The hallmark of cancer cells are their capacity for unlimited growth and their potential to invade other tissues. In contrast, normal cells display a limited capacity for growth and then undergo a process called cellular senescence or aging. Immortal cells, those with an unlimited lifespan, have escaped from normal aging controls. Such an escape mechanism may also be one of the major changes leading normal cells to become malignant tumors. Consequently, an understanding of the genes and mechanisms involved in aging and immortality would provide information about important steps in the development of cancer. Recent experimental evidence shows that several genes originally discovered as tumor suppressors, p53 and an RB-like protein, are involved in regulating cellular senescence. The long term objective is to define the molecular basis of cellular senescence in human fibroblasts and epithelial cells, with the long term goal of applying this knowledge to the biology of cancer. By identifying the protein(s) involved in cellular senescence, the proposed research should result in a better understanding if the molecular biology of human aging and cancer.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32AG005747-03
Application #
2667606
Study Section
Chemical Pathology Study Section (CPA)
Program Officer
Finkelstein, David B
Project Start
1998-02-20
Project End
Budget Start
1998-02-20
Budget End
1999-02-19
Support Year
3
Fiscal Year
1998
Total Cost
Indirect Cost
Name
University of Texas Sw Medical Center Dallas
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
City
Dallas
State
TX
Country
United States
Zip Code
75390