Bartholin gland carcinomas (BGCs) are extremely rare tumors accounting for <1% of all female genital malignancies. The current study presents a 49-year-old female with an eight-year history of BGC. A mass was identified in the vulva and the patient underwent an excisional biopsy, which revealed a left Bartholin adenoid cystic carcinoma. The patient subsequently received surgery, chemotherapy and biological therapy, and has survived. Therefore, the present case indicates that surgery is important for the treatment of BGC, however; multimodal therapy may be a more effective treatment strategy.
Background: Angiopoietin-like protein 4 (ANGPTL4) has been demonstrated highly expressed in some cancers, but it also was downregulated in others through DNA methylation. However, the expression status of ANGPTL4 in cancer of cervix remains unclear. Thus, our present study attempts to investigate the role of ANGPTL4 in the prognosis of patients with cervical cancer. Methods: Immunohistochemistry, western blotting and qRT-PCR were performed to investigate the expressive level of ANPGTL4 in cervical cancer tissues and paired noncancer tissues. The relationship of ANGPTL4 expression and clinicopathological factors was measured by Chi-square test. Overall and disease-free survival (OS and DFS) rates were estimated and compared by using Kaplan-Meier method and log-rank test, respectively. To assess the prognostic significance of ANGPTL4 in cervical cancer patients, the Cox regression model was utilized to process univariate and multivariate analyses. Results: ANGPTL4 was upregulated in cervical cancer samples and advanced tumor stage, deep stromal invasion, lymph node metastasis, lymphovascular space invasion, as well as poor OS and DFS were shown to be tightly correlated with it. Results of Cox multivariate analysis demonstrated that ANGPTL4 expression was an independent prognostic factor for OS and DFS in cervical cancer. Conclusion: Upregulated ANGPTL4 seems to be a useful marker for poor prognosis in cervical cancer.
Cervical cancer is the fourth most common malignancy in women worldwide, and resistance to chemotherapy drugs is the biggest obstacle in the treatment of cervical cancers. In the present study, the molecular mechanisms underlying cisplatin resistance in human cervical cancer cells were investigated. When human cervical cancer cells were treated with 10 µg/ml of cisplatin for 24 and 48 h, high mobility group box 1 (HMGB1) protein expression levels significantly increased in a time‑dependent manner. Comparisons between cisplatin‑sensitive HeLa cells and cisplatin‑resistant HeLa/DDP cells revealed higher levels of HMGB1 in HeLa/DDP cells than in HeLa cells. Additionally, the half maximal inhibitory concentration (IC50) value for cisplatin in HeLa/DDP cells was 5.3‑fold that in HeLa cells. Analysis of the distribution of cellular components revealed that HMGB1 translocation from the nucleus to cytoplasm contributed to cisplatin resistance. This was further confirmed by demonstration that ethyl pyruvate treatment suppressed the cytoplasmic translocation of HMGB1, resulting in inhibition of HeLa cell proliferation. Furthermore, endogenous HMGB1 was inhibited with HMGB1‑specific short hairpin (sh)RNA, and MTT assay results showed that interference with HMGB1 expression reduced cell viability and potentially reversed cisplatin resistance in HeLa cells. Transfection with HMGB1 shRNA was demonstrated to induce cell apoptosis in HeLa cells, as detected by FACS analysis. In addition, administration of recombinant HMGB1 protein in HeLa cells promoted cell autophagy, mediated by the phosphorylation of extracellular signal‑regulated kinase 1/2. Thus, cytoplasmic HMGB1 translocation and HMGB1‑induced cell autophagy are proposed to contribute to cisplatin resistance by inhibiting apoptosis of cervical cancer cells. HMGB1 could, therefore, represent a novel therapeutic target for, and a diagnostic marker of, chemotherapy resistant cervical cancers.
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