Abstract
Objective:To analyze the role of cancer stem cells (CSC) in ovarian carcinogenesis through the identification of CD133 expression in the normal ovary (NO), serous cystadenoma (SC), borderline serous tumour (BST), low-grade serous carcinoma (LGSC), and high-grade serous carcinoma (HGSC). Materials and methods:A total of 48 tissue samples contain 5 NO, 10 SC, 5 BST, 8 LGSC, and 20 HGSC were stained with anti-CD133 antibody by immunohistochemical protocol. The difference in the H-score of CD133 expression between groups and their relationship to age, histomorphology, and localization was analyzed. Results:CD133 expression varied among tumor groups, with clinicopathologic parameters showing diverse associations (age p = 0.773; histomorphology p = 0.001; and localization p = 0.026). The comparison of CD133 H-scores differed significantly between each group (p = 0.0031), in which precursor and malignant lesions possessed more robust CD133 expression. Conclusion:The presence of CD133 cellular expression and localization in different types of serous ovarian tumours suggests that these markers are involved in ovarian tumorigenesis.
Highlights
Ovarian cancer (OC), with an estimated 295,000 cases and 184,000 deaths worldwide, is the 8th most prevalent cancer diagnosis and lethal gynaecological malignancy affecting a large female population (Bray et al, 2018)
Sample Characteristics Samples were obtained from 48 cases consisting of 5 normal ovaries, 10 serous cystadenoma (SC), 5 borderline serous tumour (BST), 8 lowgrade serous carcinoma (LGSC), and 20 high-grade serous carcinoma (HGSC)
Arora et al, (2018) reported age at diagnosis to be 50-79 years, whereas our findings showed the mean age in the HGSC group falls within this range
Summary
Ovarian cancer (OC), with an estimated 295,000 cases and 184,000 deaths worldwide, is the 8th most prevalent cancer diagnosis and lethal gynaecological malignancy affecting a large female population (Bray et al, 2018). Various factors, including atypical clinical symptoms, insufficient early detection modalities, late-onset diagnosis, chemoresistance, recurrence, and metastatic spread, lead to high mortality of ovarian cancer (Burges and Schmalfeldt, 2011; Chen et al, 2017; Klapdor et al, 2017). Low-grade serous carcinoma (LGSC) grows indolently from precursor lesions: serous cystadenoma (SC) to a borderline serous tumour (BST) (Hatano et al, 2019). KRAS-BRAF and TP53 mutations are involved in these two entities, respectively (Tsuchida et al, 2016; Hatano et al, 2019) Their characterization is based on a histologic analysis showing that tumour cells resemble a sort of epithelial-like cells that most likely come from the fallopian tube epithelial (FTE) or ovarian surface epithelial (OSE)
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