Molecular Pathogenesis of Oral Squamous Cell Carcinoma

A. Jain
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引用次数: 19

Abstract

Oral carcinogenesis is a molecular and histological multistage process featuring genetic and phenotypic molecular markers which involves enhanced function of several protooncogenes, oncogenes and/or the deactivation of tumor suppressor genes, resulting in the over activity of growth factors and its cell surface receptors, which could enhance messenger signaling intracellularly, and/or leads to the increased production of transcription factors. Alone oncogenes are not responsible for carcinogenesis, genes having tumor suppressor activity, leads to a phenotypic change in cell which is responsible for increased cell proliferation, loss of cellular cohesion, and the ability to infiltrate local tissue and spread to distant sites. Understanding the molecular interplay of both onco and tumor genes will allow more accurate diagnosis and assessment of prognosis, which might lead the way for novel approaches to treatment.
口腔鳞状细胞癌的分子发病机制
口腔癌变是一个以遗传和表型分子标记为特征的分子和组织学多阶段过程,涉及多种原癌基因、癌基因和/或抑癌基因的功能增强和/或失活,导致生长因子及其细胞表面受体的过度活性,从而增强细胞内的信使信号,和/或导致转录因子的产生增加。单独的癌基因并不会导致癌变,具有肿瘤抑制活性的基因会导致细胞的表型变化,从而导致细胞增殖增加、细胞凝聚力丧失以及浸润局部组织并扩散到远处部位的能力。了解肿瘤和肿瘤基因的分子相互作用将有助于更准确的诊断和预后评估,这可能会为新的治疗方法开辟道路。
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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