Translocation Tales: Unraveling the MYC Deregulation in Burkitt Lymphoma for Innovative Therapeutic Strategies

A. Tandon, Jissy A. Kuriappan, Vaibhav Dubey
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Abstract

MYC deregulation, a cardinal event in Burkitt lymphoma (BL) pathogenesis, necessitates the elucidation of the molecular mechanisms governing MYC activation to devise innovative and effective therapeutic strategies. The t(8;14)(q24;q32) chromosomal translocation commonly observed in hematological malignancies results in MYC deregulation, endowing cancer cells with a competitive edge through heightened cell proliferation, cell cycle progression, apoptosis evasion, and metabolic reprogramming. Recent discoveries of recurrent MYC mutations in BL underscore the potential of precision medicine, employing tailored therapeutics to specifically inhibit MYC activity. However, the intricate genetic landscape of BL, featuring additional alterations, such as mutations in TP53, TCF3, and ID3, may necessitate a combinatorial approach targeting multiple oncogenic pathways for effective intervention. Despite significant strides in hematological malignancy treatment, a comprehensive understanding of the molecular mechanisms underpinning MYC’s oncogenic properties remains crucial for the potential development of highly potent and selective MYC-directed cancer therapies. This review offers an in-depth analysis of MYC translocation and its implications in Burkitt lymphoma, with a spotlight on cutting-edge advances in research and emerging therapeutic paradigms.
易位的故事:解开MYC放松管制在伯基特淋巴瘤的创新治疗策略
MYC解除管制是伯基特淋巴瘤(BL)发病机制中的一个重要事件,需要阐明MYC激活的分子机制,以设计创新和有效的治疗策略。t(8;14)(q24;q32)染色体易位通常在血液恶性肿瘤中观察到,导致MYC失调,通过增强细胞增殖、细胞周期进展、细胞凋亡逃避和代谢重编程赋予癌细胞竞争优势。最近发现的BL中复发性MYC突变强调了精准医学的潜力,即采用量身定制的治疗方法来特异性抑制MYC活性。然而,BL复杂的遗传格局,具有额外的改变,如TP53、TCF3和ID3的突变,可能需要针对多种致癌途径的组合方法来进行有效干预。尽管血液学恶性肿瘤治疗取得了重大进展,但全面了解MYC致癌特性的分子机制对于开发高效和选择性MYC导向的癌症治疗仍然至关重要。本综述深入分析了MYC易位及其在伯基特淋巴瘤中的意义,重点介绍了研究的前沿进展和新兴的治疗范例。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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