maslak, P., Cortes, J., . . . Beillard, E. (2007). An MMR control RNA for reliable monitoring of BCR-ABL transcripts in treated CML patients. In BLOOD Vol. 110 (pp. 863A-864A). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI2007 Hughes, T., Saglio, G., Martinelli, G., Kim, D. -W., Soverini, S., Mueller, M., . . . Hochhaus, A. (2007). Responses and disease progression in CML-CP patients treated with nilotinib after imatinib failure appear to be affected by the BCR-ABL mutation status and types. In BLOOD Vol. 110 (pp. 101A). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS132007 Saglio, G., Kim, D. -W., Hochhaus, A., Soverini, S., Erben, P., Branford, S., . . . Radich, J. (2007). Correlation of clinical response to nilotinib with BCR-ABL mutation status in advanced phase chronic myelogenous leukemia (CML-AP) patients with imatinib-resistance or intolerance. In BLOOD Vol. 110 (pp. 576A-577A). Atlanta, GA: AMER SOC HEMATOLOGY.
WoS42007 Stone, R. M., Kantarjian, H. M., Baccarani, M., Lipton, J. H., Hughes, T., Ezzeddine, R., . . . Hochhaus, A. (2007). Efficacy of dasatinib in patients with chronic-phase chronic myelogenous leukemia with resistance or intolerance to imatinib: 2-year follow-up data from START-C (CA180-013). In BLOOD Vol. 110 (pp. 225A). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS142007 Morley, A., Bartley, P., Martin-Harris, H., Latham, S., Ross, D., & Hughes, T. (2007). DNA-based measurement of BCR ABL in chronic myeloid leukemia (CML). In BLOOD Vol. 110 (pp. 865A-866A). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI2007 Hiwase, D. K., White, D. L., Saunders, V. A., Dang, P., Venables, A., Eadie, L., . . . Hughes, T. P. (2007). In contrast to imatinib, OCT-1 mediated influx has minimal impact on cellular uptake of dasatinib in CML patients at diagnosis. In BLOOD Vol. 110 (pp. 575A-576A). Atlanta, GA: AMER SOC HEMATOLOGY.
WoS72006 White, D., Saunders, V., Dang, P., Venables, A., Zrim, S., Reynolds, J., . . . Hughes, T. (2006). Molecular response to imatinib is dependent on dose in CML patients with low OCT-1 influx activity. Patients with high activity may respond equally well to standard or increased dose imatinib.. In BLOOD Vol. 108 (pp. 222A). Orlando, FL: AMER SOC HEMATOLOGY. 2006 White, D., Dang, P., Venables, A., Saunders, V., Zrim, S., Zannettino, A., . . . Hughes, T. (2006). ABCB1 overexpression may predispose imatinib treated CML patients to the development of Abl kinase domain mutations, and may be an important contributor to acquired resistance.. In BLOOD Vol. 108 (pp. 608A). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS22006 Branford, S., Hughes, T., Stylian, S., Schwarer, A. P., Arthur, C., Filshie, R., . . . Taylor, K. M. (2006). Significant reduction of BCR-ABL transcripts after switching to imatinib therapy in patients with CML and complete or near-complete cytogenetic responses to interferon-alpha (IFN).. In BLOOD Vol. 108 (pp. 607A-608A). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS12006 Shah, N. P., Skaggs, B., Branford, S., Hughes, T. P., Nicoll, J. M., Paquette, R. L., & Sawyers, C. L. (2006). The most common dasatinib-resistant BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia are sensitive to VX-680: Rationale for early combination kinase inhibitor therapy.. In BLOOD Vol. 108 (pp. 617A). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS22006 Hochhaus, A., Erben, P., Branford, S., Radich, J., Kim, D. W., Martinelli, G., . . . Baccarani, M. (2006). Hematologic and cytogenetic response dynamics to nilotinib (AMN107) depend on the type of BCR-ABL mutations in patients with chronic myelogeneous leukemia (CML) after imatinib failure.. In BLOOD Vol. 108 (pp. 225A). Orlando, FL: AMER SOC HEMATOLOGY.
WoS42006 Shah, N. P., Skaggs, B., Branford, S., Hughes, T. P., Nicoll, J. M., Paquette, R. L., & Sawyers, C. L. (2006). Sequential kinase inhibitor therapy in CML patients can select for cells harboring compound BCR-ABL kinase domain mutations with increased oncogenic potency: Rationale for early combination therapy of ABL kinase inhibitors.. In BLOOD Vol. 108 (pp. 225A-226A). Orlando, FL: AMER SOC HEMATOLOGY.
WoS42006 Branford, S., Cross, N. C. P., Hochhaus, A., Radich, J., Saglio, G., Kim, D. W., . . . Hughes, T. (2006). First results from a collaborative initiative to develop an international scale for the measurement of BCR-ABL by RQ-PCR based on deriving laboratory-specific conversion factors.. In BLOOD Vol. 108 (pp. 221A). Orlando, FL: AMER SOC HEMATOLOGY.
WoS12006 Branford, S., Seymour, J. F., Grigg, A., Arthur, C., Lynch, K., & Hughes, T. (2006). Increasing frequency and marked stability of complete molecular response is observed in imatinib-treated CML patients with long-term follow up.. In BLOOD Vol. 108 (pp. 131A). Orlando, FL: AMER SOC HEMATOLOGY.
WoS42006 Ross, D. M., Hughes, T. P., & Branford, S. (2006). Reverse transcription with a random pentadecamer primer increases the sensitivity of quantitative PCR for BCR-ABL.. In BLOOD Vol. 108 (pp. 662A-663A). Orlando, FL: AMER SOC HEMATOLOGY.
DOI2006 Kaeda, J., Hochhaus, A., Radich, J., Branford, S., So, C., Gathmann, I., . . . Hughes, T. (2006). Patients with chronic phase CML in the IRIS study who receive imatinib mesylate (IM) 2nd line after prior IFN/Ara-C have sustained complete cytogenetic and major molecular response rates similar to 1st line IM patients.. In BLOOD Vol. 108 (pp. 607A). Orlando, FL: AMER SOC HEMATOLOGY.
DOI WoS22005 Hughes, T. P., Branford, S., Reynolds, J., Koelmeyer, R., Seymour, J., Taylor, K., . . . Grigg, A. (2005). Maintenance of imatinib dose intensity in the first six months of therapy for newly diagnosed patients with CML is predictive of molecular response, independent of the ability to increase dose at a later point.. In BLOOD Vol. 106 (pp. 51A). Atlanta, GA: AMER SOC HEMATOLOGY.
WoS42005 Lyons, A. B., Hughes, T. P., & Viboonjuntra, P. (2005). Production of GM-CSF by CML cells can modulate the anti-proliferative and pro-apoptotic effects of imatinib on CML CD34<SUP>+</SUP> cells. In BLOOD Vol. 106 (pp. 803A). Atlanta, GA: AMER SOC HEMATOLOGY.
