Molecular mechanisms of tumour budding and its association with microenvironment in colorectal cancer.

Pub Date : 2022-04-01 DOI:10.1042/CS20210886
Phimmada Hatthakarnkul, J. Quinn, A. Ammar, Gerard Lynch, H. V. van Wyk, D. McMillan, C. Thuwajit, J. Edwards
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引用次数: 3

Abstract

Colorectal cancer (CRC) is the third most common cancer worldwide. Poor survival of CRC associated with the development of tumour metastasis led to the investigation of the potential biomarkers to predict outcomes in CRC patients. Tumour budding (TB) is a well-known independent prognostic marker for poor survival and disease metastasis. Therefore, it has been suggested that TB status is included in routine clinicopathological factors for risk assessment in CRC. In contrast with a vast majority of studies regarding the prognostic power of TB, there is no clear evidence pertaining to the underlying molecular mechanism driving this phenotype, or an understanding of TB relationship with the tumour microenvironment (TME). The aim of the present study is to present a comprehensive review of TB and tumour cell signalling pathways together with the cross-talk of immune cells that could drive TB formation in CRC.
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结直肠癌肿瘤出芽的分子机制及其与微环境的关系。
结直肠癌(CRC)是全球第三大常见癌症。结直肠癌的低生存率与肿瘤转移的发展相关,这促使研究潜在的生物标志物来预测结直肠癌患者的预后。肿瘤萌芽(TB)是一个众所周知的独立预后标志物,用于不良生存和疾病转移。因此,有人建议将结核状态纳入CRC风险评估的常规临床病理因素。与绝大多数关于结核病预后能力的研究相反,没有明确的证据表明驱动这种表型的潜在分子机制,也没有对结核病与肿瘤微环境(TME)关系的理解。本研究的目的是全面回顾结核和肿瘤细胞信号通路以及免疫细胞的相互作用,这些信号通路可以驱动结直肠癌中结核的形成。
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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