IMMUNOHISTOCHEMICAL STUDY OF OVARIAN CANCER WITH PATHOLOGICAL BIOMINERALIZATION
DOI:
https://doi.org/10.32782/2226-2008-2023-4-7Keywords:
ovarian cancer, immunohistochemistry, markers, caspase-3, CD68Abstract
Ovarian cancer (OC) is the most common gynecological oncological disease, ranking third after body and cervical cancer. Pathological biomineralization (calcification) is one of the clinical manifestations of ovarian cancer. Calcification is characteristic of serous adenocarcinoma and is presented as psammoma bodies (PB). Calcification develops in the early stages of the tumor process. The aim is to study the immunohistochemical features of OC tissue with pathological biomineralization. Materials and methods. We examined 30 ovarian cancer samples with pathological biomineralization (group I) and 30 without pathological biomineralization (group II). All samples were examined histologically and immunohistochemically using OPN, OPG, RANKL, SPARC, Casp3, and CD68. Results. An immunohistochemical study revealed a higher expression of OPN in group I (73.34 ± 4.25 cells in the field of view with a diameter of 1 mm) compared to group II (26.93 ± 1.88 cells in the field of view), p < 0.001. OPG expression was 63.07 ± 3.52 and 58.57 ± 3.54 cells in the field of view for groups I and II, respectively. A positive reaction to RANKL was detected in 56.37 ± 3.30 cells in the field of view with a diameter of 1 mm for group I and in 54.52 ± 3.49 cells in the field of view for group II. No significant difference was found when analyzing the expression of OPG and RANKL. SPARC expression was lower in group I (48.32 ± 3.26 cells in the field of view with a diameter of 1 mm) compared to group II (63.19 ± 3.39 cells in the field of view), p < 0.01. CD68 expression in group I was 52.44 ± 3.37 cells in the field of view with a diameter of 1 mm; in group II – 60.87 ± 3.14 cells in the field of view, without a significant difference according to the Student’s test. In addition, the expression of Саsp3 in I was higher (57.31 ± 2.97 cells in the field of view, p < 0.05). This fact may indicate the stimulating effect of biomineral deposits on the intensity of apoptosis in tumor tissue. This phenomenon deserves a more detailed study.
References
Arora T, Mullangi S, Lekkala MR. Ovarian Cancer. StatPearls [Internet]. 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK567760/
Fedorenko ZP, Hulak LO, Mykhailovych YuI. Cancer in Ukraine, 2021-2022. Morbidity, mortality, performance indicators of the oncology service. Biuleten Natsionalnoho kantser-reiestru Ukrainy. 2022; 22. (In Ukrainian).
Momenimovahed Z, Tiznobaik A, Taheri S, Salehiniya H. Ovarian cancer in the world: epidemiology and risk factors. Int J Womens Health. 2019 Apr 30;11:287-299. doi: 10.2147/IJWH.S197604.
Mitra AK. Ovarian Cancer Metastasis: A Unique Mechanism of Dissemination [Internet]. Tumor Metastasis. 2016. Available from: http://dx.doi.org/10.5772/64700
Tjhay F, Motohara T, Tayama S, Narantuya D, Fujimoto K, Guo J, Sakaguchi I, Honda R, Tashiro H, Katabuchi H. CD44 variant 6 is correlated with peritoneal dissemination and poor prognosis in patients with advanced epithelial ovarian cancer. Cancer Sci. 2015 Oct;106(10):1421-8. doi: 10.1111/cas.12765.
Wen J, Zhao Z, Huang L, Li L, Li J, Zeng Y, Wu J, Miao Y. Switch of the ovarian cancer cell to a calcifying phenotype in the calcification of ovarian cancer. J Cancer. 2018 Feb 28;9(6):1006-1016. doi: 10.7150/jca.22932.
Arneth B. Tumor Microenvironment. Medicina (Kaunas). 2019 Dec 30;56(1):15. doi: 10.3390/medicina56010015.
Anderson NM, Simon MC. The tumor microenvironment. Curr Biol. 2020 Aug 17;30(16):R921-R925. doi: 10.1016/j.cub.2020.06.081.
Neophytou CM, Panagi M, Stylianopoulos T, Papageorgis P. The Role of Tumor Microenvironment in Cancer Metastasis: Molecular Mechanisms and Therapeutic Opportunities. Cancers (Basel). 2021 Apr 23;13(9):2053. doi: 10.3390/cancers13092053.
Fang D, Chen H, Zhu JY, Wang W, Teng Y, Ding HF, Jing Q, Su SB, Huang S. Epithelial-mesenchymal transition of ovarian cancer cells is sustained by Rac1 through simultaneous activation of MEK1/2 and Src signaling pathways. Oncogene. 2017 Mar;36(11):1546-1558. doi: 10.1038/onc.2016.323.
Loret N, Denys H, Tummers P, Berx G. The Role of Epithelial-to-Mesenchymal Plasticity in Ovarian Cancer Progression and Therapy Resistance. Cancers (Basel). 2019 Jun 17;11(6):838. doi: 10.3390/cancers11060838.
Lampropoulou DI, Papadimitriou M, Papadimitriou C, Filippou D, Kourlaba G, Aravantinos G, Gazouli M. The Role of EMT-Related lncRNAs in Ovarian Cancer. Int J Mol Sci. 2023 Jun 13;24(12):10079. doi: 10.3390/ijms241210079.
Piddubnyi AM, Danylchenko SM, Romaniuk AM, Moskalenko RA. Prostatic calculi cause osteoblastic immunophenotype of prostate cancer. Pathology. 2019; 16 (46):170-176.
Rani S, Sehgal A, Kaur J, Pandher DK, Punia RS. Osteopontin as a Tumor Marker in Ovarian Cancer. J Midlife Health. 2022 Jul-Sep;13(3):200-205. doi: 10.4103/jmh.jmh_52_22.
Okamoto K. Role of RANKL in cancer development and metastasis. J Bone Miner Metab. 2021 Jan;39(1):71-81. doi: 10.1007/s00774-020-01182-2.
Renema N, Navet B, Heymann MF, Lezot F, Heymann D. RANK-RANKL signalling in cancer. Biosci Rep. 2016 Aug 5;36(4):e00366. doi: 10.1042/BSR20160150.
Feng J, Tang L. SPARC in Tumor Pathophysiology and as a Potential Therapeutic Target. Curr Pharm Des. 2014;20(39):6182-90. doi: 10.2174/1381612820666140619123255.
Feng X, Yu Y, He S, Cheng J, Gong Y, Zhang Z, Yang X, Xu B, Liu X, Li CY, Tian L, Huang Q. Dying glioma cells establish a proangiogenic microenvironment through a caspase 3 dependent mechanism. Cancer Lett. 2017 Jan 28;385:12-20. doi: 10.1016/j.canlet.2016.10.042.
Zhang J, Li S, Liu F, Yang K. Role of CD68 in tumor immunity and prognosis prediction in pan-cancer. Sci Rep. 2022 May 12;12(1):7844. doi: 10.1038/s41598-022-11503-2.
Moskalenko R, Romaniuk A, Iashchichyn I, Zakorko IS, Piddubnyi АM, Chernov YeO, Morozova-Roche LA. Involvement of proinflammatory S100A8/S100A9 in the atherocalcinosis of aortic valve. Patologia. 2017; 14 (1): 49-56.
