人类癌症的耐药性 - 机制和影响。
Drug resistance in human cancers - Mechanisms and implications.
发表日期:2024 Jul 12
作者:
Sudikshaa Vijayakumar, Raveena Dhakshanamoorthy, Akshaya Baskaran, B Sabari Krishnan, Ravi Maddaly
来源:
LIFE SCIENCES
摘要:
癌症具有复杂的病因学,除了社会经济影响之外,从医疗保健的角度来看也具有重大影响。与其他疾病的临床试验相比,癌症治疗的临床试验所产生的潜在希望微乎其微,这一事实可以理解癌症带来的巨大挑战。手术、化疗和放疗仍然是癌症的主要治疗选择。在这些选择带来的挑战中,诱导的化疗药物耐药性可能是预后不良和治疗无效的最重要因素。耐药性是几乎所有癌症类型都表现出的特性,包括癌、白血病、骨髓瘤、肉瘤和淋巴瘤。诱导耐药性的机制包括肿瘤微环境内的因素、负责药物代谢的基因突变、表面药物受体的变化和药物外流增加。我们在这里全面介绍癌症的耐药性及其机制。此外,除了对常用化疗药物的耐药性之外,我们还提出了对单克隆抗体等新一代治疗药物的耐药性诱导。最后,我们讨论了了解耐药性诱导机制的实验方法以及减轻诱导性耐药性的潜在方法。版权所有 © 2024。由 Elsevier Inc. 出版。
Cancers have complex etiology and pose a significant impact from the health care perspective apart from the socio-economic implications. The enormity of challenge posed by cancers can be understood from the fact that clinical trials for cancer therapy has yielded minimum potential promises compared to those obtained for other diseases. Surgery, chemotherapy and radiotherapy continue to be the mainstay therapeutic options for cancers. Among the challenges posed by these options, induced resistance to chemotherapeutic drugs is probably the most significant contributor for poor prognosis and ineffectiveness of the therapy. Drug resistance is a property exhibited by almost all cancer types including carcinomas, leukemias, myelomas, sarcomas and lymphomas. The mechanisms by which drug resistance is induced include the factors within the tumor microenvironment, mutations in the genes responsible for drug metabolism, changes in the surface drug receptors and increased drug efflux. We present here comprehensively the drug resistance in cancers along with their mechanisms. Also, apart from resistance to regularly used chemotherapeutic drugs, we present resistance induction to new generation therapeutic agents such as monoclonal antibodies. Finally, we have discussed the experimental approaches to understand the mechanisms underlying induction of drug resistance and potential ways to mitigate induced drug resistance.Copyright © 2024. Published by Elsevier Inc.