Biophysics Department, Faculty of Science, Cairo University, Giza 12613, Egypt.
Department of Oncology, Faculty of Medicine and Dentistry, University of Alberta, 11560 University Avenue, Edmonton, AB T6G 1Z2, Canada.
Int J Mol Sci. 2022 May 19;23(10):5688. doi: 10.3390/ijms23105688.
Multiple Myeloma (MM) is a B cell malignancy marked by genomic instability that arises both through pathogenesis and during disease progression. Despite recent advances in therapy, MM remains incurable. Recently, it has been reported that DNA repair can influence genomic changes and drug resistance in MM. The dysregulation of DNA repair function may provide an alternative explanation for genomic instability observed in MM cells and in cells derived from MM patients. This review provides an overview of DNA repair pathways with a special focus on their involvement in MM and discusses the role they play in MM progression and drug resistance. This review highlights how unrepaired DNA damage due to aberrant DNA repair response in MM exacerbates genomic instability and chromosomal abnormalities, enabling MM progression and drug resistance.
多发性骨髓瘤(MM)是一种 B 细胞恶性肿瘤,其特征是基因组不稳定,这种不稳定性既源于发病机制,也源于疾病进展过程。尽管最近在治疗方面取得了进展,但 MM 仍然无法治愈。最近有报道称,DNA 修复可以影响 MM 中的基因组变化和耐药性。DNA 修复功能的失调可能为 MM 细胞和源自 MM 患者的细胞中观察到的基因组不稳定性提供了另一种解释。本综述概述了 DNA 修复途径,特别关注它们在 MM 中的作用,并讨论了它们在 MM 进展和耐药性中的作用。本综述强调了由于 MM 中异常的 DNA 修复反应导致的未修复的 DNA 损伤如何加剧基因组不稳定性和染色体异常,从而促进 MM 的进展和耐药性。