Presentations for Biology Biomarkers Genomics Research
Breaking News from the WM Front
Steven Treon, MD, PhD – Dana Farber Cancer Institute, 2019 Ed Forum
Explains why complete responses are so uncommon in WM, even with targeted therapy, what are the WM-centric toxicities with commonly used therapies, how pro-survival signaling of WM cells is driven by mutated MYD88 in WM, how CXCR4 mutations permit ongoing pro-survival signaling of Wm cells by CXCL12 and makes CXCR4 resistant to ibrutinib and the impact of CXCR4 on WM response and progression free survival (PFS). Reviews studies with ibrutinib, venetoclax, a combination of both drugs, zanubrutinib, acalabrutinib, and incorporating other novel treatments to eradicate residual or resistant disease. Also explains what the knowledge gaps are for developing more effective treatments for patients with WM without MYD88 mutations, the knowledge gaps for treating Bing Neel Syndrome, and treatment outcomes of WM-related peripheral neuropathy.
Immunotherapy – Making the Immune System Target WM Cells
Stephen Ansell MD, PhD, Mayo Clinic, Rochester, 2019 Ed Forum
Explains how immunotherapy activates T-cells into killer T-cells and prevents them from being switched off, so that the T-cell has increased ability to target cancer cells. Over time, T-cells can become “exhausted” and switched off with loss of function. Strategies to block these “switched off” signals with PD1 blockade and CTLA-4 blockade are presented. T-cells in WM are not activated, strategies are presented to activate the T-cell by “waking’ them up by giving them a “poke.” T-cells in WM also do not “lock on” to their targets. Chimeric antigen receptor (CAR) T-cell therapy may give the T-cell a new way to “dock” onto WM cells.
Zachary Hunter, PhD – Dana-Farber Cancer Institute, 2019 Ed Forum
Teaches the newly diagnosed and veteran patients genetics, genomics, epigenetics, the genomics of WM, and using mutation status to understand responses to ibrutinib. Additionally, Dr. Hunter introduces us to the expression of BCL2 family members in WM, validation of CXCL13 correlation with bone marrow and hemoglobin in WM, the signaling pathways driven by mutated MYD88 in WM, the effect of cytokines that protect clones from ibrutinib, and new drugs in clinical trials (HCK inhibitors and MAPK/ERK inhibitors).
Stephen Ansell MD, PhD - Mayo Clinic Rochester, 2018 Ed Forum
Provides the IWMF-LLS Strategic Research Roadmap and addresses the uniqueness of WM, its genomics, epigenomics, MYD88 L265P and CXCR4 mutations, and treatment options
Overview of the IWMF-LLS Strategic Research Roadmap – Our Track for the Future
Stephen Ansell, MD, PhD – Mayo Clinic Rochester, 2017 Ed Forum
Provides the IWMF-LLS Strategic Research Roadmap and addresses the uniqueness of WM, its genomics, epigenomics, MYD88 L265P and CXCR4 mutations, treatment options, and survival
Steven Treon, MD, PhD – Dana-Farber Cancer Institute, 2017 Ed Forum
Discusses manifestations of WM, side effects, genomics, treatment options, upfront treatment and relapsed/refractory treatment approaches
Madhav Dhodapkar, MD – Yale University, 2017 Ed Forum
Reviews basic immunology, what makes cancer immunotherapy special, what are the some of the current approaches and existing challenges/emerging approaches
Translating Genomic Findings into New Treatment Opportunities for WM
Steven Treon, MD, PhD – Dana-Farber Cancer Institute, 2016 Ed Forum
Reviews WM-centric toxicities with commonly used therapies and discusses new directions in WM based on the MYD88 L265P somatic mutation in WM
An Overview of Epigenetics (Why understanding the epigenome will change the practice of medicine)
Ari Melnick, MD – Weill Cornell Medical College, 2016 Ed Forum
Provides an understanding of genomics and explains the genome/computer operating system vs. epigenome/computer programs metaphor. Reviews epigenetics as a blueprint for cancer cells and how epigenetics and understanding the mechanism yields therapies for turning DLBCL cells into plasma cells
Edward Stadtmauer, MD, University of Pennsylvania, 2016 Ed Forum
Covers the manifestations of WM, immunologic approaches to overcome self-tolerance in lymphoma, rationale for cellular immunotherapy in lymphoma, adoptive T-cell therapy, second generation of CAR for B-cell malignancies, overview of activated/engineered T-cell therapy, CD19-targeted CAR T-cells for B-cell malignancies, phase I trial for CLL, results with diffuse large B-cell lymphoma, follicular lymphoma and adverse events, pilot study of CART19 in multiple myeloma, CART-BCMA cells for multiple myeloma, and potential strategies to improve CART therapy in lymphoma
On March 6, 2016, Dr. Jorge Castillo spoke to the Philadelphia IWMF Support Group on Genomic-based Advances in WM. Dr. Castillo, of the Dana-Farber Cancer Institute, is one of the world’s leading clinicians for Waldenstrom’s macroglobulinemia, and provides a valuable perspective, especially since:
There are approximately 1,500 WM patients diagnosed each year in the United States.
