| Autor: |
Ohnishi, Kaori, Nakayama, Kentaro, Ishikawa, Masako, Ishibashi, Tomoka, Yamashita, Hitomi, Nakamura, Kohei, Minamoto, Toshiko, Iida, Kouji, Razia, Sultana, Ishikawa, Noriyoshi, Kyo, Satoru |
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| Zdroj: |
Archives of Gynecology & Obstetrics; Aug2020, Vol. 302 Issue 2, p487-495, 9p, 1 Color Photograph, 1 Diagram, 3 Charts, 1 Graph |
| Abstrakt: |
Purpose: Mucinous ovarian carcinomas (MOCs) are relatively rare. It has been proposed that a subset of mucinous cystadenomas (MCAs) may progress to mucinous borderline tumors (MBTs), and then to MOCs. KRAS is the predominantly mutated gene in MOC; however, other associated mutations and the mechanism underlying carcinogenesis in MOC remain unclear. Here, we assessed molecular genetic alterations in mucinous ovarian tumors and constructed mutation profiles.Methods: Using the Sanger sequencing method, we assessed genetic mutations (KRAS, BRAF, TP53, and PIK3CA) in 16 cases of MOC, 10 cases of MBT, and 12 cases of MCA.Results: Among MOC cases, the prevalence of G12D and G13D KRAS mutations was 43.8% (7/16). No MOC cases showed V600E BRAF and TP53 mutations. Among MBT cases, the prevalence of G12D KRAS mutation was 20.0% (2/10), those of TP53 and PIK3CA mutations were nil, and that of V600E BRAF mutation was 40% (4/10). None of the genetic mutations assessed were detected among MCA cases.Conclusion: These results suggest that MBT with V600E BRAF mutation may rarely progress to MOC, while MBT with G12D or G13D KRAS mutation may more commonly progress to MOC. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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