In This Section

Raghbir Athwal, PhD

Professor, Fels Institute for Cancer Research and Molecular Biology
Professor, Pathology and Laboratory Medicine

Raghbir Athwal
For Patients
Contact Information

Contact Information

Phone

215-707-6931

Fax

215-707-2989

Email

raghbir.athwal@temple.edu
About Me

Research Interests

The long term goal of our research is to elucidate molecular and genetic pathways involved in the regulation of normal cell growth leading to senescence, and their role in the development of cancer and cellular aging. Normal mammalian cells, unlike cancer cells, multiply only for a finite number of generations, and eventually enter a state of irreversible growth arrest, “the replicative senescence”. Applying a functional strategy, we have identified four cell senescence genes, three on chromosome 6q and one on 16q. The ectopic expression of one of the genes (SEN6A), cloned in a retroviral vector, induce senescence in ovarian and breast tumor cells, and lead to premature senescence in normal human fibroblasts. SEN6A is either rearranged or not expressed in many of the breast and ovarian tumor cells, suggesting that it plays a role in the etiology of breast and ovarian cancers. Further pursuit of our research includes delineation of mechanisms of SEN6A inactivation in tumor cells; and identifies signaling pathways involved in the functioning of SEN6A. Our preliminary observations revealed that SEN6A may be involved in DNA damage-repair response through a pathway related to the production of Reactive Oxygen Species (ROS). These finding evoked our interest to study genes associated with DNA damage – repair pathways in relation to cellular senescence. Signaling pathways that regulate cell senescence has gained significance as emerging targets for cancer therapy.

In another project, we are investigating the molecular mechanisms of virus induced malignant transformation of human cells. These studies are driven by the hypothesis that immortalization of human cells requires the disruption of specific genes through viral integration. Using SV40 mediated immortalization of human fibroblasts as a model system; we have isolated a human DNA segment, corresponding to the viral insertion site. The introduction of this cloned human DNA segment, into SV40 immortalized cells, led to the restoration of normal cell growth pattern and senescence. Almost 100 percent of cervical cancer is positive for the presence of HPV virus. Future studies in this project are directed to identify human genes disrupted through HPV integration, and examine their role in the etiology of cervical cancer.

The ultimate aim of our research is to identify molecular targets for diagnosis and therapeutic intervention of cancer.

Education, Training & Credentials

Educational Background

  • Research Associate, National Institutes of Health, National Cancer Institute, 1978
  • Postdoctoral Fellow, Laboratory of Biochemistry, Howard University Medical School, 1975
  • Postdoctoral Fellow, Division of Human Genetics, Department of Pediatrics, University of Missouri, 1973
  • PhD Genetics, University of Missouri, 1971
  • BSc Biology, Punjab Agricultural University, 1964
  • MSc Genetic, Punjab Agricultural University, 1966
Publications

PubMed Publications

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