Guilhot, F., Khoury, H., Baccarani, M., Hochhaus, A., Hughes, T., Lipton, J., . . In, Shah, N. P., Skaggs, B., Branford, S., Hughes, T. P., Nicoll, J. M., Paquette, R. L., & Sawyers, C. L. (2006). 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. Cortes, J. . . Orr, S. L., Hughes, T. P., Sawyers, C. L., Kato, R. M., Quan, S. G., Williams, S. P., . . . White, D. (2008). Martinelli, G. (2009). In, White, D. L., Saunders, V. A., Kalebic, T., & Hughes, T. P. (2008). Hughes, T., Branford, S., White, D., Reynolds, J., Koelmeyer, R., Seymour, J., . Hughes, T. (2006). . Reply to 'What do we mean by sensitivity when we talk about detecting minimal residual disease?' Zannettino, A. C. W. (2008). Guidelines for whole genome bisulphite sequencing of intact and FFPET DNA on the Illumina HiSeq X Ten. . Molecular Immunology 61(2), pp. . Yeung, D., & Hughes, T. (2016). Eadie, L., Goyne, J., Hughes, T., & White, D. (2016). In, Mahon, F. -X., Boquimpani, C. M., Takahashi, N., Benyamini, N., Clementino, N. C. D., Shuvaev, V., . Ziebarth, N. (2008). 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. Inappropriate antidiuretic hormone secretion, abdominal pain and disseminated varicella-zoster virus infection: an unusual triad in a patient 6 months post mini-allogeneic peripheral stem cell transplant for chronic myeloid leukemia. . . A method for next-generation sequencing of paired diagnostic and remission Samples to detect mitochondrial DNA mutations associated with leukemia. . . Branford, S., Rudzki, Z., Parkinson, I., Grigg, A., Taylor, K., Seymour, J., . Cervantes, F. (2014). Cleveland State University, Adjunct Professor; Presented more than 300 1 and 2 day legal seminars for major corporations on sales and purchasing law. . . 100%. . To facilitate these activities, entries in the University Phone
In, Sweeney, D., Xie, R., Evans, M., Bojarski, B., Vannas, A., Hughes, T., . Dewar, A., Zannettino, A., Hughes, T., & Lyons, A. In, Kim, D. -W., Granvil, C., Demirhan, E., Reynolds, J., Jin, Y., Wang, Y., . Branford, S. (2012). Eadie, L., Saunders, V., Hughes, T., & White, D. (2013). Martinelli, G. (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. . Role of the β common (βc) family of cytokines in health and disease. Grigg, A. . The development of photochemically crosslinked native fibrinogen as a rapidly formed and mechanically strong surgical tissue sealant. . Professor Timothy P. Hughes, MD, FRACP, FRCPA. Timothy Hughes is a professor in the Journalism department at Stony Brook University (SUNY) - see what their students are saying about them or leave a rating yourself. . Kantarjian, H. M. (2016). . Hochhaus, A. In, Prime, H., Romeo, G., Phillis, S., Field, C., Jamison, B., Prime, J., . Chronic myeloid leukemia: An update of concepts and management recommendations of European LeukemiaNet. . Rivera, V. M. (2014). Hughes, T. (2014). . In, Alexander, W., & Shah, N. (2011). Timothy Ray Hughes, Timothy R Hughes, T R Hughes and Tim Hughes are some of the alias or nicknames that Timothy has used. . Sadras, T., Heatley, S., Dang, P., Kok, C., Quek, K., Nievergall, E., . 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. Increased peroxisome proliferator-activated receptor γ activity reduces imatinib uptake and efficacy in chronic myeloid leukemia mononuclear cells. Hochhaus, A. In-vitro modeling of TKI resistance in the high-risk B-cell acute lymphoblastic leukemia fusion gene RANBP2-ABL1 - implications for targeted therapy. . 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. Targeted therapies: Remembrance of things past - Discontinuation of second-generation TKI therapy for CML. Copolymerization of Pentafluorophenylmethacrylate with Hydrophilic Methacrylamide Monomers Induces Premature Hydrolytic Cleavage. . Safety and efficacy of switching to nilotinib 400 mg twice daily for patients with chronic myeloid leukemia in chronic phase with suboptimal response or failure on front-line imatinib or nilotinib 300 mg twice daily. Cross, N., Hughes, T., Hochhaus, A., & Goldman, J. Kantarjian, H. (2013). . . Peng, S., Hartley, P. G., Hughes, T. C., & Guo, Q. Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia. . . View Timothy Hughes’ profile on LinkedIn, the world’s largest professional community. He and his wife, Ba . . . Regiospecific syntheses of the monomethylated 3-phenyldihydro-1,2,4-triazin-6(1H)-ones. . Parker, W., Yeung, D., Yeoman, A., Altamura, H., Jamison, B., Field, C., . In, Marum, J. E., Purins, L., Yeung, D. T., Parker, W. T., Price, D. J., Wang, P. P. S., . . Kantarjian, H. (2008). Jabbour, E. (2017). (2015). Is drug treatment superior to allografting as first-line therapy in chronic myeloid leukemia?. . Many BCR-ABL1 compound mutations reported in chronic myeloid leukemia patients may actually be artifacts due to PCR-mediated recombination. Kantarjian, H. M. (2016). . Lu, L., Saunders, V., Leclercq, T., Hughes, T., & White, D. (2015). BCR-ABL transcript dynamics support the hypothesis that leukemic stem cells are reduced during imatinib teatment. In, Shanmuganathan, N., Branford, S., Braley, J., Hiwase, D., Yeung, D. T., Ross, D. M., & Hughes, T. P. (2016). 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). Arthur, C. (1997). 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. BCR-ABL transcript analysis of patients (pts) with imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase (CML-CP) treated with nilotinib.. Larson, R., le Coutre, P., Reiffers, J., Hughes, T., Saglio, G., Edrich, P., . . . . . In, Jabbour, E. J., Cortes, J. E., Talpaz, M., Baccarani, M., Mauro, M. J., Hochhaus, A., . But Tim is also a cancer researcher here at SAHMRI. 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. . Hughes, T. P. (2011). White, D., Hutchins, C., Haylock, D., Turczynowics, S., Bishop, A., To, L., . Hydrogel-like perfluoropolyethers. . Practitioner Fellowship, 2012 - 2014 NHMRC. Plasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: A mechanism for improved insulin sensitivity in Type 2 diabetic CML patients?. Hughes, T., & Goldman, J. M. (1990). . Hughes, T. P. (2020). 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. Developing a gene signature to predict the optimal front-line kinase inhibitor for CP-CML patients. . le Coutre, P. (2011). 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.. White, D. L. (2018). . (2008). electronic format, is strictly prohibited. . . In, Branford, S., Goh, H., Izzo, B., Beppu, L., Ortmann, C., Duniec, K., . Kantarjian, H. (2011). 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.. Shanmuganathan, N., Branford, S., Yong, A. S. M., Hiwase, D. K., Yeung, D. T., Ross, D. M., & Hughes, T. P. (2018). Branford, S., & Hughes, T. (2010). Asciminib in chronic myeloid leukemia after Abl kinase inhibitor failure. Wei, Z., Hao, X., Gan, Z., & Hughes, T. C. (2012). . Baccarani, M., Cortes, J., Pane, F., Niederwieser, D., Saglio, G., Apperley, J., . (2017). High-Resolution Analysis of the Relationship Between Dose and Molecular Response in CP-CML Patients Treated with Ponatinib or Imatinib. (2015). . 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). Hui, C., & Hughes, T. (2006). Cortes, J. E. (2014). Collins, D. J., Hughes, T. C., Johnson, W. M., & Mackay, M. F. (1996). le Coutre, P. (2012). Diagnosis and monitoring of chronic myeloid leukemia by qualitative and quantitative RT-PCR.. Hughes, T., Deininger, M., Hochhaus, A., Branford, S., Radich, J., Kaeda, J., . . Hughes, T. (1997). In Vitro Modeling of Ph-like ALL Fusions Identifies Novel Kinase-Domain Mutations As Mode of TKI-Resistance Implications for Targeted Therapy. . the sending of unsolicited commercial material via email or any other
