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黑色素瘤的替代治疗方法:靶向BCL-2家族成员以减少肿瘤体积并杀死癌症干细胞。

Alternative Treatments For Melanoma: Targeting BCL-2 Family Members to De-Bulk and Kill Cancer Stem Cells.

作者信息

Mukherjee Nabanita, Schwan Josianna V, Fujita Mayumi, Norris David A, Shellman Yiqun G

机构信息

Department of Dermatology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.

Department of Dermatology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA; Department of Veterans Affairs Medical Center, Dermatology Section, Denver, Colorado, USA.

出版信息

J Invest Dermatol. 2015 Sep;135(9):2155-2161. doi: 10.1038/jid.2015.145. Epub 2015 May 7.

DOI:10.1038/jid.2015.145
PMID:25947358
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4537369/
Abstract

For the first time new treatments in melanoma have produced significant responses in advanced diseases, but 30-90% of melanoma patients do not respond or eventually relapse after the initial response to the current treatments. The resistance of these melanomas is likely due to tumor heterogeneity, which may be explained by models such as the stochastic, hierarchical, and phenotype-switching models. This review will discuss the recent advancements in targeting BCL-2 family members for cancer treatments, and how this approach can be applied as an alternative option to combat melanoma, and overcome melanoma relapse or resistance in current treatment regimens.

摘要

黑色素瘤的新疗法首次在晚期疾病中产生了显著疗效,但30%至90%的黑色素瘤患者对当前治疗无反应或在初始反应后最终复发。这些黑色素瘤的耐药性可能归因于肿瘤异质性,随机、分层和表型转换模型等模型或许可以解释这一现象。本综述将讨论靶向BCL-2家族成员进行癌症治疗的最新进展,以及该方法如何作为一种替代方案来对抗黑色素瘤,并克服当前治疗方案中的黑色素瘤复发或耐药问题。

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本文引用的文献

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Understanding melanoma stem cells.了解黑色素瘤干细胞。
Melanoma Manag. 2015;2(2):179-188. doi: 10.2217/mmt.15.4.
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BRAF inhibitor resistance mediated by the AKT pathway in an oncogenic BRAF mouse melanoma model.致癌性BRAF小鼠黑色素瘤模型中由AKT通路介导的BRAF抑制剂耐药性
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A stress-induced early innate response causes multidrug tolerance in melanoma.应激诱导的早期固有反应导致黑色素瘤的多药耐受。
Identification and validation of autophagy‑related genes in hypertrophic cardiomyopathy.
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MCL1 inhibition targets Myeloid Derived Suppressors Cells, promotes antitumor immunity and enhances the efficacy of immune checkpoint blockade.MCL1 抑制靶向髓系来源抑制细胞,促进抗肿瘤免疫并增强免疫检查点阻断的疗效。
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Nischarin expression may have differing roles in male and female melanoma patients.Nischarin 表达可能在男性和女性黑色素瘤患者中有不同的作用。
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7
Zebrafish Patient-Derived Xenograft Model as a Preclinical Platform for Uveal Melanoma Drug Discovery.斑马鱼患者来源异种移植模型作为葡萄膜黑色素瘤药物发现的临床前平台
Pharmaceuticals (Basel). 2023 Apr 15;16(4):598. doi: 10.3390/ph16040598.
8
Drug and apoptosis resistance in cancer stem cells: a puzzle with many pieces.癌症干细胞中的药物与凋亡抗性:一个由诸多碎片组成的谜题。
Cancer Drug Resist. 2022 Aug 2;5(4):850-872. doi: 10.20517/cdr.2022.20. eCollection 2022.
9
Resistance to drugs and cell death in cancer stem cells (CSCs).癌症干细胞(CSCs)中的耐药性与细胞死亡
J Transl Sci. 2020 Jun;6(3). doi: 10.15761/jts.1000341. Epub 2019 Jun 24.
10
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J Invest Dermatol. 2022 Jul;142(7):1912-1922.e7. doi: 10.1016/j.jid.2021.11.035. Epub 2021 Dec 20.
Oncogene. 2015 Aug 20;34(34):4545. doi: 10.1038/onc.2014.432. Epub 2015 Jan 26.
4
Targeting the metabolic plasticity of multiple myeloma with FDA-approved ritonavir and metformin.使用美国食品药品监督管理局(FDA)批准的利托那韦和二甲双胍靶向多发性骨髓瘤的代谢可塑性。
Clin Cancer Res. 2015 Mar 1;21(5):1161-71. doi: 10.1158/1078-0432.CCR-14-1088. Epub 2014 Dec 26.
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The delicate balance of melanoma immunotherapy.黑色素瘤免疫治疗的微妙平衡。
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The melanoma revolution: from UV carcinogenesis to a new era in therapeutics.黑色素瘤革命:从紫外线致癌作用到治疗新时代。
Science. 2014 Nov 21;346(6212):945-9. doi: 10.1126/science.1253735.
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J Invest Dermatol. 2015 Mar;135(3):842-850. doi: 10.1038/jid.2014.464. Epub 2014 Oct 28.
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N Engl J Med. 2014 Nov 13;371(20):1867-76. doi: 10.1056/NEJMoa1408868. Epub 2014 Sep 29.
10
Combined BRAF and MEK inhibition versus BRAF inhibition alone in melanoma.BRAF 和 MEK 联合抑制与单独 BRAF 抑制治疗黑色素瘤。
N Engl J Med. 2014 Nov 13;371(20):1877-88. doi: 10.1056/NEJMoa1406037. Epub 2014 Sep 29.