Oncogenes and tumor-suppressor genes
- National Cancer Institute, Bethesda, MD (United States)
The functional role of oncogenes in human lung carcinogenesis has been investigated by transfer of activated oncogenes into normal cells or an immortalized bronchial epithelial cell line, BEAS-2B. Transfection of v-Ha-ras, Ki-ras, or the combination of myc and raf into BEAS-2B cells produced tumorigenic cell lines, while transfection of raf or myc alone produced nontumorigenic cell lines. In addition to studying the pathogenic role of oncogenes, the authors are attempting to define negative growth-regulating genes that have tumor-suppressive effects for human lung carcinomas. Their strategy to identify tumor-suppressor genes involves loss of heterozygosity studies, monochromosome-cell fusion, and cell-cell fusion studies. Loss of heterozygosity studies revealed consistent allelic DNA sequence deletions on chromosome 17p in squamous cell carcinomas, while large cell carcinomas and adenocarcinomas retained this locus. Mutations in p53, a tumor-suppressor gene located on chromosome 17p, have been observed. Cell-cell hybrid clones produced from fusion of nontumorigenic BEAS-2B cells with tumorigenic HuT292DM cells generally are nontumorigenic. The mechanistic role of the known tumor-suppressor genes Rb-1 and p53 in the development of human lung carcinomas is being investigated in this epithelial cell model of human bronchogenic carcinogenesis.
- OSTI ID:
- 6096698
- Journal Information:
- Environmental Health Perspectives; (United States), Vol. 93; ISSN 0091-6765
- Country of Publication:
- United States
- Language:
- English
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GENES
INACTIVATION
ONCOGENES
MOLECULAR BIOLOGY
CARCINOGENESIS
CHEMICAL ACTIVATION
EPITHELIUM
HYBRIDIZATION
LUNGS
MAN
ANIMAL TISSUES
ANIMALS
BODY
MAMMALS
ORGANS
PATHOGENESIS
PRIMATES
RESPIRATORY SYSTEM
TISSUES
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