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. 2022 May 18;29(5):3658-3667.
doi: 10.3390/curroncol29050294.

Mutation Profiles of Ovarian Seromucinous Borderline Tumors in Japanese Patients

Hiroki Sasamori  1 , Kentaro Nakayama  1 , Sultana Razia  1 , Hitomi Yamashita  1 , Tomoka Ishibashi  1 , Masako Ishikawa  1 , Seiya Sato  1 , Satoru Nakayama  2 , Yoshiro Otsuki  3 , Ritsuto Fujiwaki  4 , Noriyoshi Ishikawa  5 , Satoru Kyo  1
Affiliations

Mutation Profiles of Ovarian Seromucinous Borderline Tumors in Japanese Patients

Hiroki Sasamori et al. Curr Oncol. .

Abstract

Ovarian seromucinous tumors (SMBTs) are relatively rare, and their carcinogenesis is largely unknown. In this study, the molecular features of SMBTs in Japan are assessed. DNA was extracted from microdissected paraffin-embedded sections from 23 SMBT cases. Genetic mutations (KRAS, BRAF, PIK3CA, and ERBB2) were evaluated using Sanger sequencing. Immunohistochemistry for p53, ARID1A, and PTEN was also performed as a surrogate for the loss of functional mutations in these tumor suppressor genes. The prevalence of KRAS, BRAF, PIK3CA, and ERBB2 mutations was 4.3% (1/23), 8.6% (2/23), 8.6% (2/23), and 17.3% (4/23), respectively. Overexpression or loss of p53 expression occurred in 26% (6/23), loss of ARID1A expression in 4.3% (1/23), and none of the cases showed expression of PTEN loss. These findings suggest that KRAS/BRAF/PIK3CA and PTEN mutations are rare carcinogenic events in SMBTs. The high frequency of positive p53 staining and a low frequency of loss of ARID1A staining suggests that SMBT carcinogenesis may be related to the alteration of p53 rather than that of ARID1A. ERBB2 oncogenic mutations may play an important role in the tumorigenesis of Japanese SMBTs.

Keywords: mutation; oncogene; ovarian seromucinous borderline tumor; ovarian tumor; tumor suppressor gene.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Representative histological characteristics of seromucinous borderline tumor (SMBT). (a) Low magnification (×10); (b) high magnification (×20).
Figure 2
Figure 2
Chromatograms of ERBB2 mutation statuses in SMBTs. Each SMBT showed mutations (A) D769N (2305G>A), (B) G815R (2443G>A), (C) L786V (2356C>G), and (D) T793A (2377A>G) in the ERBB2 gene, respectively.
Figure 3
Figure 3
Representative immunohistochemical staining of ARID1A, PTEN, p53 and ERBB2 in SMBTs. Normal (A) and loss of ARID1A expression (B). Normal PTEN (C); overexpression (D) and loss of p53 expression (E); low (F) and overexpression (G) of ERBB2 in SMBTs.
Figure 3
Figure 3
Representative immunohistochemical staining of ARID1A, PTEN, p53 and ERBB2 in SMBTs. Normal (A) and loss of ARID1A expression (B). Normal PTEN (C); overexpression (D) and loss of p53 expression (E); low (F) and overexpression (G) of ERBB2 in SMBTs.
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This research was funded by JSPS KAKENHI (grant numbers 18K09229 and 18K09291).