The aim of this work was to study the expression of SOX2 gene in triple negative breast cancer and its role. One hundred and twenty specimens of paraffin-embedded triple negative breast cancer (TNBC) tissues were collected from Harbin Medical University Cancer Hospital, Heilongjiang, China between January 2014 and March 2018. The expression of SOX2 was detected using immunohistochemistry, and the relationship between the expression of SOX2 and clinical features was analyzed. Breast cancer cell lines (normal group, SOX2 interference group, SOX2 overexpression group) were cultured in vitro to detect the proliferation and cloning ability of the cell lines. The expression of SOX2 was related to lymph node metastasis and stage of breast cancer (P less than 0.05), but was not related to age, menopause or tumor size (P > 0.05); the expression of SOX2 in the overexpression group was significantly greater than that in the normal group after 72 hours, and no significant difference between the overexpression group and the interference group was observed. The number of clone cells with a diameter of 0.5 mm in the interference group was lower compared to the normal group, and that of the overexpression group was higher, but not significant. SOX2 is associated with the high invasiveness of breast cancer and can be used as a therapeutic target to inhibit the metastasis of cancer cells. SOX2 can promote the proliferation of breast cancer cells and affect the size of clone cells in its involvement in clone.

OBJECTIVEKinesin family member 14 (KIF14) is a mitotic kinesin and plays an important role in tumor progression. KIF14 overexpression has been observed in multiple cancers and has been correlated with a poor prognosis. However, its protein expression and prognostic significance in epithelial ovarian cancer (EOC) remain unclear. In this research, we aimed to explore the relationship of KIF14 expression with clinicopathological parameters and prognosis in EOC.MATERIALS AND METHODSIn this study, we measured KIF14 expression in 170 EOC carcinoma tissue samples with immunohistochemistry and correlated these data with clinicopathological characteristics.RESULTSThe expression of KIF14 in EOC tissues was significantly higher than that in normal tissues. Furthermore, KIF14 expression was significantly associated with metastasis (p = 0.047), histological type (p = 0.001), Ki67 expression (p = 0.004) and residual tumor (p = 0.038). Also, Kaplan-Meir survival curves showed that a high level of KIF14 expression was a predictor for worse PFS (p = 0.013) and OS (p = 0.009) in patients with EOC.CONCLUSIONSKIF14 expression may be associated with poor prognosis, suggesting that it has potential value as an effective prognostic predictor in EOC patients.

Allelic losses of multiple chromosome loci in gastric adenocarcinoma suggest that inactivation of tumour suppressor genes in these regions may be important for tumourigenesis. To define deletion intervals and find candidate tumour suppressor genes involved in gastric adenocarcinoma pathogenesis, a genome-wide search for loss of heterozygosity (LOH) was conducted in 45 patients with primary gastric adenocarcinoma. Investigations using 29 microsatellite markers spanning chromosomes 17 and 18 showed allelic deletion in 29 (64%) specimens at one or more loci. Five LOH overlap regions, three newly identified as deletion regions, were defined: RI, D17S831–D17S921 at 17p12-13.3; RII, D17S1868–D17S787 at 17q21.3-22; RIII, D17S785–D17S928 at 17q25.3; RIV, D18S61–D18S1161 at 18q22; and RV, D18S462–D18S70 at 18q22-q23. Eleven (24%) patients with chromosome 17 allelic loss also showed LOH on 18q, with at least one region of overlapping. LOH mapping showed allelic losses were widespread on both chromosomes and suggests the possibility that multiple tumour suppressor genes, including one or more that are unknown, might be inactivated in the aetiology of gastric adenocarcinoma.

Cytogenetic analysis was performed on eight primary gastric cancers. Three of them had simple chromosome changes: 47,XX,+X/48,XX,+X,+X; 48,XX,+8,+19,t(3;5) (q21;q31) and 47,XY,+del(7)(q22). The five others had complicated chromosome changes; both 3p- and 7q- were noted in four cases and i(5p) was noted in two cases.

In direct preparation of five primary esophageal cancers, chromosomes 1, 3, and 12 were most frequently involved in structural abnormalities; 12p- was consistently seen in all five cases and, thus, could be considered as one of the characteristic chromosome changes in esophageal cancer. Moreover, 2p-, 4p-, and 7q- were seen in three cases.