Given the complex number of germline and somatic alterations of oncogenes and tumor suppressor genes associated with human breast cancer, it is difficult to derive a singular pathogenic pathway which incorporates all these components. Rather, it would appear that breast cancer represents a family of phenotypically similar diseases with varying molecular etiologies. Non-familial breast cancer accounts for some 90% of cases diagnosed. Both in vitro and in vivo studies suggest that hyperexpression of the oncogenes ras, myc and c-erbB-2 are involved in the initiation of carcinogenesis in the majority of these tumors, while other genes may be involved in their promotion and ultimate metastases. Familial breast cancer accounts for some 10% of cases diagnosed. Approximately 80% of these said cases can be explained by a germline loss of heterozygosity at one of two genes, BRCA-1 and BRCA-2. Considerable research is ongoing to identify the gene(s) responsible for the remaining 20%. Currently, the clinical relevance to categorization of patients according to the subsets among the above observations lies in assigning a prognosis to individuals at risk for or suffering from breast cancer. This should lead to more successful disease prevention and detection and allow for stratification of patients on therapeutic clinical trials. Hopefully, however, our increased knowledge of the myriad molecular cascades involved in the pathogenesis of human breast cancer will lead to novel therapeutic strategies in the future.
|Original language||English (US)|
|Number of pages||28|
|Journal||Archives of STD/HIV Research|
|State||Published - Jan 1 1996|
ASJC Scopus subject areas
- Immunology and Allergy
- Microbiology (medical)