WoS12005 Shah, N. P., Nicoll, J. M., Branford, S., Hughes, T. P., Paquette, R. L., Talpaz, M., . . . Sawyers, C. L. (2005). Molecular analysis of dasatinib resistance mechanisms in CML patients identifies novel BCR-ABL mutations predicted to retain sensitivity to imatinib: Rationale for combination tyrosine kinase inhibitor therapy.. In BLOOD Vol. 106 (pp. 318A). Atlanta, GA: AMER SOC HEMATOLOGY.
WoS112005 Roberts, M. M., Ross, D. M., Hughes, T. P., & To, L. B. (2005). Lymphoid foci in bone marrow of patients with chronic myeloid leukaemia treated with imatinib.. In BLOOD Vol. 106 (pp. 568A). Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS12004 Shah, N. P., Branford, S., Hughes, T. P., Nicoll, J. M., Decillis, A. P., & Sawyers, C. L. (2004). Major cytogenetic responses to BMS-354825 in patients with chronic myeloid leukemia are associated with a one to two log reduction in <i>BCR</i>-<i>ABL</i> transcript.. In BLOOD Vol. 104 (pp. 288A). San Diego, CA: AMER SOC HEMATOLOGY.
WoS42004 Hughes, T. C., Chan, G. Y. N., Evans, M. D. M., Johnson, G., Le, T. P. T., McFarland, G., . . . Xie, R. Z. (2004). Perfluoropolyether corneal onlays: Adhesive development. In Transactions - 7th World Biomaterials Congress (pp. 1653). 2004 Hughes, T. C., Chan, G. Y. N., Evans, M. D. M., Johnson, G., Knower, W. S., Le, T. P. T., . . . Xie, R. Z. (2004). Hydrogel-like perfluoropolyethers. In Transactions - 7th World Biomaterials Congress (pp. 1607).
Scopus12004 McLean, K. M., Beumer, G. J., Bojarski, B., Chan, G. Y. N., Chaouk, H., Evans, M. D. M., . . . Xie, R. Z. (2004). Corneal implants for refractive error correction. In Transactions - 7th World Biomaterials Congress (pp. 1605). 2003 Branford, S., Rudzki, Z., Miller, B., Grigg, A., Seymour, J. F., Schwarer, A., . . . Hughes, T. P. (2003). Mutations in the catalytic core (P-Loop) of the BCR-ABL kinase domain of imatinib-treated chronic myeloid leukemia patients in chronic phase are strongly associated with imminent progression to blast crisis.. In BLOOD Vol. 102 (pp. 71A). SAN DIEGO, CALIFORNIA: AMER SOC HEMATOLOGY.
WoS32003 Branford, S., Rudzki, Z., Grigg, A., Seymour, J. F., Taylor, K., Herrmann, R., . . . Hughes, T. P. (2003). The incidence of BCR-ABL kinase mutations in chronic myeloid leukemia patients is as high in the second year of imatinib therapy as the first but survival after mutation detection is significantly longer for patients with mutations detected in the second year of therapy.. In BLOOD Vol. 102 (pp. 414A). SAN DIEGO, CALIFORNIA: AMER SOC HEMATOLOGY.
WoS62003 Hughes, T. P., Branford, S., Matthews, J., Seymour, J., Taylor, K., Guzzo-Pernell, N., . . . Grigg, A. (2003). Trial of higher dose imatinib with selective intensification in newly diagnosed CML patients in the chronic phase.. In BLOOD Vol. 102 (pp. 31A). SAN DIEGO, CALIFORNIA: AMER SOC HEMATOLOGY.
WoS162003 Baccarani, M., Cortes, J., Daley, G. Q., Druker, B. J., Guilhot, F., Hochhaus, A., . . . Mahon, F. X. (2003). Comments on the hammersmith policy. In Seminars in Hematology Vol. 40 (pp. 104-113). Elsevier BV.
DOI1997 Moore, S., Levesque, J. P., Haylock, D. N., McDiarmid, L., Samels, L., To, L. B., . . . Hughes, T. P. (1997). Kit ligand as the sole stimulatory agent induces marked proliferation of CD34+ CML cells without a concomitant increase in adhesion.. In BLOOD Vol. 90 (pp. 1746). W B SAUNDERS CO.
WoS11995 Juttner, C. A., To, L. B., Haylock, D. N., Dyson, P. G., Simmons, P. J., Bayly, J., . . . Thorp, D. (1995). Blood progenitor cells: Biologic and clinical issues. In Bone Marrow Transplantation Vol. 15. 1995 Lewis, L. D., Haylock, D. N., Moore, S., To, L. B., Juttner, C. A., & Hughes, T. P. (1995). Identification of normal primitive progenitors in blood and mobilised blood in chronic myeloid leukaemia.. In BLOOD Vol. 86 (pp. 2085). W B SAUNDERS CO.
WoS11993 Cullis, J. O., Szydlo, R. M., Cross, N. C. P., Marks, D. I., Schwarer, A. P., Hughes, T. P., . . . Goldman, J. M. (1993). Matched unrelated donor bone marrow transplantation for chronic myeloid leukaemia in chronic phase: Comparison of ex vivo and in vivo T-cell depletion. In Bone Marrow Transplantation Vol. 11 (pp. 107-111). England.
Scopus12 Europe PMC41991 Goldman, J. M., & Hughes, T. (1991). Detection and significance of minimal residual disease in patients with leukaemia and lymphoma. In Bone Marrow Transplantation Vol. 7 (pp. 66-69). England.
Scopus3 Europe PMC21991 Hughes, T. P., O'Shea, P., Morgan, G., Martiat, P., & Goldman, J. M. (1991). Persistence of BCR/ABL transcripts after BMT for CML detected by PCR reflects a high risk of relapse. In Bone Marrow Transplantation Vol. 7 (pp. 23). England.
