Epigenetics at the Interface of Aging, Exposures and Cancer

When:
February 20, 2014 @ 12:00 pm – 1:00 pm
2014-02-20T12:00:00-07:00
2014-02-20T13:00:00-07:00
Where:
Biodesign Auditorium
727 E. Tyler St. Tempe
AZ 85287
Contact:
Chevas Samuels
480-965-6784

issa-con

Speaker(s):
Jean-Pierre Issa, MD is Professor of Medicine and Director of Temple University School of Medicine’s Fels Institute for Cancer Research and Molecular Biology. As principal investigator and project leader of several multi-million-dollar NIH/NCI-funded research projects, Dr. Issa has overseen ground-breaking studies. Particularly impressive are the important contributions his work has made to our understanding of epigenetics in the pathophysiology and treatment of cancer. His work has helped to reveal that different cancers arise along different molecular routes – predominantly genetic vs. predominantly epigenetic, an important concept in the pathophysiology of cancer. His focus on whole genome epigenetic studies has led to promising biomarkers for cancer detection, prognosis and prediction, and his proof-of-principle for epigenetic therapy of cancer is now standard of care in several types of leukemias.

Location:

Web Cast: Web Cast:

Date & Time: February 20th, 2014 12:00 p.m.

Title: Epigenetics At The Interface of Aging, Exposures and Cancer

Abstract:
The epigenome is reset during embryogenesis and matures around the end of development. Large scale genomic studies have now shown considerable proliferation dependent epigenome changes (drift) in aging cells (DNA methylation instability, chromatin instability). Comparison of rodent, primate and human aging shows that DNA methylation drift is conserved, depends primarily on chronologic age, and can be predicted to a certain degree by local genomic features (e.g. retrotransposons). It can therefore be argued that this epigenomic instability is a necessary result of the evolution of complex genomes that lack reprogramming capabilities in adult cells. Epigenetic drift creates gene expression variation in aging tissues that serve as an enabler of Darwinian evolution at the tissue level. Selective pressures result in cells with unique epigenetic programs that lead to diseases such as cancer or atherosclerosis. Importantly, epigenetic drift can be modulated by exposures (inflammation and perhaps diet), providing a mechanistic link between lifestyle and disease. In turn, epigenetic reprogramming could be useful for prevention and treatment of age-related pathology. In leukemias, reprogramming by DNA methylation inhibitors has gained acceptance as effective therapy for myeloid leukemias, and drugs for other epigenetic targets are rapidly proceeding towards clinical trials.

If you have questions please contact Chevas Samuels. Coffee will be served!

Chevas Samuels, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

(480) 965-0342 | Fax: (480) 965-6362

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