Role of BRCA gene dysfunction in breast and ovarian cancer predisposition.
Tumor suppressor genes that perform apparently generic cellular functions nonetheless cause tissue-specific syndromes in the human population when they are mutated in the germline. The two major hereditary breast/ovarian cancer predisposition genes, BRCA1 and BRCA2, appear to participate in a common pathway that is involved in the control of homologous recombination and in the maintenance of genomic integrity. How might such functions translate into the specific suppression of cancers of the breast and ovarian epithelia? Recent advances in the study of BRCA1 and BRCA2, discussed herein, have provided new opportunities to address this question.
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Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA. ralph_scully@dfci.harvard.edu
D019313:BRCA1 Protein / Q000502:physiology*; D024682:BRCA2 Protein; D001943:Breast Neoplasms / Q000235:genetics*; D002453:Cell Cycle; D004260:DNA Repair; D005260:Female; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D018095:Germ-Line Mutation; D006801:Humans; D009363:Neoplasm Proteins / Q000502:physiology*; D010051:Ovarian Neoplasms / Q000235:genetics*; D011995:Recombination, Genetic; D014157:Transcription Factors / Q000502:physiology*
D019313:BRCA1 Protein; D024682:BRCA2 Protein; D005819:Genetic Markers; D009363:Neoplasm Proteins; D014157:Transcription Factors