Scopus5 -
Conference Items
Year Citation 2018 Shanmuganathan, N., Branford, S., Yong, A. S. M., Hiwase, D. K., Yeung, D. T., Ross, D. M., & Hughes, T. P. (2018). The e13a2 BCR-ABL1 Transcript Is Associated with Higher Rates of Molecular Recurrence after Treatment-Free Remission Attempts: Retrospective Analysis of the Adelaide Cohort. Poster session presented at the meeting of BLOOD. San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS52018 Asari, K., Leclercq, T., Srihari, S., Fitter, S., Yeung, D., Hughes, T., . . . White, D. L. (2018). in vitro modelling of Ph-like ALL uncovers novel genomic alterations associated with TKI-resistance as a consequence of targeted therapy. Poster session presented at the meeting of Childhood Leukaemia and Lymphoma Symposium. Helsinki, Finland. 2018 Heatley, S. L., Mayne, B. T., McClure, B. J., Kok, C., Sadras, T., Dang, P., . . . White, D. L. (2018). Exploring the genomic diversity of AYA and adult high-risk B-ALL cases by mRNA sequencing. Poster session presented at the meeting of 23rd Congress of European Hematology Association. Stockholm, Sweden. 2018 Heatley, S. L., McClure, B. J., Kok, C., Sadras, T., Dang, P., Galbraith, K., . . . White, D. L. (2018). Exploring the genomic diversity of adult and AYA cases with high-risk B-ALL by mRNA sequencing. Poster session presented at the meeting of NDLR. 2018 Pagani, I. S., Kok, C., Saunders, V., Schwarer, A., Hughes, T. P., White, D. L., & Ross, D. M. (2018). Association of mitochondrial DNA (mtDNA) mutations at diagnosis with treatment response in chronic myeloid leukaemia (CML) patients. Poster session presented at the meeting of NDLR. 2018 Lu, L., Kok, C., Saunders, V., Nievergall, E., White, D. L., & Hughes, T. P. (2018). TGF-α predicts TKI treated CML patients who fail to achieve early molecular response. Poster session presented at the meeting of NDLR. 2018 Downes, C. E., McClure, B. J., Mayne, B. T., Bruning, J. B., Heatley, S. L., Kok, C., . . . White, D. L. (2018). Identification and computational modelling of ruxolitinib resistant mutations in JAK2-rearranged B-cell acute lymphoblastic leukaemia. Poster session presented at the meeting of APG Student Awards. 2018 Downes, C. E., McClure, B. J., Mayne, B. T., Bruning, J. B., Heatley, S. L., Kok, C., . . . White, D. L. (2018). Identification of ruxolitinib resistance mutations in Pro-B cells driven by a high-risk JAK2 fusion in B-cell acute lymphoblastic leukaemia. Poster session presented at the meeting of ASMR. 2018 Downes, C. E., McClure, B. J., Mayne, B. T., Bruning, J. B., Heatley, S. L., Kok, C., . . . White, D. L. (2018). Identification and Characterisation of Ruxolitinib Resistant Mutations in JAK2-rearranged B-cell Acute Lymphoblastic Leukaemia. Poster session presented at the meeting of AGTA. 2018 Downes, C. E., McClure, B. J., Mayne, B. T., Bruning, J. B., Heatley, S. L., Kok, C., . . . White, D. L. (2018). Identification of mutations that cause ruxolitinib resistance in Pro-B cells driven by a high-risk B-ALL JAK2-fusion.. Poster session presented at the meeting of ANZCHOG. 2018 Downes, C. E., McClure, B. J., Mayne, B. T., Bruning, J. B., Heatley, S. L., Kok, C., . . . White, D. L. (2018). Identification and computational modelling of ruxolitinib resistant mutations in JAK2-rearranged B-cell acute lymphoblastic leukaemia. Poster session presented at the meeting of SAHMRI Scientific Seminar. 2018 Downes, C. E., McClure, B. J., Mayne, B. T., Bruning, J. B., Heatley, S. L., Kok, C., . . . White, D. L. (2018). Identification and computational modelling of ruxolitinib resistant mutations in JAK2-rearranged B-cell acute lymphoblastic leukaemia. Poster session presented at the meeting of EMBL Australia Postgraduate Symposium. 2017 El-Khawanky, N., Hughes, A., Yu, W., Clarson, J., Lopez, A. F., Brown, M., . . . Yong, A. (2017). CD123 Chimeric Antigen Receptor T-cells in Chronic and Acute Myeloid Leukaemia: pre-clinical in vitro studies. Poster session presented at the meeting of HAA. 2017 El-Khawanky, N., Hughes, T. P., Clarson, J., Yu, W., White, D. L., & Yong, A. (2017). Anti-CD123 Chimeric Antigen Receptor (CAR) T-cells in Chronic and Acute Myeloid Leukaemia: pre-clinical in vitro studies. Poster session presented at the meeting of ASMR. 2017 McClure, B. J., Heatley, S. L., Kok, C., Sadras, T., An, J., Quek, K., . . . White, D. L. (2017). EP300-ZNF384 is a recurrent fusion gene with distinct gene expression in adolescent/young adult pre-B-ALL patients. Poster session presented at the meeting of ANZCHOG. 2017 Heatley, S. L., Sadras, T., Kok, C., Nievergall, E., Quek, K., Dang, P., . . . White, D. L. (2017). High Prevalence of Relapse in Australian Children with Ph-like Acute Lymphoblastic Leukemia Despite Risk-Adapted Treatment. Poster session presented at the meeting of ANZCHOG. 2017 Asari, K., Sadras, T., Srihari, S., Fitter, S., An, J., Zannettino, A. C., . . . White, D. L. (2017). in vitro Modelling of Ph-like ALL Fusions Uncovers Novel Kinase-domain Mutations as a Mode of TKI-resistance and Potential Consequence of Targeted TKI Therapy. Poster session presented at the meeting of ANZCHOG. 2017 Ross, D. M., Pagani, I. S., Shanmuganathan, N., Seymour, J. F., Mills, A., Filshie, R., . . . Hughes, T. P. (2017). Long-Term Follow-up of the ALLG CML8 Twister Study of Treatment-Free Remission (TFR) in Patients with Chronic Myeloid Leukemia (CML). Poster session presented at the meeting of 59th ASH Annual Meeting & Exposition. 2017 Hughes, A., Clarson, J., White, D. L., Yeung, D., Hughes, T. P., & Yong, A. S. M. (2017). Nilotinib/Interferon-α Combination Rapidly Enhances Leukaemia-Associated Antigen Specific Cytotoxic T-Lymphocyte Immune Responses, Limits Natural Killer Cell Maturation and Triggers B Cell Remodelling. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
WoS42017 Yeung, D., Grigg, A., Shanmuganathan, N., Cunningham, I., Shortt, J., Rowling, P., . . . Hughes, T. P. (2017). Nilotinib in Combination with Pegylated Interferon Alfa-2b for CP-CML Leads to High Molecular Response Rates: Interim Results of the Pinnacle Study. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY. 2017 Pagani, I. S., Dang, P., Kommers, I. O., Goyne, J., Saunders, V. A., Prime, J. A., . . . Ross, D. M. (2017). COMPARISON OF GENOMIC DNA AND REVERSE TRANSCRIPTASE Q-PCR FOR THE MONITORING OF FIRST-LINE IMATINIB TREATMENT: AN ALLG CML9 SUB-STUDY. Poster session presented at the meeting of HAEMATOLOGICA. Madrid, SPAIN: FERRATA STORTI FOUNDATION. 2017 Cortes, J. E., Kantarjian, H. M., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., Chuah, C., . . . Mueller, M. C. (2017). 5-YR RESULTS FROM THE PIVOTAL PHASE 2 PONATINIB PACE TRIAL: EFFICACY, SAFETY AND LANDMARK ANALYSIS IN HEAVILY PRETREATED PATIENTS (PTS) WITH CHRONIC-PHASE CHRONIC MYELOID LEUKEMIA (CP-CML). Poster session presented at the meeting of HAEMATOLOGICA. Madrid, SPAIN: FERRATA STORTI FOUNDATION. 2017 Hochhaus, A., Jabbour, E., Kantarjian, H., Guilhot, F., Kota, V., Hughes, T. P., . . . Cortes, J. E. (2017). 5-YEAR EFFICACY OF DASATINIB AND IMATINIB IN NEWLY DIAGNOSED PATIENTS WITH CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE (CML-CP) WITH DOSE MODIFICATIONS FROM DASISION. Poster session presented at the meeting of HAEMATOLOGICA. Madrid, SPAIN: FERRATA STORTI FOUNDATION. 2017 Downes, C. E., McClure, B. M., Heatley, S. H., Sadras, T. S., Hughes, T. H., Kok, C. K., . . . White, D. W. (2017). Identification and cloning of a novel GOLGA4-JAK2 fusion from an adult patient with B-cell Acute Lymphoblastic Leukaemia. Poster session presented at the meeting of Poster session presented at the ASMR SA Scientific Meeting. Adelaide. 2017 Heatley, S., Sadras, T., Kok, C., Nievergall, E., Quek, K., Dang, P., . . . White, D. (2017). High prevalence of relapse in children with Philadelphia-like acute lymphoblastic leukemia despite risk-adapted treatment. Poster session presented at the meeting of Abstracts of the 57th Annual Meeting of the American Society of Hematology, as published in Blood. Orlando, FL: American Society of Hematology.
