WNT and β-Catenin in Cancer: Genes and Therapy

IF 4.7 2区 医学 Q1 ONCOLOGY
R. Jackstadt, M. Hodder, O. Sansom
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引用次数: 32

Abstract

The WNT pathway is a pleiotropic signaling pathway that controls developmental processes, tissue homeostasis, and cancer. The WNT pathway is commonly mutated in many cancers, leading to widespread research into the role of WNT signaling in carcinogenesis. Understanding which cancers are reliant upon WNT activation and which components of the WNT signaling pathway are mutated is paramount to advancing therapeutic strategies. In addition, building holistic insights into the role of WNT signaling in not only tumor cells but also the tumor microenvironment is a vital area of research and may be a promising therapeutic strategy in multiple immunologically inert cancers. Novel compounds aimed at modulating the WNT signaling pathway using diverse mechanisms are currently under investigation in preclinical/early clinical studies. Here, we review how the WNT pathway is activated in multiple cancers and discuss current strategies to target aberrant WNT signaling.
癌症的WNT和β-儿茶素基因及其治疗
WNT通路是一种多向性信号通路,控制发育过程、组织稳态和癌症。WNT通路在许多癌症中普遍发生突变,这使得人们对WNT信号在癌变中的作用进行了广泛的研究。了解哪些癌症依赖于WNT激活以及WNT信号通路的哪些成分发生突变,对于推进治疗策略至关重要。此外,全面了解WNT信号在肿瘤细胞和肿瘤微环境中的作用是一个重要的研究领域,可能是多种免疫惰性癌症的一种有希望的治疗策略。旨在通过多种机制调节WNT信号通路的新型化合物目前正在临床前/早期临床研究中进行研究。在这里,我们回顾了WNT通路在多种癌症中是如何被激活的,并讨论了当前针对异常WNT信号的策略。
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来源期刊
CiteScore
14.50
自引率
1.30%
发文量
13
期刊介绍: The Annual Review of Cancer Biology offers comprehensive reviews on various topics within cancer research, covering pivotal and emerging areas in the field. As our understanding of cancer's fundamental mechanisms deepens and more findings transition into targeted clinical treatments, the journal is structured around three main themes: Cancer Cell Biology, Tumorigenesis and Cancer Progression, and Translational Cancer Science. The current volume of this journal has transitioned from gated to open access through Annual Reviews' Subscribe to Open program, ensuring all articles are published under a CC BY license.
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