作者: Andrew M. Kaz , William M. Grady
DOI: 10.1007/978-90-481-8833-8_3
关键词: Genetics 、 Mouse model of colorectal and intestinal cancer 、 Chromosome instability 、 Bioinformatics 、 Molecular genetics 、 Epigenetics 、 Genome instability 、 Gene mutation 、 Colorectal cancer 、 Cancer 、 Biology
摘要: Colorectal cancer arises as the result of accumulation genetic alterations (including gene mutations and amplification) epigenetic modifications (such aberrant DNA methylation chromatin modifications) that transform normal colonic epithelial cells into adenocarcinoma cells. Loss genomic stability resulting changes appears to be a crucial molecular pathogenic step occurs early in tumourigenic process permits sufficient number tumour suppressor genes oncogenes accumulate clone their eventual transformation cancer. Substantial progress has been made recently concerning potential causes chromosomal instability colorectal determining effects various forms on biological clinical behavior colon tumours. Furthermore, terms understanding specific signalling pathways are frequently deregulated cancers. Although discovery involved metastasis remains challenge, advancements our genetics this have occurred, both with traditional familial/linkage studies also utilizing state-of-the-art genome-wide searches. The evaluation cause role events formation yield more effective prevention treatment strategies for disease.