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多发性骨髓瘤的代谢改变:从肿瘤发生到蛋白酶体抑制剂耐药性

Metabolic Alterations in Multiple Myeloma: From Oncogenesis to Proteasome Inhibitor Resistance.

作者信息

Weir Philip, Donaldson David, McMullin Mary Frances, Crawford Lisa

机构信息

Department of Haematology, Belfast City Hospital, Belfast BT9 7AB, UK.

Patrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.

出版信息

Cancers (Basel). 2023 Mar 9;15(6):1682. doi: 10.3390/cancers15061682.

DOI:10.3390/cancers15061682
PMID:36980568
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10046772/
Abstract

Despite significant improvements in treatment strategies over the past couple of decades, multiple myeloma (MM) remains an incurable disease due to the development of drug resistance. Metabolic reprogramming is a key feature of cancer cells, including MM, and acts to fuel increased proliferation, create a permissive tumour microenvironment, and promote drug resistance. This review presents an overview of the key metabolic adaptations that occur in MM pathogenesis and in the development of resistance to proteasome inhibitors, the backbone of current MM therapy, and considers the potential for therapeutic targeting of key metabolic pathways to improve outcomes.

摘要

尽管在过去几十年中治疗策略有了显著改进,但由于耐药性的产生,多发性骨髓瘤(MM)仍然是一种无法治愈的疾病。代谢重编程是癌细胞(包括MM细胞)的一个关键特征,它有助于促进细胞增殖增加、营造有利的肿瘤微环境并促进耐药性。本文综述了MM发病机制以及对蛋白酶体抑制剂(当前MM治疗的主要药物)产生耐药性过程中发生的关键代谢适应性变化,并探讨了靶向关键代谢途径进行治疗以改善治疗效果的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53b0/10046772/3bc1fc78c419/cancers-15-01682-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53b0/10046772/7d48644c10a3/cancers-15-01682-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53b0/10046772/3bc1fc78c419/cancers-15-01682-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53b0/10046772/7d48644c10a3/cancers-15-01682-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53b0/10046772/3bc1fc78c419/cancers-15-01682-g002.jpg

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