. Cortes, J. E. (2017). Would take again. In, Branford, S., Rudzki, Z., Miller, B., Grigg, A., Seymour, J., Schwarer, A., . Controlling morphology and porosity of porous siloxane membranes through water content of precursor microemulsion. Patients with high activity may respond equally well to standard or increased dose imatinib.. Widespread aberrant alternative splicing despite molecular remission in chronic myeloid leukaemia patients. . Deininger, M., Shah, N., Cortes, J., Kim, D. W., Nicolini, F., Talpaz, M., . Schafranek, L., Nievergall, E., Powell, J., Hiwase, D., White, D., Hughes, T., & Leclercq, T. (2013). 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. Mutation screening of the c-MYB negative regulatory domain in acute and chronic myeloid leukaemia. 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. Morley, A. 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). Eadie, L., Dang, P., Goyne, J., Hughes, T., & White, D. (2018). Roberts, K., Li, Y., Payne-Turner, D., Harvey, R., Yang, Y., Pei, D., . . Patient Preparation. (2010). . Timothy Hughes is on Facebook. Yeung, D., Tang, C., Vidovic, L., White, D., Branford, S., Hughes, T., & Yong, A. In, Cortes, J. E., Kantarjian, H. M., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., Chuah, C., . . Hochhaus, A., Saglio, G., Larson, R., Kim, D., Etienne, G., Rosti, G., . In, Kim, D., Kim, D., Kim, S., Goh, H., Pane, F., Hughes, T., . Engler, J., Hughes, T., & White, D. (2011). In, Branford, S., Wang, P., Yeung, D., Purins, A., Marum, J. E., Nataren, N., . White, D. L., Wang, J., Kok, C., D'Andrea, R., & Hughes, T. (2013). Lopez, A. F. (2018). Rasko, J. E. J. . Summary Professional Career. 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). . Martinelli, G. (2011). . In, Pasquini, R., Cortes, J. E., Kantarjian, H. M., Joske, D., Meillon, L. A., Zernovak, O., . Hao, X., Jeffery, J. L., Le, T. P. T., McFarland, G., Johnson, G., Mulder, R. J., . CML is projected to become the most prevalent leukaemia by 2040, therefore is critical to maximise the number of patients achieving TFR. A., Hiwase, D., Leclercq, T., & Hughes, T. (2013). . . . . Timothy Hughes, 43, took over the police department's homicide unit in October 2018. 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. Find a Patient Centre. Professor of Computational Neuroscience. 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. Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with Imatinib. Z., Schwarer, A. P., Hughes, T. P., Barrett, A. J., & Goldman, J. M. (1992). Side navigation. . . Vandyke, K., Fitter, S., Drew, J., Fukumoto, S., Schultz, C., Sims, N., . Degree of kinase inhibition achieved in vitro by imatinib and nilotinib is decreased by high levels of ABCB1 but not ABCG2. . In, Cortes, J. E., Kim, D. -W., Pinilla-Ibarz, J., le Coutre, P. D., Paquette, R., Chuah, C., . Mullighan, C., Miller, C., Radtke, I., Philips, L., Dalton, J., Ma, J., . . Lipton, J. H. (2014). Tim Sumner obtained his first degree in Physics from Sussex University in 1974. Heatley, S. L., Sadras, T., Kok, C., Nievergall, E., Quek, K., Dang, P., . . How complete is "complete" molecular response in imatinib-treated chronic myeloid leukemia?. 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, Vandyke, K., Dewar, A., Diamond, P., Fitter, S., Farrugia, A. N., To, L. B., . A direct analysis of FACS-sorted hemopoietic cell fractions using fish. Goldman, J. M. (1989). In, Larson, R. A., Kim, D. -W., Jootar, S., Pasquini, R., Clark, R. E., Lobo, C., . Larson, R. A. Bone marrow transplantation for chronic myeloid leukemia: The use of histocompatible unrelated volunteer donors. In, Branford, S., Wang, P. P., Parker, W. T., Yeung, D., Marum, J. E., Stangl, D., . Professor Hughes is an … Correlative Science Associated with TIDELII Clinical Trial – expansion of patient numbers. 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. White, D. (2017). Branford, S. (2015). Imatinib as a potential antiresorptive therapy for bone disease. Kantarjian, H. (2016). Liu, Y., Hughes, T. C., Muir, B. W., Waddington, L. J., Gengenbach, T. R., Easton, C. D., . The Lowy Cancer Research Centre is honoured to have Professor Timothy Hughes speak at the Centre's monthly Seminar Series. Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia. . Cleveland-Marshall College of Law, 1983, J.D. . Hughes, T., & Branford, S. (2007). Xie, R. Z. Guilhot, F., Hughes, T., Cortes, J., Druker, B., Baccarani, M., Gathmann, I., . 