DOI WoS22016 Mueller, M., Baccarani, M., Deininger, M. W., Guilhot, F., Hochhaus, A., Hughes, T. P., . . . Cortes, J. E. (2016). LANDMARK ANALYSES IN THE PIVOTAL PONATINIB PACE TRIAL: IMPACT OF EARLY RESPONSES ON 3-YEAR OUTCOMES IN HEAVILY PRETREATED CP-CML PATIENTS. Poster session presented at the meeting of HAEMATOLOGICA. Copenhagen, DENMARK: FERRATA STORTI FOUNDATION. 2016 Kok, C. H., Watkins, D., Wang, J., Saunders, V., Goyne, J., Pagani, I., . . . White, D. (2016). HIGH GENE EXPRESSION OF HIST1H2AG AND HIST1H4A REDUCES IMATINIB UPTAKE INTO CML CELLS AND PREDICTS POOR RESPONSE TO FRONTLINE IMATINIB THERAPY. Poster session presented at the meeting of HAEMATOLOGICA. Copenhagen, DENMARK: FERRATA STORTI FOUNDATION. 2016 Hughes, T. P., Boquimpani, C., Takahashi, N., Benyamini, N., Clementino, N. C. D., Shuvaev, V., . . . Mahon, F. X. (2016). RESULTS FROM ENESTOP: TREATMENT-FREE REMISSION (TFR) FOLLOWING SWITCH TO NILOTINIB (NIL) IN PATIENTS (PTS) WITH CHRONIC MYELOID LEUKEMIA IN CHRONIC PHASE (CML-CP). Poster session presented at the meeting of HAEMATOLOGICA. Copenhagen, DENMARK: FERRATA STORTI FOUNDATION.
WoS52016 Cortes, J. E., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., Chuah, C., Nicolini, F. E., . . . Kantarjian, H. M. (2016). LONG-TERM EFFICACY AND SAFETY OF PONATINIB IN HEAVILY PRETREATED LEUKEMIA PATIENTS: 4-YEAR RESULTS FROM THE PIVOTAL PHASE 2 PACE TRIAL. Poster session presented at the meeting of HAEMATOLOGICA. Copenhagen, DENMARK: FERRATA STORTI FOUNDATION.
WoS12016 Sadras, T., Heatley, S., Dang, P., Kok, C., Quek, K., Nievergall, E., . . . White, D. L. (2016). A nine-gene signature defines 2 groups of CRLF2 rearranged B-ALL patients with distinctive genetic features. Poster session presented at the meeting of .. Athens. 2016 Pagani, I. S., Kok, C., Saunders, V., Goyne, J., McLean, J., Vanderhoek, M., . . . Ross, D. (2016). The genomic landscape of mitochondrial DNA mutations in chronic myeloid leukaemia. Poster session presented at the meeting of .. Barcelona, Spain. 2016 Eadie, L., Saunders, V., Branford, S., Hughes, T., & White, D. (2016). Resistance mechanisms of the new allosteric inhibitor ABL001. Poster session presented at the meeting of ,. Houtson, USA. 2016 Eadie, L., Goyne, J., Hughes, T., & White, D. (2016). ABCC6 plays a significant role in the transport of nilotinib in both cells lines and primary patient cells, and may contribute to resistance. Poster session presented at the meeting of ,. Houston, USA. 2016 Saunders, V. A., Wang, J., Lu, L., Eadie, L. N., McLean, J. A., Goyne, J. M., . . . Hughes, T. P. (2016). A Low Concentration of ABL001 Potentiates <i>In Vitro</i> TKI-Induced Bcr-Abl Kinase Inhibition in CML Cells. Poster session presented at the meeting of BLOOD. San Diego, CA: AMER SOC HEMATOLOGY.
DOI WoS12016 Eadie, L. N., Goyne, J., Hughes, T., & White, D. L. (2016). The ABCC6 Transporter Plays a Significant Role in the Efflux of Nilotinib and Dasatinib, and May Contribute to Tyrosine Kinase Inhibitor Resistance. Poster session presented at the meeting of .. San Diego, USA: AMER SOC HEMATOLOGY.
DOI2016 Eadie, L., Hughes, T., & White, D. (2016). ABCB1 overexpression predicts outcome of CML patients undergoing first-line imatinib treatment. Poster session presented at the meeting of Abstract presented at the New Directions in Leukaemia Research 2016 Meeting. Noosa, QLD. 2016 Eadie, L., Saunders, V., Leclercq, T., Branford, S., White, D. L., & Hughes, T. (2016). Abl001 Is Susceptible To Resistance Mediated By Overexpression Of Drug Transporters Abcb1 and Abcg2. Poster session presented at the meeting of .. Noosa, QLD. 2016 Sadras, T., Heatley, S., Kok, C., Quek, K., Dang, P., Nievergall, E., . . . White, D. L. (2016). CRLF2 rearranged B-ALL cases with a Ph-like gene signature are enriched for JAK2 mutations. Poster session presented at the meeting of .. Noosa, QLD. 2016 Lu, L., Saunders, V., Kok, C., Leclercq, T., Hughes, T., & White, D. (2016). Modelling ponatinib resistance in BCR-ABL1+ cell lines: implications for ponatinib therapy. Poster session presented at the meeting of New Directions in Leukaemia Research 2016. Noosa, QLD. 2016 McClure, B., Heatley, S., Sadras, T., Nievergall, E., Kok, C., Dang, P., . . . White, D. L. (2016). Identification of a significantly high prevalence of relapse in Australian children with Ph-like ALL. Poster session presented at the meeting of .. Noosa, QLD. 2016 Asari, K., Heatley, S., Leclercq, T., Fitter, S., Zannettino, A., Hughes, T., & White, D. L. (2016). In vitro Modelling of Therapeutic Resistance to Elucidate Mechanisms of TKI-Resistant High-Risk ALL. Poster session presented at the meeting of .. Noosa, QLD. 2016 Pagani, I., Kok, C., Saunders, V., Goyne, J., McLean, J., Vanderhoek, M., . . . White, D. L. (2016). Do mitochondrial mutations in chronic myeloid leukaemia identify a pre-leukemic clone?. Poster session presented at the meeting of .. Noosa, QLD. 2016 Eadie, L., Dang, P., Saunders, V., Hughes, T., & White, D. L. (2016). The clinical significance of early imatinib induced ABCB1 overexpression in chronic phase CML patients treated sequentially with imatinib and nilotinib: A TIDEL II sub-study. Poster session presented at the meeting of ,. Adelaide, SA. 2016 White, D. L., McClure, B., Heatley, S., Sadras, T., Quek, K., & Hughes, T. (2016). Investigation of the transforming capacity of a recently identified EP300-ZNF384 fusion gene in adult acute lymphoblastic leukaemia. Poster session presented at the meeting of Poster Session. Adelaide, SA. 2016 