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Frederick Pei Li

Born  1940
Died  

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American physician, born 1940, Canton, China.

Biography of Frederick Pei Li

The information below is taken from the website of the Harvard School of Public Health as well as that of Asian American Network for Cancer Awareness, Research, and Training:

Frederick Pei Li was born in Canton, China, and raised in New York City where his parents operated a Chinese restaurant. He received a B.A. in physics from New York University, an M.D. from the University of Rochester, and M.A. in demography from Georgetown University. In 1967 he joined the Epidemiology Branch of the NCI. He served for 24 years, mostly at the NCI's field station at the Dana-Farber Cancer Institute in Boston. In 1991, he became head of Dana-Farber's Division of Cancer Epidemiology and Control.

Currently, Dr. Li is Professor of Clinical Cancer Epidemiology at the Harvard School of Public Health, Professor of Medicine at the Harvard Medical School, and the Harry and Elsa Jiler American Cancer Society Clinical Research Professor. In 1996, Dr. Li was appointed by President Clinton to NCI's National Cancer Advisory Board.

This is Li's presentation of himself and his work:
Research Interests : Molecular Epidemiology of Hereditary Cancers
Recent data have established that the basic molecular defects in cancer are genetic changes that result in loss of normal cellular control mechanisms. Some of these mutations can be inherited through the germline. I have been studying inherited susceptibility of cancer through affected families. The goal is to identify genes that are involved in cancer development.

I was attracted to studies of cancer families because epidemiological studies show that virtually all cancers manifest a tendency to aggregate in families. Close relatives of a cancer patient are at increased risk of that neoplasm, and perhaps other forms of cancer. The excess site-specific cancer risk is exceptionally high for carriers of certain cancer genes, in whom the attack rate can approach 100 percent. In candidate cancer families, the possibility that clustering is on the basis of chance must be excluded through epidemiological studies that establish the presence of an excess cancer risk. Predisposed families are candidates for laboratory studies to identify the inherited susceptibility factors. These investigations have lead to the identification and isolation of human cancer genes, the tumor suppressor genes. These cancer genes are among more than 200 single-gene traits associated with the development of cancer. Approximately a dozen inherited susceptibility genes have been definitively identified, and many more are being sought. From studies of retinoblastoma and other rare cancers, important new information was generated about the fundamental biology of cancers that arise in many patients. Isolation of an inherited cancer susceptibility gene provides opportunities for presymptomatic testing of at-risk relatives. However, testing of healthy individuals also raise important issues regarding informed consent, confidentiality and potential for adverse psychological, social and economic effects.

My colleagues and I are using families with inherited mutations in the p53 gene, which predisposes to breast cancer and diverse childhood cancers, as a model for developing a genetic testing program.

Bibliography

  • F.P. Li:
    Phenotypes, genotypes, and interventions for hereditary cancers.
    Cancer Epidemiology, Biomarkers and Prevention, Baltimore, 1995, 4:579-582.
  • A.F. Patenaude, L. Basili, D.L. Fairclough, and F.P. Li :
    Attitudes of 47 mothers of pediatric oncology patients towards genetic testing for cancer predisposition.
    Journal of Clinical Oncology, Duluth, Minnesota, in press.
  • J. A. Talcott, W.A. Thurber, A.F. Kantor, E.A. Gaensler, J.F. Danahy, K.H. Antman, and F.P. Li:
    Asbestos-associated diseases in a cohort of cigarette-filter workers.
    The New England Journal of Medicine, Boston, 1989, 321: 1220-1223.
  • J. Pelletier, W. Bruening, F.P. Li, D.A. Haber, T. Glaser, and D.E. Housman:
    WT1 mutations contribute to abnormal genital system development and hereditary Wilms' tumour. Nature, London, 1991, 353: 431-434. See also bilbiography for Joseph F. Fraumeni.

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