Time slots Sessions Location December 5 th (Friday) Friday Scientific Workshop on Myeloid Development

Transcription

1 Overview of CML related sessions at the 56 th ASH Annual Meeting in San Francisco (USA) December 5-9, 2014 Time slots Sessions Location December 5 th (Friday) Friday Scientific Workshop on Myeloid Development The Workshop on Myeloid Development will examine the latest scientific findings in myeloid biology in a highly interactive environment that permits exchange of ideas among investigators. The workshop will include sessions on stem cells, transcription factors and epigenetics, signalling, animal models, and myeloid malignancies. This is a true workshop, where each session leader will briefly summarize the current questions facing the field and then lead discussions on how best to answer those questions. New findings or novel techniques that provide insight into these questions will be an essential part of this discussion. This workshop is directed at laboratorybased investigators, but the broad-ranging content and highly interactive format is suitable for clinically oriented investigators and is particularly appealing to students and trainees, giving them the opportunity to interact directly with experts in the fields of hematopoiesis and myeloid biology. South Gateway Ballroom 103 Co-Chairs: Leonard I. Zon, MD, Howard Hughes Medical Institute, Boston Children's Hospital, Harvard Medical School Boston, MA Alan G. Rosmarin, MD, University of Massachusetts Memorial Medical Worcester, MA

2 December 6th (Saturday) Educational Session: Minimal Residual Disease: Chronic Myeloid Leukemia and Acute Lymphocytic Leukemia Chair: Michael J Mauro MD, Memorial Sloan Kettering Cancer, New York North This session will delve into the critical question of identifying, quantifying, and characterizing minimal residual disease (MRD) in leukemia. With increased clarity regarding molecular characterization of acute leukemias as well as significantly greater depth of response potential in chronic myeloid leukemia, both methods and definitions have been redefined to judge the therapeutic index of novel therapies, relapse risk specific to the molecular signature identified, and likelihood of long term durable response after therapy. Speakers: David Grimwade, PhD, King's College London School of Medicine London: United Kingdom Defining Minimal Residual Disease: Which Platforms are Ready for "Prime Time"? Michael J. Mauro, MD, Memorial Sloan Kettering Cancer New York, NY: Goals for Chronic Myeloid Leukemia Tyrosine Kinase Inhibitor Treatment: How Little Disease is Too Much? Martin Schrappe, MD University Hospital Schleswig-Holstein Kiel, Germany: Detection and Management of Minimal Residual Disease in Acute Lymphocytic Leukemia

3 Educational Session: Minimal Residual Disease: Chronic Myeloid Leukemia and Acute Lymphocytic Leukemia Chair: Dr. Michael J Mauro MD, Memorial Sloan Kettering Cancer, New York This session will delve into the critical question of identifying, quantifying, and characterizing minimal residual disease (MRD) in leukemia. With increased clarity regarding molecular characterization of acute leukemias as well as significantly greater depth of response potential in chronic myeloid leukemia, both methods and definitions have been redefined to judge the therapeutic index of novel therapies, relapse risk specific to the molecular signature identified, and likelihood of long term durable response after therapy. Speakers: David Grimwade, PhD, King's College London School of Medicine London: United Kingdom Defining Minimal Residual Disease: Which Platforms are Ready for "Prime Time"? Michael J. Mauro, MD, Memorial Sloan Kettering Cancer New York, NY: Goals for Chronic Myeloid Leukemia Tyrosine Kinase Inhibitor Treatment: How Little Disease is Too Much? Martin Schrappe, MD University Hospital Schleswig-Holstein Kiel, Germany: Detection and Management of Minimal Residual Disease in Acute Lymphocytic Leukemia

4 Poster session: Chronic Myeloid Leukemia: Biology and Pathophysiology excluding Therapy, Poster I Chronic Myeloid Leukemia: Therapy, Poster I Level 1 December 7 th (Sunday) Oral Poster presentation: CML: Outcomes with TKI Therapy Michele Baccarani, MD, University of Bologna Daniel J. DeAngelo, MD/PhD, Harvard University/Dana Farber Cancer Institute San Francisco Marriott Marquis Yerba Buena Ballroom Salon : Interim analysis of a pan European stop tyrosine kinase inhibitor trial in chronic myeloid leukemia: the EURO-SKI study 16.45: Final study results of the phase 3 dasatinib versus imatinib in newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) trial (DASISION, CA ) 17.00: Survival and prognosis in patients with first-line imatinib treatment under particular consideration of death to chronic myeloid leukemia 17.15: Second malignancies following treatment of chronic myeloid leukemia in the tyrosine kinase inhibitor ERA 17.30: Defining therapy goals for major molecular remission in chronic myeloid