Asari, K., Heatley, S., Leclercq, T., Fitter, S., Kok, C. H., Zannettino, A., . . . White, D. L. (2016). Investigating Modes of Therapeutic Resistance via In Vitro Modelling of TKI-resistant High-Risk Philadelphia-chromosome-positive and Philadelphia-chromosome-like Acute Lymphoblastic Leukaemia. Poster session presented at the meeting of Poster Session. Adelaide, SA. 2016 Watts, S., Saunders, V., Wee, A., Kutyna, M., White, D. L., Hughes, T., & Hiwase, D. (2016). Understanding the mechanism of secondary resistance to Azacitidine in Myelodysplastic syndromes using the cell-line model MOLM-13. Poster session presented at the meeting of Poster Session. Adelaide, SA. 2016 Kok, C. H., Watkins, D., Wang, J., Saunders, V., Goyne, J., Pagani, I. S., . . . White, D. L. (2016). High Gene Expression of hist1h2ag and hist1h4a Reduces Imatinib Uptake into CML Cells and Predicts Poor Response to Frontline Imatinib Therapy. Poster session presented at the meeting of Poster Session. Melbourne, VIC. 2016 Heatley, S., Sadras, T., McClure, B., Kok, C. H., Dang, P., Nievergall, E., . . . White, D. L. (2016). The Incidence of Ph-like Acute Lymphoblastic Leukaemia (ALL) Increases with Age and is Characterised by Poor Outcome. Poster session presented at the meeting of Poster Session. Melbourne, VIC. 2016 Pagani, I. S., Kok, C. H., Wang, J., Saunders, V., Van der Hoek, M., Heatley, S., . . . Ross, D. (2016). Mitochondrial DNA Mutations at Diagnosis are Linked to Response in TKI treated Chronic Myeloid Leukaemia Patients. Poster session presented at the meeting of Poster Session. Melbourne, VIC. 2016 Watts, S., Wee, A., Saunders, V., Kutyna, M., White, D. L., Hughes, T., & Hiwase, D. (2016). Determining Mechanisms of Resistance to Azacitidine (Aza) in Myelodysplastic (MDS) Syndromes and Acute Myeloid Leukaemia (AML) using an in-vitro model. Poster session presented at the meeting of Poster Session. Melbourne, VIC. 2016 Lu, L., Saunders, V., Kok, C. H., Leclercq, T., Hughes, T., & White, D. L. (2016). Modelling Ponatinib Resistance In BCR-ABL1+ Cell Lines: Implications For Ponatinib Therapy. Poster session presented at the meeting of Poster Session. Adelaide, SA. 2015 Guilhot, F., Khoury, H. J., Baccarani, M., Hochhaus, A., Hughes, T. P., Lipton, J. H., . . . Mauro, M. J. (2015). ELEVATED BLOOD PRESSURE (BP) AND ADVERSE EVENTS OF HYPERTENSION (HTN) IN PHASE 1, 2, AND 3 TRIALS OF PONATINIB IN LEUKEMIA. Poster session presented at the meeting of HAEMATOLOGICA. Vienna, AUSTRIA: FERRATA STORTI FOUNDATION.
WoS12015 Cortes, J., Kim, D. W., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., Chuah, C., . . . Kantarjian, H. M. (2015). PONATINIB EFFICACY AND SAFETY IN HEAVILY PRETREATED LEUKEMIA PATIENTS: 3-YEAR RESULTS OF THE PACE TRIAL. Poster session presented at the meeting of HAEMATOLOGICA. Vienna, AUSTRIA: FERRATA STORTI FOUNDATION.
WoS122015 Mueller, M. C., Baccarani, M., Deininger, M. W., Guilhot, F., Hochhaus, A., Hughes, T. P., . . . Cortes, J. E. (2015). Responses to Ponatinib at early landmark time points are associated with Progression-Free Survival (PFS) and Overall Survival (OS) in heavily pretreated Chronic-Phase (CP) Chronic Myeloid Leukemia (CML) patients (Pts). Poster session presented at the meeting of Oncology Research and Treatment. KARGER. 2015 Foreman, C., Russo, P., Davies, N., Hissaria, P., Hughes, T., Proudman, S., & Limaye, V. (2015). AN AUDIT OF IVIG USE FOR INFLAMMATORY MYOPATHIES IN SOUTH AUSTRALIA. Poster session presented at the meeting of INTERNAL MEDICINE JOURNAL. WILEY-BLACKWELL. 2014 Branford, S., Yeung, D., Ross, D., Parker, W., Braley, J., Seymour, J., & Hughes, T. (2014). The adverse effect of high sokal risk for first line imatinib treated patients is overcome by a rapid rate of BCR-ABL decline measured as early as 1 month of treatment. Poster session presented at the meeting of Abstract of power point presentation at 56th ASH Annual Meeting, published in Blood. San Francisco, California: American Society of Hematology. 2014 Yeung, D. T., Vidovic, L., Tang, C., White, D. L., Branford, S., Hughes, T. P., & Yong, A. S. M. (2014). KIR2DL5B Genotype Independently Predicts Poor Outcomes in CML-CP Patients Switched to Nilotinib after Suboptimal Responses to Imatinib and May Refine Prognosis in Patients with EMR Failure. Poster session presented at the meeting of BLOOD. San Francisco, CA: AMER SOC HEMATOLOGY. 2014 Nievergall, E., Reynolds, J., Kok, C. H., Watkins, D., Biondo, M., Busfield, S. J., . . . Hughes, T. P. (2014). High plasma levels of TGF-α and IL-6 at diagnosis predict early molecular response failure and transformation in CML. Poster session presented at the meeting of Abstract of presentation to 56th ASH Annual Meeting, published in Blood. San Francisco, California: American Society of Hematology.
DOI WoS12014 Branford, S., Ross, D., Yeung, D., Braley, J., & Hughes, T. (2014). Achieving the deep molecular response levels required for an imatinib discontinuation trial is strongly associated with the BCR-ABL level at the first qualifying timepoint. Poster session presented at the meeting of Abstract of power point presentation at 56th ASH Annual Meeting, published in Blood. San Francisco, California: American Society of Hematology.
WoS22014 Parker, W. T., Phillis, S. R., Yeung, D. T., Lawrence, D., Schreiber, A., Wang, P., . . . Branford, S. (2014). Detection of BCR-ABL1 Compound and Polyclonal Mutants in Chronic Myeloid Leukemia Patients Using a Novel Next Generation Sequencing Approach That Minimises PCR and Sequencing Errors. Poster session presented at the meeting of BLOOD. San Francisco, CA: AMER SOC HEMATOLOGY.
