APC, signal transduction and genetic instability in colorectal cancer.
Colorectal cancer arises through a gradual series of histological changes, each of which is accompanied by a specific genetic alteration. In general, an intestinal cell needs to comply with two essential requirements to develop into a cancer: it must acquire selective advantage to allow for the initial clonal expansion, and genetic instability to allow for multiple hits in other genes that are responsible for tumour progression and malignant transformation. Inactivation of APC--the gene responsible for most cases of colorectal cancer--might fulfil both requirements.
Fodde
R
R
Department of Human and Clinical Genetics, and Center for Biomedical Genetics, Leiden University Medical Center, The Netherlands. r.fodde@lumc.nl
Smits
R
R
Clevers
H
H
D000818:Animals; D020137:Base Pair Mismatch; D002869:Chromosome Aberrations; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000378:metabolism; D003598:Cytoskeletal Proteins / Q000502:physiology; D004260:DNA Repair; D017491:Genes, APC / Q000502:physiology*; D006801:Humans; D019656:Loss of Heterozygosity; D018895:Microsatellite Repeats; D009154:Mutation; D012641:Selection, Genetic; D015398:Signal Transduction; D015534:Trans-Activators; D051176:beta Catenin
C495270:CTNNB1 protein, human; D003598:Cytoskeletal Proteins; D015534:Trans-Activators; D051176:beta Catenin