Abstract
Chemotherapy-induced ovarian damage and fertility preservation in young patients with cancer are emerging disciplines. The mechanism of treatment-related gonadal damage provides important information for targeting prevention methods. The genomic aspects of ovarian damage after chemotherapy are not fully understood. Several studies have demonstrated that gene alterations related to follicular apoptosis or accelerated follicle activation are related to ovarian insufficiency and susceptibility to ovarian damage following chemotherapy. This may accelerate follicular apoptosis and follicle reservoir utilization and damage the ovarian stroma via multiple molecular reactions after chemotherapy. This review highlights the importance of genomic considerations in chemotherapy-induced ovarian damage and multidisciplinary oncofertility strategies for providing high-quality care to young female cancer patients.
Highlights
It is estimated that 9.2 million women were newly diagnosed with malignancy worldwide in 2020 [1]
This article reviews the genetics of chemotherapy-induced ovarian dysfunction and explores the gene-targeted prevention of ovarian damage
A retrospective study on the in vitro fertilization of Brca mutation carriers showed no significant differences in the procedure cycles or in the number of oocytes compared to non-carriers [76]
Summary
It is estimated that 9.2 million women were newly diagnosed with malignancy worldwide in 2020 [1]. Among adolescents and young adults aged 15–39 years, 89,500 patients were newly diagnosed with cancer, and 9270 mortalities were reported in the United States [2] In these patients, oncologic therapies can harm normal ovarian function and result in ovarian damage [3]. 2. Genes Involved in the Regulation of Ovarian Follicular reserve In females, number of primordial follicles (PFs) declines towards menopause because of their finite nature [8]. Non-growing follicle endowment is composed of the formation, commitment, migration, and colonization of ovarian primordial germ cells (PGCs). Rspo, Bmp, Bmp, Bmp8a, Smads, KltL, Oct, GNdafn9,oBs1m,pN15a,nZops31,, ZKpiTt2a,,fD4Zbpa3z,l,CBxc4l3-,xR, sPpion21, ,InPhoag,, Gja, Bax Msx, EMsrs1x,2F,sDhri,cNerp,pANc,hoNrt,cpChrlb,a,FsKto4rl,laiPss,otEalgirnk1, /S2t,rEag8f,r,SBtaaxg,, Follicular Primordial Germ assembly Cells Formation and. Other meiotic gene mutations, including Stag, Pof1b, Pof2b, and Hfm, have been associated with ovarian reserve impairment in humans [46,47,48]
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