DOI WoS42014 Branford, S., Yeung, D., Parker, W. T., Purins, L., Braley, J., Seymour, J. F., . . . Hughes, T. P. (2014). PROGNOSIS FOR CML PATIENTS WITH >10% BCR-ABL AFTER 3 MONTHS OF IMATINIB DEPENDS ON THE INITIAL RATE OF BCR-ABL DECLINE. Poster session presented at the meeting of HAEMATOLOGICA. Milan, ITALY: FERRATA STORTI FOUNDATION. 2014 Kantarjian, H. M., Kim, D. -W., Pinilla-Ibaz, J., Le Coutre, P. D., Paquette, R., Chuah, C., . . . Cortes, J. E. (2014). Ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph plus ) leukemias resistant or intolerant to dasatinib or nilotinib, or with the T315I mutation: Longer-term follow up of the PACE trial.. Poster session presented at the meeting of JOURNAL OF CLINICAL ONCOLOGY. Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
DOI WoS52014 Lu, L., Saunders, V., Kok, C. H., Leclercq, T., Hughes, T. P., & White, D. L. (2014). Modeling Ponatinib Resistance in <i>BCR-ABL1</i>+ Cell Lines: Implications for Ponatinib Resistance in TKI-Resistant and TKI-naive Patients. Poster session presented at the meeting of BLOOD. AMER SOC HEMATOLOGY. 2014 Deininger, M. W., Cortes, J. E., Kim, D. -W., Nicolini, F. E., Talpaz, M., Baccarani, M., . . . Hughes, T. P. (2014). Impact of Baseline Mutations on Response to Ponatinib and End of Treatment Mutation Analysis in Patients With Chronic Myeloid Leukemia. Poster session presented at the meeting of CLINICAL LYMPHOMA MYELOMA & LEUKEMIA. CIG MEDIA GROUP, LP.
DOI2014 Lipton, J. H., Chuah, C., Guerci-Bresler, A., Rosti, G., Simpson, D., Assouline, S., . . . Deininger, M. W. (2014). Epic: A Phase 3 Trial of Ponatinib Compared with Imatinib in Patients with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CP-CML). Poster session presented at the meeting of BLOOD. AMER SOC HEMATOLOGY.
WoS32013 White, D. L., Schafranek, L., Nievergall, E., Powell, J. A., Hiwase, D., Leclercq, T., & Hughes, T. (2013). STAT5 is a critical component of the time-dependent sensitivity of CML cells to TKI treatment in a Bcr-Abl-dependent, but JAK2-independent manner.. Poster session presented at the meeting of American Society of Haematology. New Orleans, USA. 2013 White, D., Saunders, V., Eadie, L., David, Y., & Hughes, T. P. (2013). The Depth Of <i>In Vivo</i> Kinase Inhibition Achieved Over The First Month Of Nilotinib Therapy Predicts For Subsequent Molecular Response, and Is Closely Related To Nilotinib Plasma Levels. Poster session presented at the meeting of BLOOD. New Orleans, LA: AMER SOC HEMATOLOGY.
WoS12013 Wang, J., Kok, C. H., D'Andrea, R. J., Hughes, T. P., & White, D. L. (2013). Role Of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) and Its Ligands In The Regulation Of Functional OCT-1 Activity In CML Cells. Poster session presented at the meeting of BLOOD. New Orleans, LA: AMER SOC HEMATOLOGY.
DOI2013 White, D. L., Eadie, L., & Hughes, T. (2013). Increasing Expression of the Efflux Transporter ABCB1 may Predispose CML Cells to Overt TKI Resistance.. Poster session presented at the meeting of American Society of Haematology. New Orleans, USA. 2013 Deininger, M. W. N., Cortes, J. E., Kim, D. -W., Nicolini, F. E., Talpaz, M., Baccarani, M., . . . Hughes, T. P. (2013). Impact of baseline mutations on response to ponatinib and end of treatment mutation analysis in patients with chronic myeloid leukemia.. Poster session presented at the meeting of JOURNAL OF CLINICAL ONCOLOGY. Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS.
WoS42013 Spector, N., Leber, B., Lipton, J. H., De Souza, C., Moiraghi, B., Steegmann, J. L., . . . Rea, D. (2013). Switching patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP) with residual disease on long-term imatinib (IM) to nilotinib (NIL): ENESTcmr 24-mo follow-up. Poster session presented at the meeting of JOURNAL OF CLINICAL ONCOLOGY. Chicago, IL: LIPPINCOTT WILLIAMS & WILKINS. 2013 Parker, W., Yeoman, A., Altamura, H., Roberts, N., Yeung, D., Jamison, B., . . . Branford, S. (2013). Additional BCR-ABL1 Mutations Identified By Sensitive Mass Spectrometry In Chronic Phase CML Patients With T315I Treated With Ponatinib Are Associated With Relatively Inferior Responses and Outcome. Poster session presented at the meeting of Blood. Amer Soc Hematology. 2013 Hiwase, D., Yeung, D., Carne, L., Ross, D., Grigg, A., & Hughes, T. (2013). Hypercholesterolemia In Imatinib Intolerant/Resistant CML-CP Patients Treated With Nilotinib: A Retrospective Analysis. Poster session presented at the meeting of Blood. Amer Soc Hematology.
WoS82013 Deininger, M., Shah, N., Cortes, J., Kim, D. W., Nicolini, F., Talpaz, M., . . . Branford, S. (2013). Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML). Poster session presented at the meeting of Blood. Amer Soc Hematology.
WoS32013 Parker, W., Phillis, S., Yeung, D., Hughes, T., Scott, H., & Branford, S. (2013). PCR-mediated recombination can lead to artificial chimera formation, which may pose as BCR-ABL1 compound mutations. Poster session presented at the meeting of Oral Sessions from the 55th ASH Annual Meeting and Exhibition, as published in Blood. New Orleans, Louisiana: American Society of Hematology. 2012 Branford, S., Ross, D., Prime, J., Field, C., Altamura, H., Yeoman, A., . . . Hughes, T. (2012). Early Molecular Response and Female Sex Strongly Predict Achievement of Stable Undetectable <i>BCR</i>-<i>ABL1</i>, a Criterion for Imatinib Discontinuation in Patients with CML. Poster session presented at the meeting of BLOOD. GA, Atlanta: AMER SOC HEMATOLOGY.
DOI WoS62012 Watkins, D. B., Kok, C. H., D'Andrea, R. J., Hughes, T. P., & White, D. L. (2012). Global DNA methylation analysis identifies key pathway differences between poor (low OCT-1 activity) and standard risk CP-CML patients at diagnosis. Poster session presented at the meeting of “Abstracts of the 54th Annual Meeting and Exposition of the American Society of Hematology, as published in Blood. Atlanta, GA: America Society of Hematology. 2012 Nievergall, E., White, D. L., Yong, A. S. M., Ramshaw, H. S., Busfield, S. J., Vairo, G., . . . Hiwase, D. K. (2012). Effective Elimination of CML Progenitor and Stem Cells Through Combination of α-CD123 Antibody-Dependent Cell-Mediated Cytotoxicity and Tyrosine Kinase Inhibitor Treatment. Poster session presented at the meeting of BLOOD. GA, Atlanta: AMER SOC HEMATOLOGY.