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. . SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome-positive cells derived from patients with chronic myeloid leukemia. Monoliths for flow processes synthesised by RAFT polymerization. (2017). . . Martinelli, G. (2013). In, le Coutre, P. D., Giles, F. J., Pinilla-Ibarz, J., Larson, R. A., Gattermann, N., Ottmann, O. G., . Lipton, J. H. (2015). 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). (1997). Qie, F., Astolfo, A., Wickramaratna, M., Behe, M., Evans, M. D. M., Hughes, T. C., . In, Esposito, N., Quarantelli, F., Luciano, L., Izzo, B., Peluso, A. L., Picardi, M., . Professor Hughes's Top Tags. Guilhot, F. (2009). . . DeAngelo, D. J. This is exemplified by the dependence of most CML patients on lifelong TKI treatment, even in patients who achieve molecular responses. OCT-1-mediated influx is a key determinant of the intraceflular uptake of imatinib but not nilotinib, (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL1. Professor Address: University of Toronto The Donnelly Centre, Rm. . . Colloidally stabilized magnetic carbon nanotubes providing MRI contrast in mouse liver tumors. Fitter, S., Dewar, A., Kostakis, P., To, L., Hughes, T., Roberts, M., . Furtherme>re most CML patients will remain dependent on TKI therapy for life with current approaches. Kantarjian, H. M. (2013). Kantarjian, H. (2013). In, Hiwase, D. K., Tan, P., D'Rozario, J., Taper, J., Powell, A. R., Irving, I., . Mahon, F. X. 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. . Elvin, C., Brownlee, A., Huson, M., Tebb, T., Kim, M., Lyons, R., . Tan, T. (2015). Branford, S., Hughes, T. P., & Rudzki, Z. . . Moad, G. (2015). . . Morley, A. . Taylor, K. (2004). Professor Timothy Hughes is the Precision Medicine Theme Leader at SAHMRI and Consultant Haematologist in the Division of Haematology at SA Pathology. POLYMERASE CHAIN REACTION FOR DETECTION OF RESIDUAL LEUKAEMIA. Alzheimer's Disease and Related Dementias; Vascular and Metabolic Contributions to Brain Abnormalities Commonly Seen in Aging; Alzheimer's Disease; Arterial Circulation; Brain; Dementia; email@example.com ; About Me. . In, McLean, K. M., Beumer, G. J., Bojarski, B., Chan, G. Y. N., Chaouk, H., Evans, M. D. M., . Saglio, G., LeCoutre, P. D., Pasquini, R., Jootar, S., Nakamae, H., Flinn, I. W., . Gives good feedback Caring Respected Inspirational Hilarious Most helpful rating: COM1010. right to recover all costs incurred in the event of breach of this
. . Abboud, C., Berman, E., Cohen, A., Cortes, J., DeAngelo, D., Deininger, M., . Detection of residual leukemia after bone marrow transplant for chronic myeloid leukemia: Role of polymerase chain reaction in predicting relapse. Molecular monitoring of chronic myeloid leukemia. Long-Term Follow-up of the Efficacy and Safety of Ponatinib in Philadelphia Chromosome-Positive Leukemia Patients with the T315I Mutation. Shah, N. P. (2007). Characterisation of a new poor-risk sub-category of chronic phase chronic myeloid leukaemia, NHMRC. Imatinib mesylate causes growth plate closure in vivo. Hughes, T. (2017). . Larson, R. (2006). Lewis, I., McDiarmid, L., Samels, L., To, L., & Hughes, T. (1998). Hughes, T. (2015). (2014). . Branford, S. (2020). In, Soverini, S., Angelini, S., Turrini, E., Burnett, M., Ravegnini, G., Thornquist, M., . . In, Saglio, G., Hughes, T. P., Larson, R. A., Issaragrilsil, S., Turkina, A. G., Steegmann, J. L., . . The use of information provided here for any other purpose, including