5 leukemia: results of the randomized CML-Study IV 17.45: Comparing the prognostic significance of early predictors of survival in chronic myeloid leukemia (CML) treated with imatinib an analysis of the randomized CML-Study IV Poster session: Chronic Myeloid Leukemia: Biology and Pathophysiology excluding Therapy, Poster II Chronic Myeloid Leukemia: Therapy, Poster II : Level 1 December 8 th (Monday) Oral poster presentation: CML: Biology and Pathophysiology, excluding Therapy: Strategies to Circumvent Therapy Resistance Thomas O'Hare, PhD, Huntsman Cancer Institute, University of Utah Wendy T Parker, PhD, Centre for Cancer Biology 10.30: Induced pluripotent stem cell model in chronic myeloid leukemia revealed olfactomedin 4 as a novel survival factor for primitive leukemia cells 10.45: ABL001, a potent allosteric inhibitor of BCR-ABL, prevents emergence of resistant disease when administered in combination with nilotinib in an in vivo murine model of chronic myeloid leukemia 11.00: 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 North

6 11.15: CD70/CD27 signalling mediates resistance of chronic myeloid leukemia stem cells to tyrosine kinase inhibitors by compensatory activation of the Wnt pathway 11.30: Combination of tyrosine kinase inhibitor with β-catein/cbp modulator C82 reverses TKI resistance, eradicates quiescent CML stem/progenitors cells, and overcomes MSC-associated micro environmental protection 11.45: Integrin-linked kinase as a key mediator of stromal cell-enhanced resistance of primitive CML cells to tyrosine kinase inhibitors Oral poster presentation: CML: Prognosis and Therapy Jane F. Apperley, MD, Hammersmith Hospital Imperial College, London Mauricette Michaellet, MD, PhD, Centre Hospitalier Lyon Sud : Spirit 2: an NCRI randomised study comparing dasatinib with imatinib in patients with newly diagnosed CML 15.00: Achieving early landmark response is predictive of outcomes in heavily pretreated patients with chronic phase myeloid leukemia (CP-CML) treated with ponatinib 15.15: Epic: A phase 3 trial of ponatinib compared with imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CP-CML) 15.30: Seven years follow-up of patients with imatinib-resistant or intolerant chronic phase myeloid leukemia (CML-CP) receiving dasatinib in study CA : final study results 15.45: The experience of the international registry for chronic myeloid leukemia

7 (CML) in children and adolescent (i-cml-ped study): prognostic consideration 16.00: Impairment of longitudinal growth by tyrosine kinase inhibitor (TKI) treatment data from a large pediatric cohort with chronic myeloid leukemia (CML) Oral poster presentation: CML: Biology and Pathophysiology, excluding Therapy: Disease Progression and the Microenvironment: Therapeutic Implications Christopher J. Walker, PhD, The Ohio State University Comprehensive Cancer Tim H Brummendorf, MD, University Hospital RWTH Aachen : Malignant reprogramming of progenitors into leukemia stem cells is enhanced by upregulation of CD44 transcript variant 3 in malignant microenvironments 15.00: Cooperative targeting of BcL-2 family proteins by ABT-199 (GDC-0199) and tyrosine kinase inhibitors to eradicate blast crisis CML and CML stem/progenitor cells 15.15: BACH2 promotes lineage-specific fate decisions in BCR-ABL1-driven leukemia 15.30: Pyrvinium selectively targets blast phase chronic myeloid leukemia through inhibition of mitochondrial respiration 15.45: Evaluation of extrinsic and intrinsic cues involved in BCR-ABL-induced leukemogenisis 16.00: The vascular niche is involved in regulating leukemic stem cells in

8 murine chronic myelogenous leukemia Poster session: Chronic Myeloid Leukemia: Biology and Pathophysiology excluding Therapy, Poster III Chronic Myeloid Leukemia: Therapy, Poster III Oral Poster presentation: Health Services and outcomes Research Malignant Diseases: New/Refined Prognostic Schemes/Pharmacoeconomics Richard Aplenc, MD, PhD, Children's Hospital of Philadelphia Kristen M. Sanfilippo, MD, MPHS, Saint Louis Veterans Administration Medical Level : What is the most cost-effective strategy for treating newly diagnosed chronic phase myeloid leukemia (CML) after imatinib loses patent exclusivity? December 9 th (Tuesday) Oral poster presentation: CML Therapy: TKI Cessation, Monitoring and Resistance Martin C. Müller, MD, University Hospital Mannheim, Germany Franck Emmanuel Nicolini, MD, PhD, Centre Hospitalier Lyon Sud

9 7.30: Dasatinib or nilotinib discontinuation in chronic phase (CP-) chronic myeloid leukemia (CML) patients with durably undetectable BCR-ABL Transcripts: Interim analysis of the STOP 2G-TKI Study with a minimum followup of 12 months on behalf of the French CML group 7.45: Early disease relapse after tyrosine kinase inhibitor treatment discontinuation in CML is related both to a low number and impaired function of NK-Cells 8.00: The risk of relapse in CML patients who discontinued imatinib can be predicted based on patients' age and the results of dpcr analysis 8.15: KIR 2DL 5D genotype independently predicts poor outcomes in CML-CP patients switched to nilotinib after suboptimal responses to imatinib and may redefine prognosis and patients with EMR failure 8.30 In chronic myeloid leukemia patients an 2 nd line tyrosine kinase inhibitor therapy, deep sequencing at the time of warning may allow sensitive detection of emerging BCR-ABL1 mutants 8.45 The adverse effect of high sokal risk for first line imatinib treated patients is overcome by a rapid rate of BCR-ABL decline measure as early as 1 month of treatment