DOI2012 Schafranek, L., Nievergall, E., Powell, J. A., Hiwase, D. K., White, D. L., & Hughes, T. P. (2012). Commitment of CML Cells to Apoptotic Cell Death Depends On the Length of Exposure to Das and the Level of STAT5 Activity. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS32012 Yeung, D. T., Osborn, M. P., White, D. L., Branford, S., Kornhauser, M., Slader, C., . . . Hughes, T. P. (2012). Early Switch to Nilotinib Does Not Overcome the Adverse Outcome for CML Patients Failing to Achieve Early Molecular Response On Imatinib, Despite Excellent Overall Outcomes in the TIDEL II Trial. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS82012 Parker, W. T., Yeoman, A. L., Jamison, B. A., Yeung, D. T., Scott, H. S., Hughes, T. P., & Branford, S. (2012). The patient's BCR-ABL1 Kinase Domain Mutation History Is Important for Decisions Regarding Tyrosine Kinase Inhibitor Therapy. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
DOI2012 White, D. L., Saunders, V., Yeung, D., Grigg, A., & Hughes, T. (2012). Early Molecular Response to Imatinib in CP-CML Patients: The Significance of Early Dose Intensity and OCT-1 Activity in Responders and Efficacy of Dose Escalation and Switch to Nilotinib in Non-Responders.. Poster session presented at the meeting of American Society of Haematology. Atlanta, USA. 2012 Delphine, R., Gautier, J. -F., Breccia, M., Saglio, G., Hughes, T. P., Kantarjian, H. M., . . . Hochhaus, A. (2012). Incidence of Hyperglycemia by 3 Years in Patients (Pts) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Treated with Nilotinib (NIL) or Imatinib (IM) in ENESTnd. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS42012 Hochhaus, A., Hughes, T. P., Saglio, G., Guilhot, F., Al-Ali, H. K., Rosti, G., . . . Kantarjian, H. M. (2012). Outcome of Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Based On Early Molecular Response and Factors Associated with Early Response: 4-Year Follow-up Data From Enestnd (Evaluating Nilotinib Efficacy and Safety in Clinical Trials Newly Diagnosed Patients). Poster session presented at the meeting of BLOOD. GA, Atlanta: AMER SOC HEMATOLOGY.
DOI WoS192012 Cortes, J. E., Pasquini, R., Kantarjian, H. M., Joske, D., Meillon, L. A., Shen, Z., . . . Hughes, T. P. (2012). First-Line Treatment and Management of Chronic Myeloid Leukemia (CML) in Clinical Practice: Update of > 1800 Patients (Pts) in the WORLD CML Registry. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
DOI2012 Kantarjian, H. M., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P., Paquette, R., Chuah, C., . . . Cortes, J. E. (2012). Efficacy and Safety of Ponatinib in Patients with Accelerated Phase or Blast Phase Chronic Myeloid Leukemia (AP-CML or BP-CML) or Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ ALL): 12-Month Follow-up of the PACE Trial. Poster session presented at the meeting of BLOOD. Atlanta, GA: AMER SOC HEMATOLOGY.
DOI WoS32011 Saglio, G., Kantarjian, H., Reiffers, J., Jootar, S., Kalaycio, M. E., Shibayama, H., . . . Hochhaus, A. (2011). The incidence of BCR-ABL mutations in patients (pts) with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CP) treated with nilotinib or imatinib in ENESTnd: 24-month follow-up. Poster session presented at the meeting of JOURNAL OF CLINICAL ONCOLOGY. AMER SOC CLINICAL ONCOLOGY.
DOI WoS22011 Larson, R. A., Kim, D., Rosti, G., Stenke, L., Pasquini, R., Hoenekopp, A., . . . Kantarjian, H. (2011). Comparison of nilotinib and imatinib in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd 24-month follow-up. Poster session presented at the meeting of JOURNAL OF CLINICAL ONCOLOGY. AMER SOC CLINICAL ONCOLOGY.
DOI WoS12011 Soverini, S., Angelini, S., Barnett, M., Ravegnini, G., Pane, F., Hughes, T. P., . . . Martinelli, G. (2011). Pharmacogenetics of drug transporters may be useful to identify chronic myeloid leukemia patients who are less likely to achieve molecular responses to imatinib: Implications for treatment optimization in the era of new tyrosine kinase inhibitors. Poster session presented at the meeting of CANCER RESEARCH. AMER ASSOC CANCER RESEARCH.
DOI2011 Yin, O. Q., Giles, F. J., Baccarani, M., le Coutre, P., Chia, Y. L., Gallagher, N., . . . Larson, R. A. (2011). CONCURRENT USE OF PROTON PUMP INHIBITORS (PPI) OR H2-BLOCKERS DID NOT ADVERSELY AFFECT NILOTINIB RESPONSE IN PATIENTS WITH CHRONIC MYELOID LEUKEMIA (CML). Poster session presented at the meeting of CLINICAL PHARMACOLOGY & THERAPEUTICS. Dallas, TX: NATURE PUBLISHING GROUP. 2011 Hughes, T. P., Kim, D. -W., Etienne, G., De Souza, C., Kurokawa, M., Kalaycio, M., . . . Hochhaus, A. (2011). The Incidence of BCR-ABL Mutations and Their Impact on Outcome in Patients with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Treated with Nilotinib or Imatinib in ENESTnd: 36-Month Follow-up. Poster session presented at the meeting of BLOOD. San Diego, CA: AMER SOC HEMATOLOGY.
WoS22011 Hochhaus, A., Ossenkoppele, G., Reiffers, J., Yao, M., Shibayama, H., Gatterman, N., . . . Kantarjian, H. M. (2011). Results From the ENESTnd Extension Study: Efficacy and Safety of Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP), Treated with Nilotinib 400 Mg Twice Daily (BID) After Suboptimal Response (SoR) or Treatment Failure (TF) to Imatinib 400 Mg Once Daily (QD) or Nilotinib 300 Mg BID. Poster session presented at the meeting of BLOOD. San Diego, CA: AMER SOC HEMATOLOGY. 2011 Larson, R. A., Bunworasate, U., Turkina, A. G., Goldberg, S. L., Dorlhiac-Llacer, P., Lopez, J. L., . . . Hughes, T. P. (2011). Nilotinib Shows Safety and Efficacy in Older Patients (≥ 65 years) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase Comparable with That in Younger Patients with Chronic Myeloid Leukemia in Chronic Phase: Results From ENESTnd. Poster session presented at the meeting of BLOOD. San Diego, CA: AMER SOC HEMATOLOGY.
WoS22011 Saglio, G., LeCoutre, P. D., Pasquini, R., Jootar, S., Nakamae, H., Flinn, I. W., . . . Kantarjian, H. M. (2011). Nilotinib Versus Imatinib in Patients (pts) with Newly Diagnosed Philadelphia Chromosome-Positive (Ph+) Chronic Myeloid Leukemia in Chronic Phase (CML-CP): ENESTnd 36-Month (mo) Follow-up. Poster session presented at the meeting of BLOOD. San Diego, CA: AMER SOC HEMATOLOGY.