Dr. Castillo sees approximately 750 WM patients each year!
Most community oncologists see 0, 1, 2, or 3 WM patients in their career, Dr. Castillo probably sees more WM patients in a morning than most oncologists see in a lifetime.
This video is almost 2 hours in length.
No slides available
The Strategic Research Roadmap for WM
Lee Greenberger, PhD - The Leukemia and Lymphoma Society, 2015 Ed Forum
Covers who is LLS, what are their interests in WM, what have they funded, what is the road ahead, and how will we fund the future
Steven Treon, MD, PhD - Dana Farber Cancer Institute, 2015 Ed Forum
Explains the WM-centric toxicities with commonly used therapies and new treatment directions in WM, including MYD88 L265P mutation and the MYD88 L265P signal pathway, Ibrutinib studies and its effect on side effects and survival, WHIM-like CXCR4 C-tail mutations in WM, unmutated MYD88 disease in WM, Idelalisib, clinical trial of ABT-199 (BCL2 inhibitor) in relapsed/refractory WM, resistance to Ibrutinib, and Ixazomib clinical trial
Mary L. McMaster, MD - National Institutes of Health, 2015 Ed Forum
Explores why WM sometimes clusters in families, is WM in families different from non-familial WM, why some people are susceptible to WM, factors that increase risk for WM, genetics, and environmental lifestyle
Julie Nielsen, PhD - Deeley Research Centre, British Columbia Cancer Foundation, 2015 Ed Forum
Provides an overview of the immune response to cancer, what T cells are and how they work, immune-based therapies for cancer, using T cells to target patient-specific mutations, targeting MYD88 with T cells, CD19 Car T cells, and mutations in WM
Stephen Ansell, MD, PhD - Mayo Clinic, Rochester, 2015 Ed Forum
Reviews how lymphocytes become plasma cells and then produce antibodies and activate the B-cell receptor pathway, the Toll-like receptor pathway, causes of increased production of IgM in WM, cytokines, chemokines, receptor/ligand interactions and cell communications
Advances in the Management of WM Revealed by Whole Genome Sequencing (Genomic Based Treatment Advances in WM)
Steven Treon, MD, PhD - Dana Farber Cancer Institute, 2014 Ed Forum
Discusses the NCCN options for treatment of WM, WM-centric toxicities with commonly used therapies, MYD88 L265P in WM /IgM MGUS, MYD88 L265P Signal Pathway and Ibrutinib (inhibitor of BTK), and Idelalisib (inhibitor of P13K-delta)
New Developments in WM Research (updates of research in WM)
Irene Ghobrial, MD – Dana Farber Cancer Institute, 2014 Ed Forum
Discusses tissue bank research studies, the development of an integrated tissue bank that is linked to clinical characteristics from patients with different stages of WM, and early results from that study
Covers CXCR4 in MM and WM and C10113G/CXCR4 variant in WM and treatment options
Stephen Ansell, MD, PhD – Mayo Clinic, Rochester, 2014 Ed Forum
Covers why WM cells need to communicate and how they communicate, cytokine networks, B-cell receptor pathway, Toll-like receptor pathway, what goes wrong in WM, what causes the increased production of IgM in WM, B-lymphocyte stimulator (BLyS) increase in WM, and why we need to stop the communication