Molecular genetic markers of ovarian cancer tumor cells and their microenvironment, study methods, and clinical value: A review

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Abstract

Ovarian cancer (OC) is a common malignancy of the female reproductive system. In most patients, OC is diagnosed in the later stages, leading to an abysmal prognosis. The standard treatment for OC is surgery and chemotherapy; however, relapse often occurs after treatment, especially in patients with advanced disease. New therapeutic options based on advances in tumor genetics and molecular biology are needed to improve treatment outcomes. Manipulations with genes and the proteins they express, affecting oncogenesis and treatment resistance, seem promising, and proteins and gene fragments identified using molecular methods become valuable markers in the supportive pharmacodiagnosis and tailoring of complex therapy. This article describes the research achievements in genetic markers in OC.

About the authors

Margarita A. Kalfa

Vernadsky Crimean Federal University

Email: rita.kalfa@mail.ru
ORCID iD: 0000-0002-7179-3402

cand. sci. (med.)

Russian Federation, Simferopol

Ilya O. Golovkin

Vernadsky Crimean Federal University

Email: golovkin.io.1996@gmail.com
ORCID iD: 0000-0002-3578-5130

res. assist.

Russian Federation, Simferopol

Artem E. Lazarev

Vernadsky Crimean Federal University

Email: artik.lazarev@gmail.com
ORCID iD: 0000-0003-2684-3834

аssistant

Russian Federation, Simferopol

Lena P. Golubinskaya

Vernadsky Crimean Federal University

Email: missive@mail.ru
ORCID iD: 0000-0003-3917-924X

d. sci. (med.)

Russian Federation, Simferopol

Olga Yu. Gritskevich

Vernadsky Crimean Federal University

Email: editor@omnidoctor.ru
ORCID iD: 0000-0002-3556-1399

аssistant

Russian Federation, Simferopol

Evgenia Yu. Zyablitskaya

Vernadsky Crimean Federal University

Author for correspondence.
Email: evgu79@mail.ru
ORCID iD: 0000-0001-8216-4196

d. sci. (med.)

Russian Federation, Simferopol

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Supplementary files

Supplementary Files
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1. JATS XML
2. Fig. 1. Recruitment and stabilization of RAD51: RPA is a replicative protein A that prevents single-stranded DNA from pairing into duplexes, as replication is only possible in unpaired DNA [15].

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3. Fig. 2. MMR system function: MutSβ or MutSα recognize and bind to the mismatch site, then other complexes are recruited, mainly MutLα, proliferating cell nuclear antigen (PCNA), and replication factor C (RFC). The assembly initiates the PMS2 endonuclease activity, inducing single-strand breaks near the mismatch site, and opens the site for the entry of exonuclease 1 (EXO1), leading to the final dissociation of the damaged DNA region, and the polymerase (Pol) restores the complementary chain.

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