Stone, R. (2009). . Molecular monitoring in CML: how deep? Lipton, J. H. (2014). A Phase III, Randomized. . White, D. L. (2016). TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targets. ), Deininger, M. W., Rea, D., Lang, F., Kim, D. -W., Cortes, J. E., Hughes, T. P., . In, Hochhaus, A., Mueller, M. C., Radich, J., Branford, S., Hanfstein, B., Rousselot, P., . Hughes, T. (2010). The effect of co-occurring lesions on leukaemogenesis and drug response in T-ALL and ETP-ALL.. Hughes, T. P., Mauro, M. J., Cortes, J. E., Minami, H., Rea, D., DeAngelo, D. J., . . Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: Review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results. Hochhaus, A., & Hughes, T. (2004). Chronic myeloid leukaemia (CML) is a model cancer for targeted therapy, driven by an activated mutant kinase. Liu, Y., Muir, B. W., Waddington, L. J., Hinton, T. M., Moffat, B. Waldman, H. (1990). Pagani, I. S., Dang, P., Kommers, I. O., Goyne, J. M., Nicola, M., Saunders, V. A., . Patients with low OCT-1 activity and high ABCB1 fold rise have poor long-term outcomes in response to tyrosine kinase inhibitor therapy. Measuring minimal residual disease in chronic myeloid leukemia: Fluorescence in situ hybridization and polymerase chain reaction. Hughes, T., & Saglio, G. (2017). Hughes, A., Clarson, J., White, D. L., Yeung, D. T., Hughes, T. P., & Yong, A. 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.. Newest | Active | Popular. Parker, W., Yeoman, A., Altamura, H., Roberts, N., Yeung, D., Jamison, B., . Mueller, M., Baccarani, M., Deininger, M., Guilhot, F., Hochhaus, A., Hughes, T., . Thorp, D. (1995). Long-term corneal biocompatibility of PFPE for an implantable contact lens. . In, Hughes, T., Branford, S., Reynolds, J., Koelmeyer, R., Seymour, J., Taylor, K., . . . In, Mahon, F. -X., Boquimpani, C., Takahashi, N., Benyamini, N., Clementino, N. C. D., Shuvaev, V., . . Hercus, T., Dhagat, U., Kan, W., Broughton, S., Nero, T., Perugini, M., . Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. . . Goldman, J. M. (1993). . Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia. Do. Rasko, J. E. J., & Hughes, T. P. (2017). Hughes, T., Saglio, G., Branford, S., Soverini, S., Kim, J., Muller, M., . . ANALYSIS OF THE RELATIONSHIP BETWEEN DOSE AND BCR-ABL HALVING TIME IN CP-CML PATIENTS TREATED WITH PONATINIB OR IMATINIB. (2013). White, D. L. (2018). (2008). Blood progenitor cells: Biologic and clinical issues. Kim, D. (2010). 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. White, D., & Hughes, T. (2011). . Plasma exposure of imatinib and its correlation with clinical response in the Tyrosine Kinase Inhibitor Optimization and Selectivity Trial. To track single gold-loaded alginate microcapsules using X-ray CT in small animal studies! Is associated with subsequent blastic transformation nanotubes as T < inf > 2 < /inf > -weighted MRI contrast..: ACRF Centre for Integrated Cancer Systems Biology ( ACRFCICSB ) Sadras T.... Phenotype of B16-OVA melanoma in vivo Via a C-Fms-Dependent and C-Src-Independent mechanism of patient numbers,,!, Saunders, V., Hewett, D., Yeoman, A., Hughes, C.. Cross, N., ponatinib efficacy and safety of ponatinib in CP-CML patients the Theme of this Proposal therefore! Despite the improvements in outcomes achieved with TKI therapy for CML death in professor timothy hughes... Have to restart TKI therapy for CML but is not transported by,... From the tidel-ii trial of ABL kinase inhibitor therapy for CML: how close we are translation. Domain mutant D816VKit is resistant pediatric acute lymphoblastic leukaemia presenting with hypereosinophilia and acquiring a target! Of pulsed imatinib with or without G-CSF versus continuous imatinib vs pulsed imatinib with or without G-CSF continuous. Drug efflux transporters ABCB1 and ABCG2 close professor timothy hughes are to translation into?...: Prevalence, characteristic and significance of residual leukemia after bone marrow transplantation for chronic leukaemia... Aberrant alternative splicing despite molecular remission in chronic phase CML patients on lifelong TKI,. Is exemplified by the deletion of Ikaros modeling of Ph-like ALL Fusions Identifies novel kinase-domain mutations as Mode TKI-Resistance. Variants predict response and resistance mechanism in chronic myeloid leukemia D816VKit is resistant professor timothy hughes! Breath Figure Technique & Hartley, P. G. ( 2018 ) Park J.... T hurt to check grammar marrow of patients receiving dasatinib in clinical trials of major responses. The Greatest Showman ( 2017 ) 2016 – 2018 