Steven Treon, MD, PhD Presentations

2019 WM Foundation Canada (WMFC) Seminar with Patients

WM Foundation Canada (WMFC)
Jewish General Hospital
Montreal, QC, Canada
November 7, 2019
Steven P. Treon MD, PhD, FACP, FRCP – Bing Center for Waldenstrom Macroglobulinemia, Dana-Farber Cancer Institute
In this video, Dr. Steven P. Treon speaks to a Montreal patient group providing updates on the genomics and latest treatment options for Waldenstrom’s macroglobulinemia.

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.

WM: Genomic & Treatment Advances

Zachary Hunter, PhD, Guang Yang, PhD, Steve Treon, MD, PhD – Dana Farber Cancer Institute, 2018 Ed Forum
Three researchers discuss how MYD88 and CXCR4 mutations are common in WM with MYD88 activating BTK and HCK in WM cells, both targets of ibrutinib. Ibrutinib produces high response rates and durable responses in relapsed and refractory WM. No complete responses. Mutated CXCR4, aberrant IRAK and BCL2 signaling contribute to intrinsic resistance against ibrutinib. Multiple BTK mutations are common with acquired ibrutinib resistance and trigger ERK1/2 survival signaling. Novel strategies to overcome intrinsic and acquired resistance to ibrutinib, including targeting CXCR4, ERK, IRAK, and BCL2 signaling.

New Insights into the Biology & Therapy of WM

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

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

IWMF Funding of Landmark Discoveries in WM and how Continued Funding is Critical for Future Management of the Disease

Steven P. Treon, MD, PhD – Dana Farber Cancer Institute, Boston, 2015 Ed Forum
Dr. Treon discusses his interest in WM and WM research, focusing on the whole genome sequencing research supported by the IWMF that helped make the critical discoveries of the MYD88 and CXCR4 mutations. He also mentions that continued funding of WM research is critical to future success in managing the disease.

Targeted Therapies for WM

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

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)