Writing and Publishing Scientific Articles
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This assertion is supported by the observation, as expected, of significant increases in the frequencies of loss at the BRCA1 and BRCA2 loci in tumors from BRCA1 and BRCA2 carriers, respectively. [Interpretation of findings] To provide a better indication of the most critical events, we used a hierarchical cluster algorithm to group alterations that tended to occur together. The apparent clustering of a limited number of regions of loss and gain indicates a select series of targets [The targets do not have to be named here, because they were named in the Results section] for future studies aimed at identifying genes in ovarian cancer. [Avenue for further studies] Some studies indicate that there are differences in the clinical and/or histopathological characteristics of breast and ovarian tumors between tumors from BRCA1, BRCA2, and non-BRCA1/2 mutation carriers (7 – 13). The reasons for this variation are unknown. BRCA1 and BRCA2 may have a direct effect on the behavior of breast and ovarian epithelial cells, which could vary depending on germ-line BRCA1/2 mutation status. Alternatively, BRCA1/2 mutation status might influence subsequent somatic genetic events in tumorigenesis, with these events being responsible for the observed variation in tumor phenotype. The somatic genetic differences that we observed between BRCA1, BRCA2, non-BRCA1/2, and sporadic ovarian tumors provide support for the latter of these hypotheses. A more detailed comparison of the histopathological characteristics of ovarian tumors in BRCA1/2 mutation and nonmutation carriers will be needed to obtain a better understanding of this association. [Avenue for further study] In conclusion, we used metaphase CGH to characterize the spectrum of somatic genetic events that occur in the development of epithelial ovarian cancer in tumors from BRCA1 and BRCA2 mutation carriers, familial non-BRCA1/2, and sporadic cases. In doing so, we identified molecular genetic differences between these 4 tumor groups that suggest there are different mechanisms for tumor development that may influence the phenotype and clinical outcome of ovarian cancers. The genetic differences we found may be useful in tailoring treatment for breast cancer patients. [Implication of findings]
Adapted with permission from Ramus SJ et al. BRCA1/2 mutation status influences somatic genetic progression in inherited and sporadic epithelial ovarian cancer cases. Cancer Res 63:417 – 423, 2003.
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