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MD Anderson Events

The Center for Cancer Epigenetics Distinguished Lecture Series

The Center for Cancer Epigenetics Distinguished Lecture Series

The Center for Cancer Epigenetics Distinguished Lecture

Talk Title: “Epigenetic Mechanism & Therapy for B-Cell Lymphoma

Speaker: Dr. Ari Melnick

Professor, Department of Medicine & Pharmacology

Weil Cornell Medical School

New York City, New York

Date: Feb. 23

Location: AT&T Auditorium, B2.4750

 

Host: Dr. Xiaobing Shi

Date: 2/23/18, 11am to 12pm
Time: 2/23/18, 11am to 12pm
Location: AT&T Auditorium, Main Building, Floor 2 (B2.4750)
Format: Lecture
Facilitator: Xiaobing Shi
Speaker: Ari Melnick
Speaker Bio: Dr. Melnick focuses on transcriptional and epigenetic mechanisms of lymphoid and myeloid neoplasms. His group uses transcriptional biochemistry and molecular biology, epigenomics, animal models and systems biology in their research. His laboratory has both wet bench and dry bench components. Dr. Melnick is known for his work describing the mechanism of action of the BCL6 transcriptional repressor, results that led his developing the first example of a rationally designed transcription factor inhibitor (Polo et al Nat Med 2004). He has gone on to define the epigenetic and biological mechanisms through which somatic mutations in histone modifying proteins such as EZH2 and KMT2D drive lymphomagenesis. This line of research has led to the realization of how founder somatic mutations in lymphoma have in common the function of maintaining the germinal center phenotype by disrupting the epigenetic programs linked to proliferation control, terminal differentiation, and immune synapsis in 8-cells. Dr. Melnick has also been a pioneer in the epigenomics field. He performed the first large scale epigenomics profiling studies in human cancer specimens which showed for the first time how disruption of focal and highly specific epigenetic patterning is a hallmark of tumors. To accomplish this he established extensive international collaborations with colleagues from Europe, Asia and Australia. These studies led to important findings detailing the mechanism through which mutations in IDH1 and IDH2 disrupt the epigenome, how oncogenes cooperate to drive transformation through aberrant cytosine methylation patterning, and the discovery that epigenetic heterogeneity is an independent risk factor for adverse outcome and that clonal selection is not uniquely driven by genetic mutations. Dr. Melnick has an active drug discovery program in his lab, in addition to BCL6 he has developed other novel targets which have led to contracts with Pharma companies.
Contact: Jessica Fields - (713) 834-6267 - jfnields@mdanderson.org