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. 2023 Jul 9;14(11):2128–2144. doi: 10.7150/jca.84930

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This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

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Major mechanisms of chemotherapy resistance in ovarian cancer are divided into primary and acquired resistance. Amplification of 19q12 contains CCNE1 related to TPX2 amplification, and 20q11.22-q13 are two dominant structural variants associated with primary chemotherapy failure. Tumor desmoplasia reaction is associated with poor response to chemotherapy despite a homologous-recombination defection. CSCs markers ALDH1, CD133, and SOX2 are associated with non-response to chemotherapy. Platinum resistance is attributed to enhanced NER because of the increased capacity of the cells to repair platinum-induced DNA damage. Essential mechanisms of acquired PARPi resistance are restoring the homologous recombination repair because of secondary mutations of RCA1/2, loss of 53BP1 resulting in HR reactivation, and alterations in the PARP and the PARG proteins leading to the same replication fork protection.