Epithelial ovarian cancer: Difference between revisions

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[[File:Pathogenesis of high grade serous carcinoma.jpg|alt=Pathogenesis of high grade serous carcinoma|center|frame|Pathogenesis of high grade serous carcinoma<ref name="pmid27898521">{{cite journal |vauthors=Kroeger PT, Drapkin R |title=Pathogenesis and heterogeneity of ovarian cancer |journal=Curr. Opin. Obstet. Gynecol. |volume=29 |issue=1 |pages=26–34 |date=February 2017 |pmid=27898521 |pmc=5201412 |doi=10.1097/GCO.0000000000000340 |url=}}</ref>   
[[File:Pathogenesis of high grade serous carcinoma.jpg|alt=Pathogenesis of high grade serous carcinoma|center|frame|Pathogenesis of high grade serous carcinoma<ref name="pmid27898521">{{cite journal |vauthors=Kroeger PT, Drapkin R |title=Pathogenesis and heterogeneity of ovarian cancer |journal=Curr. Opin. Obstet. Gynecol. |volume=29 |issue=1 |pages=26–34 |date=February 2017 |pmid=27898521 |pmc=5201412 |doi=10.1097/GCO.0000000000000340 |url=}}</ref>   
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.   19746182
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.<ref name="pmid27898521">{{cite journal |vauthors=Kroeger PT, Drapkin R |title=Pathogenesis and heterogeneity of ovarian cancer |journal=Curr. Opin. Obstet. Gynecol. |volume=29 |issue=1 |pages=26–34 |date=February 2017 |pmid=27898521 |pmc=5201412 |doi=10.1097/GCO.0000000000000340 |url=}}</ref>]]
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==References==
{{reflist|2}}

Revision as of 14:25, 26 February 2019


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]

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.