Biology of colorectal cancer.
Biology of colorectal cancer.
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DOI：
10.3332/ecancer.2015.520
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发表时间：
2015
影响因子：
1.8
通讯作者：
Cotte C
中科院分区：
文献类型：
--
作者：
Arvelo F;Sojo F;Cotte C
结直肠癌是一个严重的健康问题，是研究的挑战，也是研究其发展分子机制的模型。根据其发病率，这种病理表现为三种形式：家族性、遗传性和最常见的散发性，显然与任何遗传或家族因素无关。对于具有遗传模式和家族倾向的类型，肿瘤的发展经历了从腺瘤性病变到恶性肿瘤表现的明确阶段。已经确定环境和遗传因素会导致结直肠癌的发生，癌基因（抑制和修复 DNA 的基因）突变的积累表明，存在多种可能导致肿瘤出现的途径。就抑制性和突变性轨迹而言，其特征是与腺瘤/癌形态进展序列的表型变化相关的遗传性疾病。此外，BRAF 和 KRAS 基因突变的替代途径与息肉进展为癌症有关。本综述调查了在细胞和分子水平上所做的研究，旨在寻找对抗结直肠癌的特定替代治疗靶点。
Colorectal cancer is a serious health problem, a challenge for research, and a model for studying the molecular mechanisms involved in its development. According to its incidence, this pathology manifests itself in three forms: family, hereditary, and most commonly sporadic, apparently not associated with any hereditary or familial factor. For the types having inheritance patterns and a family predisposition, the tumours develop through defined stages ranging from adenomatous lesions to the manifestation of a malignant tumour. It has been established that environmental and hereditary factors contribute to the development of colorectal cancer, as indicated by the accumulation of mutations in oncogenes, genes which suppress and repair DNA, signaling the existence of various pathways through which the appearance of tumours may occur. In the case of the suppressive and mutating tracks, these are characterised by genetic disorders related to the phenotypical changes of the morphological progression sequence in the adenoma/carcinoma. Moreover, alternate pathways through mutation in BRAF and KRAS genes are associated with the progression of polyps to cancer. This review surveys the research done at the cellular and molecular level aimed at finding specific alternative therapeutic targets for fighting colorectal cancer.