DEPARTMENT OF COMPARATIVE PATHOBIOLOGY

 

 

 

SPECIAL SEMINAR

 

 

Kenneth P. Nephew, Ph.D.

Professor, Department of Cellular and Integrative Physiology

Adjunct Professor of Obstetrics and Gynecology

Indiana University School of Medicine

Bloomington, Indiana

 

 

An Epigenetic Approach To Understanding The Pathobiology Of Cancer”

 

 

Thursday, October 25, 2007

Lynn 1136

10:30 am

 

ABSTRACT:

The term epigenetics refers to heritable DNA modifications that occur outside of primary base-coding sequences.  The most common of these is methylation of cytosine, usually located within the dinucleotide CpG, catalyzed by enzymes known as DNA methyltransferases (DNMTs). CpG islands, regions of DNA with a high GC content and typically located near the promoter of a gene, are usually unmethylated in normal cells.  However, it has now been well established that CpG islands often become hypermethylated and transcriptionally silenced in tumors, despite an overall global decrease in DNA methylation (i.e., global hypomethylation) in the tumor. Other commonly occurring epigenetic modifications within silenced genes are hypoacetylation and methylation of their associated histones.  A number of histone lysines have been discovered as methylated; these modifications can be transcriptionally activating or repressing, depending on the specific residue. The comprehensive collection of genome-wide epigenetic phenomena, DNA-methylation patterns and chromatin modifications, is called the epigenome.  Furthermore, most if not all human cancers are at least partially associated with epigenetic dysregulation of gene expression, forming a rational basis for future treatment strategies designed to alter this fundamental processes in cancer. We have investigated the role of the epigenome in the pathobiology of ovarian and breast cancer and have identified potential epigenetic biomarkers for these diseases. Unlike genetic changes, the epigenetic changes in cancer are potentially reversible, and the ability to reactivate epigentically-silenced tumor suppressor genes and key control pathways and reverse the cancer cell phenotype is a promising strategy.  Epigenetic drugs, including demethylating agents and histone deacetylase inhibitors, can be used singly or in combination with currently available cancer chemotherapies.  An approach we are taking in the clinic is to use a demethylating agent to re-sensitize drug-resistant cancer cells to standard chemotherapeutic approaches.  A new opportunity in cancer research is that many cancers are now believed to contain a small population of “cancer stem cells” responsible for growing an entire tumor. While conventional cancer chemotherapies kill most of the cells in a tumor, they may miss these cancer stem cells, allowing the tumor to re-grow. Epigenetic changes may be a way to characterize cancer stem cells, and new drugs that alter those DNA structural changes may represent a new type of therapy against those cells, allowing complete killing of the tumor.