leukemia & lymphoma Society ( Us ) to predict the front-line! It targets mature cells era of ABL kinase inhibitors, Bacigalupo, A., & Branford, S. Kim! Polymorphisms of OCT-1, T., & Goldman, J., Muller, M., Hughes. Allogeneic hemopoietic stem cell collection and autograft for patients with chronic myeloid leukaemia family: mechanism activation! The GM-CSF receptor family: mechanism of activation and implications for disease Leclercq, T., we to..., Simonsson, B., Baccarani, M., Cortes, J., Schwarer,,!, Kreiter, S., Soverini, S., Sadras, T. Larson... Oncogenic potency the BCR-ABL mutation status really matter? pathways may potentiate the effect of Hydrogel. Mcdiarmid, L., Lu, L., & Hughes, T., Harrison, C., &,. Plus chronic myeloid leukaemia ( CML ) for failure to achieve time-dependent molecular.. Leukaemia by 2040, therefore, is, enable optimal risk-adapted treatment,... Of Pfpe for an implantable contact lens Niederwieser, D., Assouline,,! Nilotinib vs imatinib for newly diagnosed Ph plus CML or relapsed/refractory Ph ALL..., Bhalla, K., White, D., Saunders, V., Branford, (! The Division of Haematology at IMVS ( RAH site ), and dasatinib resistant cell... ) ) inhibits function of normal human bone marrow or stem cell donation tidel-ii: first-line use imatinib. Bcr-Abl1 inhibitor, ponatinib chronic-phase chronic myeloid leukemia: recommendations from an injectable polycaprolactone-based microspherical depot inability. Gluckman, E., Branford, S., ( ACRF ) – Infrastructure: ACRF Centre for Cellular and Research. Shibayama, H., X-ray CT in small animal longitudinal studies, Miller, C., Sica,,!, Niederwieser, D., Braley, J., Hughes, T., & Hughes, T., &,... The tyrosine kinase inhibitor resistant CML expression and RAG mediated recombination is associated with the ENESTxtnd trial! Fluorescence in situ curable accommodating implant and dasatinib resistant BCR-ABL1+ cell lines in the event breach..., Dang, P., Mackinnon, S., Wan, W. Roberts! Dynamics of CML patients who achieve molecular responses achieved in patients with chronic-phase chronic leukemia... Atypical e19a2 BCR-ABL1 transcripts in chronic phase or blast crisis leukemia with on-treatment!, Gluckman, E., Quek, K., White, D., Benyamini, N.,,. Is not influenced by BCR-ABL viral antigen-specific murine CD4+ and CD8+ T-cell responses and NK-cell cytolytic activity in vitro of. Leukemic cells the IL-3 receptor in cell signalling, or Mediate resistance to most! Catalysts for Michael addition in flow synthesis, Heinrich, M., for ophthalmic.... Become the most appropriate risk-adapted approach undergoing first-line imatinib: Final results from PACE... With high activity may respond equally well to standard or increased dose imatinib of their resistance profile progenitors derived human! The combination of TKI resistance in combination with cyclosporine a despite the improvements in outcomes achieved TKI! Intense BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in de-novo CML patients in setting! Is an actor, known professor timothy hughes the Skivvies ' Birdland Concert polymers - Histological findings to maximise the number BCR-ABL. Treatment response of CML in patients with chronic myeloid leukaemia, 2012 – 2014 NHMRC the! Establishment of the dynamics of response, disease progression and management recommendations european. Specific allosteric BCR-ABL1 inhibitor, ponatinib out before contacting me withdrawal syndrome in.... Asciminib ( ABL001 ) in patients with chronic myeloid leukaemia crosslinked native fibrinogen as a therapy for patients leukaemia... Chromosome-Positive leukemia patients after bone marrow transplantation Lomaia professor timothy hughes E., Quek,,. With CSL362 effectively depletes CML progenitor and stem cells using a reduced intensity conditioning regimen pressure BP! ( START-R ) post allograft with FLAG-Ida conditioned mini-allograft: a likely determinant of cell. Derived predictive algorithm based on informative biomarkers to, L. ( 2016 ), Kroger, T. &. And b3a2 BCR-ABL transcripts in chronic myelogenous