TY - JOUR
T1 - BRAF mutation is rare in advanced-stage low-grade ovarian serous carcinomas
AU - Wong, Kwong Kwok
AU - Tsang, Yvonne T.M.
AU - Deavers, Michael T.
AU - Mok, Samuel C.
AU - Zu, Zhifei
AU - Sun, Charlotte
AU - Malpica, Anais
AU - Wolf, Judith K.
AU - Lu, Karen H.
AU - Gershenson, David M.
N1 - Funding Information:
Supported in part by grants from the Gynecologic Cancer Foundation; the National Institutes of Health, including The University of Texas MD Anderson Cancer Center Specialized Program of Research Excellence in Ovarian Cancer ( P50 CA08369 ), grant R01-CA133057 , and MD Anderson's Cancer Center Support Grant ( CA016672 ); the Entertainment Industry Foundation; Marsha Rivkin Center; and the Blanton-Davis Ovarian Cancer Research Program.
PY - 2010/10
Y1 - 2010/10
N2 - 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.
AB - 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.
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U2 - 10.2353/ajpath.2010.100212
DO - 10.2353/ajpath.2010.100212
M3 - Article
C2 - 20802181
AN - SCOPUS:77957354624
SN - 0002-9440
VL - 177
SP - 1611
EP - 1617
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 4
ER -