WoS12008 Vandyke, K., Dewar, A. L., Davis, A. N., Fiuer, S., Hughes, T. P., To, L. B., & Zannettino, A. C. W. (2008). The tyrosine kinase inhibitor dasatinib decreases osteoclast formation and activity in vitro. Poster session presented at the meeting of 30th Annual Meeting of the American Society for Bone and Mineral Research, as published in Journal of Bone and Mineral Research. Montreal, Canada: Wiley.
DOI
2021 - 2026 Medical Research Future Fund (MRFF) - Research Grants - Precision Medicine for Chronic Myelomonocytic Leukaemia: Phase II Trial Studying the Efficacy of Lenzilumab or High Dose Ascorbate plus Azacitidine Based on Molecular Profiling Compared to Risk-matched Historical Cohort.
2020 Cancer Council SA Beat Cancer Research Project Grant. Developing an artificial intelligence-based algorithm to enable a risk-adapted approach to frontline therapy in chronic myeloid leukaemia (CML)
2018 Australian Cancer Research Fund (ACRF) – Infrastructure: ACRF Centre for Integrated Cancer Systems Biology (ACRFCICSB).
2018 - 2021 NHMRC Project Grant. Chronic Myeloid Leukaemia: Changing the treatment paradigm
2018 - 2022 NHMRC. Principal Research Fellowship. Improving Leukaemia Outcomes
2016 – 2018 Leukemia & Lymphoma Society (US). Translational Research Program Grant
2015 - 2019 NHMRC Program Grant: Cytokine dysregulation in leukaemia
2015 Bristol Meyer Squibb Australia. Correlative Science Proposal Associated with the DIRECT study.
2014 - 2017 Determining the prerequisites for the achievement of treatment-free remission in chronic myeloid leukaemia to facilitate the development of new therapeutic approaches with curative intent.
2014 Bristol Meyer Squibb Australia. Correlative Science Proposal Associated with the REGALLIA clinical trial registry.
2014 Bristol Meyer Squibb Australia. Correlative Science Proposal Associated with the REGALLIA clinical trial registry.
2014 Novartis Australia. Correlative Science Proposal Associated with the ENESTxtnd clinical trial.
2013 - 2015 Screening for recently defined genetic lesions in poor risk adult and childhood ALL, and developing treatment approaches to target causative pathways
2013 - 2017 NHMRC. Practitioner Fellowship
2012 - 2014 NHMRC. Assessment of markers of genomic instability for the prediction of treatment response of chronic myeloid leukaemia
2012 – 2014 NHMRC. Characterisation of a new poor-risk sub-category of chronic phase chronic myeloid leukaemia
2012 – 2014 NHMRC. Development of a treatment algorithm for kinase inhibitor therapy in CML
2011 - 2012 Leukaemia Foundation of Australia. Developing a gene signature to predict the optimal front-line kinase inhibitor for CP-CML patients
2011 - 2013 Novartis Pharmaceuticals Australia. Correlative Science Proposal Associated with the ENESTxtnd clinical trial.
2011 Novartis Pharmaceuticals Australia. Correlative Science Associated with TIDELII Clinical Trial – expansion of patient numbers.
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Current Higher Degree by Research Supervision (University of Adelaide)
Date Role Research Topic Program Degree Type Student Load Student Name 2023 Co-Supervisor Investigating the role of lipid metabolism in chronic myeloid leukaemia Doctor of Philosophy Doctorate Full Time Miss Molly Gladys Tolland 2021 Co-Supervisor Investigation of current, innovative treatments and the roles of secondary genomic lesions in BCR-ABL1 positive leukaemias Doctor of Philosophy Doctorate Part Time Mr Elias Lagonik 2021 Co-Supervisor Genomic Mechanisms Influencing Outcome In Chronic Myeloid Leukaemia Doctor of Philosophy Doctorate Full Time Miss Adelina Catherina B. Fernandes -
Past Higher Degree by Research Supervision (University of Adelaide)
Date Role Research Topic Program Degree Type Student Load Student Name 2019 - 2023 Principal Supervisor Unravelling Resistance Mechanisms in Philadelphia Positive Leukemias: Targeted Treatment Strategies to Overcome Resistance Doctor of Philosophy Doctorate Full Time Mr Govinda Poudel 2012 - 2014 Principal Supervisor The role of cytokines in governing the expansion of the T315I mutation in Chronic myeloid leukaemia Master of Philosophy (Medical Science) Master Full Time Dr Oi-Lin Lee 2012 - 2016 Co-Supervisor In Vitro Investigation of Intracellular Ponatinib Transport and Modeling Ponatinib Resistence in BCR-ABL1+ Cell Lines: Implications for Therapeutic Strategies Doctor of Philosophy Doctorate Full Time Miss Liu Lu 2012 - 2016 Co-Supervisor Prognostic Markers Associated With Tyrosine Kinase Inhibitor Treatment Response and Maintenance of Treatment Free Remission in Chronic Myeloid Leukaemia Doctor of Philosophy Doctorate Full Time Prof David Yeung 2010 - 2014 Principal Supervisor Assessment of Critical Survival Mechanisms Exploited by BCR-ABL1+ Cells to Evade Tyrosine Kinase Inhibitor-Induced Death; Determination of Novel Therapeutic Targets in Chronic Myeloid Leukaemia Doctor of Philosophy Doctorate Full Time Miss Lisa Schafranek 2010 - 2014 Co-Supervisor Defining CP-CML patient subsets associated with poor imatinib uptake and response Doctor of Philosophy Doctorate Full Time Mr Dale Benjamin Watkins 2009 - 2013 Principal Supervisor Nilotinib Efflux and Resistance Development: The Effects of Combination and Concomitant Therapies on the Transport and Efficacy of Nilotinib Doctor of Philosophy Doctorate Full Time Ms Laura Eadie 2008 - 2013 Principal Supervisor Investigating Drugs that Enhance Imatinib Uptake and Factors which Contribute to the Functional Activity of OCT-1 in CML Cells Doctor of Philosophy Doctorate Full Time Miss Jueqiong Wang 2008 - 2012 Principal Supervisor TKI Resistance in CML Cell Lines: Investigating Resistance Pathways Doctor of Philosophy Doctorate Full Time Mrs Carine Tang 2007 - 2011 Principal Supervisor Cell Lineage, Cell Maturity and BCR-ABL: Factors Which Influence Imatinib Uptake in Chronic Myeloid Leukaemia Doctor of Philosophy Doctorate Full Time Ms Jane Engler 2006 - 2009 Principal Supervisor Minimal Residual Disease in Chronic Myeloid Leukaemia after Imatinib Treatment Doctor of Philosophy Doctorate Full Time Dr David Ross 2005 - 2009 Co-Supervisor Investigating the Effects of ABL Kinase Inhibitors on the Signalling and Function of Normal Leukocytes and Leukemic Cells Doctor of Philosophy Doctorate Full Time Mr Stephen Blake 2004 - 2008 Principal Supervisor Factors which Impact on the Response of CML Patients to ABL Kinase Inhibitor Therapy: A Study of Imatinib and Nilotinib Doctor of Philosophy Doctorate Part Time Prof Deborah Lee White 2001 - 2006 Co-Supervisor GM-CSF Protection of CML CD34+ Cells from the Inhibitory Effect of Imatinib Doctor of Philosophy Doctorate Full Time Mr Pongtep Viboonjuntra
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