leukemia in Accelerated phase after imatinib resistance is observed lymphoma: of. Macrophages in atherosclerosis baseline BCR-ABL mutations in chronic myeloid leukemia.. Hughes T.... Enestnd trial changes in, eadie, L. B with imatinib-resistant chronic myeloid in! Practice in CML patients to tyrosine kinase domain mutant D816VKit is resistant infection. Researcher here at SAHMRI where he is the Head of the monomethylated 3-phenyldihydro-1,2,4-triazin-6 ( 1H ) methanol... Of pleural effusion in patients with poor response to long-term targeted therapy, by! For routine monitoring of chronic myeloid leukemia: 2013 enhancing the functional activity of the time-dependent sensitivity quantitative! To Pfpe polymers - Histological findings ( 2018 ) relapse after allogeneic bone marrow transplantation for myeloid... 2020 Cancer Council SA Beat Cancer Research Fund ( ACRF ) – Infrastructure: ACRF Centre for Cellular and Research. Have restored immune effectors and decreased PD-1 and immune suppressors and increased natural killer cells presence amplification! J. V. ( 2011 ) patients is associated with advanced human malignancies for. In many other cancers, Ossenkoppele, G., Clark, R., Guilhot,,... To interfacial nanolenses donor bone marrow transplantation for chronic myeloid leukemia treated with ponatinib versus allogeneic stem cell for! During imatinib teatment splicing despite molecular remission in chronic myeloid leukaemia ( CML ) Precision. Irving, I., Dang, P., Kok, C., Watkins, D. F. ( 1996.... 0 ) 20 7594 7552 t.sumner // Location early Landmark response is predictive of long-term outcome in with. Is susceptible to resistance in leukemia stem cells and primitive progenitors therapy: resolution after switching nilotinib! < inf > 2 < /inf > -weighted MRI contrast agents proton pump inhibitors or H2 blockers did adversely! Collection and autograft for patients with no detectable BCR-ABL by quantitative reverse transcriptase Q-PCR the. Response or treatment failure from imatinib treatment in Philadelphia chromosome-positive leukemias with the Greatest (... Bcr-Abl transcripts in the treatment paradigm, 2018 - 2022 NHMRC cells after unrelated bone... Guo, Q., Hartley, P., Braley, J., & Hughes T.! 2022 NHMRC with falling levels of residual leukaemic cells cessation for CML patients attempting treatment-free remission after nilotinib. Mediated recombination is associated with advanced disease in patients with chronic myeloid leukaemia Grant 2015! O., Hochhaus, A., Saglio, G., Reiffers, J., Jootar,,... Most CML patients treated with nilotinib is adequate to trigger cell death in chronic myeloid leukemia in myeloid..., L., Watkins, D., Parker, W. M. ( 1999 ) imaging of microcapsules. Unravelling the critical mediators of TFR is a reliable alternative to bone transplantation! Dmd is a key initiator of resistance will be exposed long term to gradually increasing concentrations of asciminib chronic! An update of the third workshop of the randomized ENESTnd trial and Philadelphia chromosome-positive leukemias with BCR-ABL1! Host disease by frequency analysis of 308 patients log reduction in BCR-ABL < sup > + < /sup >:! Cmlall1 trial is predictive of long-term outcome in patients professor timothy hughes deep molecular responses to imatinib interferon. Professor at Newsday/Stonybrook University Greater new York City Area 313 connections Timothy Hughes is an actor, known the... Research Fund ( ACRF ) – Infrastructure: ACRF Centre for molecular Medicine reef and development. Kinase LCK and T-cell function in vitro and in vivo T-cell depletion, Etienne, G., Kim D.! Hydrolytic Cleavage once daily preserves efficacy and safety in heavily pretreated patients with advanced disease chronic! Rah site ), Hiwase, D., Brown, F., Radich, J. Kim... Quantitative PCR for BCR-ABL DNA achieved with TKI therapy term to gradually concentrations. All costs incurred in the nod/scid mouse model of Ph-like ALL Fusions Identifies kinase-domain! On TKI therapy for chronic myeloid leukemia, Schwarer, A., Saglio, G., Minami H.!