Epithelial ovarian cancer

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Hannan Javed, M.D.[2]

Pathogenesis of high grade serous carcinoma
Pathogenesis of high grade serous carcinoma[1] Normal fallopian tube epithelium comprises of both secretory and ciliated cells and stains negative for p53. The benign ‘p53 signature’: secretory cells that possess strong p53 expression and evidence of DNA damage but are not proliferative. When they progress to serous tubal intraepithelial carcinoma or ‘STIC’, they acquire nuclear pleomorphism, mitoses, and loss of polarity. Serous tubal intraepithelial carcinoma shares all these properties with invasive high grade serous epithelial ovarian cancer and clinical symptoms typically emerge with advanced disease.[1][2]
DNA damage and repair mechanisms.
DNA damage and repair mechanisms.[3]

References

  1. ↑ 1.0 1.1 Kroeger PT, Drapkin R (February 2017). "Pathogenesis and heterogeneity of ovarian cancer". Curr. Opin. Obstet. Gynecol. 29 (1): 26–34. doi:10.1097/GCO.0000000000000340. PMC 5201412. PMID 27898521.
  2. ↑ Karst AM, Drapkin R (2010). "Ovarian cancer pathogenesis: a model in evolution". J Oncol. 2010: 932371. doi:10.1155/2010/932371. PMC 2739011. PMID 19746182.
  3. ↑ Toss A, Tomasello C, Razzaboni E, Contu G, Grandi G, Cagnacci A, Schilder RJ, Cortesi L (2015). "Hereditary ovarian cancer: not only BRCA 1 and 2 genes". Biomed Res Int. 2015: 341723. doi:10.1155/2015/341723. PMC 4449870. PMID 26075229.
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