Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 177, Issue 4, Pages 1611-1617Publisher
AMER SOC INVESTIGATIVE PATHOLOGY, INC
DOI: 10.2353/ajpath.2010.100212
Keywords
-
Categories
Funding
- Gynecologic Cancer Foundation
- National Institutes of Health, The University of Texas MD Anderson Cancer Center [P50 CA08369, R01-CA133057]
- MD Anderson's Cancer Center [CA016672]
- Entertainment Industry Foundation
- Marsha Rivkin Center
- Blanton-Davis Ovarian Cancer Research Program
Ask authors/readers for more resources
Low-grade ovarian serous carcinomas are believed to arise via an adenoma-serous borderline tumor-serous carcinoma sequence. In this study, we found that advanced-stage, low-grade ovarian serous carcinomas both with and without adjacent serous borderline tumor shared similar regions of loss of heterozygosity. We then analyzed 91 ovarian tumor samples for mutations in TP53, BRAF, and KRAS. TP53 mutations were not detected in any serous borderline tumors (n = 30) or low-grade serous carcinomas (n = 43) but were found in 73% of high-grade serous carcinomas (n = 18). BRAF (n = 9) or KRAS (n = 5) mutation was detected in 47% of serous borderline tumors, but among the low-grade serous carcinomas (39 stage III, 2 stage II, and 2 stage I), only one (2%) had a BRAF mutation and eight (19%) had a KRAS mutation. The low frequency of BRAF mutations in advanced-stage, low-grade serous carcinomas, which contrasts with previous findings, suggests that aggressive, low-grade serous carcinomas are more likely derived from serous borderline tumors without BRAF mutation. In addition, advanced-stage, low-grade carcinoma patients with BRAF or KRAS mutation have a better apparent clinical outcome. However, further investigation is needed. (Am J Pathol 2010, 177:1611-1617; DOI: 10.2353/ajpath.2010.100212)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available