There has been a significant annual increase in the number of cases of uterine leiomyomas or fibroids (UF) among women of all races and ages across the world. A fortune is usually spent by the healthcare sector for fibroid-related treatments and management. Molecular studies have established the higher mutational heterogeneity in UF as compared to normal myometrial cells. The contribution of DNA damage and defects in repair responses further increases the mutational burden on the cells. This in turn leads to genetic instability, associated with cancer risk and other adverse reproductive health outcomes. Such and many more growing bodies of literature have highlighted the genetic/molecular, biochemical and clinical aspects of UF; none the less there appear to be a lacuna bridging the bench to bed gap in addressing and preventing this disease. Presented here is an exhaustive review of not only the molecular mechanisms underlying the predisposition to the disease but also possible strategies to effectively diagnose, prevent, manage, and treat this disease.

中文翻译：

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DNA 损伤和修复机制在子宫肌瘤/平滑肌瘤中的作用：综述。

全世界所有种族和年龄的女性中，子宫平滑肌瘤或肌瘤 (UF) 的病例数每年都显着增加。医疗保健部门通常会花费大量资金用于与肌瘤相关的治疗和管理。分子研究表明，与正常子宫肌层细胞相比，UF 具有更高的突变异质性。DNA 损伤和缺陷在修复反应中的贡献进一步增加了细胞的突变负担。这反过来会导致遗传不稳定，与癌症风险和其他不利的生殖健康结果相关。越来越多的文献都强调了 UF 的遗传/分子、生化和临床方面；尽管如此，在解决和预防这种疾病方面似乎还存在差距。