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套细胞淋巴瘤(MCL)是一种富于挑战性的B细胞淋巴瘤。MCL最具特征的遗传学上异常是t(11;14)(q13;q32)易位,这一易位导致位于11q13的CCND1基因并列到位于14号染色体的免疫球蛋白重链增强子基因的附近,从而引起其产物cyclinD1过表达。随着对MCL分子遗传学发病机制的研究的深入,目前推测MCL的发病机制是由于三种主要的因素聚集在一起的结果,即细胞周期通路失调、DNA损伤反应通路缺陷以及细胞生存通路失调。通过对MCL分子遗传学发病机制以及它们是如何影响肿瘤的生物学行为的研究,为MCL患者提供新的治疗策略。
Mantle cell lymphoma (MCL) is a challenging B-cell lymphoma. The most characteristic genetic abnormality in MCL is the t (11; 14) (q13; q32) translocation, which translocates the CCND1 gene located at 11q13 to the immunoglobulin heavy chain enhancer gene located on chromosome 14 Nearby, causing its product cyclinD1 overexpression. With the development of molecular pathogenesis of MCL, it is hypothesized that the pathogenesis of MCL is the result of three major factors, such as imbalance of cell cycle pathways, defects of DNA damage response pathways and disorders of cell survival pathways. By studying the molecular mechanisms of molecular genetics in MCL and how they affect the biological behavior of tumors, new therapeutic strategies for MCL patients are provided.