Colorectal cancer (CRC) is a heterogeneous disease that is common in both men and women. Chromosome instability is the most common alteration and is present in almost 85% of all cases. Cases of hereditary predisposition to colorectal cancer fall into in two categories: familial adenomatous polyposis (FAP; OMIM phenotypic series MIM:PS175100) and hereditary nonpolyposis colorectal cancer (HNPCC; OMIM phenotypic series MIM:PS120435). Disease models related to colorectal cancer in Drosophila include 'familial adenomatous polyposis 1' (FBhh0000135), 'colorectal cancer, multigenic' (FBhh0000658), 'cancer, intestinal stem cell, SRC-related' (FBhh0000475), and 'cancer, intestinal stem cell, APC-RAS-related' (FBhh0000912).
[updated Oct. 2018 by FlyBase; FBrf0222196]
[COLORECTAL CANCER; CRC](https://omim.org/entry/114500)
[PHOSPHOLIPASE A2, GROUP IIA; PLA2G2A](https://omim.org/entry/172411)
[NRAS PROTOONCOGENE, GTPase; NRAS](https://omim.org/entry/164790)
[BUB1 MITOTIC CHECKPOINT SERINE/THREONINE KINASE; BUB1](https://omim.org/entry/602452)
[CATENIN, BETA-1; CTNNB1](https://omim.org/entry/116806)
[PHOSPHATIDYLINOSITOL 3-KINASE, CATALYTIC, ALPHA; PIK3CA](https://omim.org/entry/171834)
[FIBROBLAST GROWTH FACTOR RECEPTOR 3; FGFR3](https://omim.org/entry/134934)
[TOLL-LIKE RECEPTOR 2; TLR2](https://omim.org/entry/603028)
[APC REGULATOR OF WNT SIGNALING PATHWAY; APC](https://omim.org/entry/611731)
[MCC REGULATOR OF WNT SIGNALING PATHWAY; MCC](https://omim.org/entry/159350)
[PROTEIN-TYROSINE PHOSPHATASE, NONRECEPTOR-TYPE, 12; PTPN12](https://omim.org/entry/600079)
[B-RAF PROTOONCOGENE, SERINE/THREONINE KINASE; BRAF](https://omim.org/entry/164757)
[DLC1 RHO GTPase ACTIVATING PROTEIN; DLC1](https://omim.org/entry/604258)
[PLATELET-DERIVED GROWTH FACTOR RECEPTOR-LIKE; PDGFRL](https://omim.org/entry/604584)
[RAD54 HOMOLOG B; RAD54B](https://omim.org/entry/604289)
[PROTEIN-TYROSINE PHOSPHATASE, RECEPTOR-TYPE, J; PTPRJ](https://omim.org/entry/600925)
[CYCLIN D1; CCND1](https://omim.org/entry/168461)
[DNA MISMATCH REPAIR PROTEIN MLH3; MLH3](https://omim.org/entry/604395)
[AKT SERINE/THREONINE KINASE 1; AKT1](https://omim.org/entry/164730)
[BUB1 MITOTIC CHECKPOINT SERINE/THREONINE KINASE B; BUB1B](https://omim.org/entry/602860)
[TUMOR PROTEIN p53; TP53](https://omim.org/entry/191170)
[FOLLICULIN; FLCN](https://omim.org/entry/607273)
[AXIS INHIBITOR 2; AXIN2](https://omim.org/entry/604025)
[DCC NETRIN 1 RECEPTOR; DCC](https://omim.org/entry/120470)
[BCL2-ASSOCIATED X PROTEIN; BAX](https://omim.org/entry/600040)
[SRC PROTOONCOGENE, NONRECEPTOR TYROSINE KINASE; SRC](https://omim.org/entry/190090)
[AURORA KINASE A; AURKA](https://omim.org/entry/603072)
[E1A-BINDING PROTEIN, 300-KD; EP300](https://omim.org/entry/602700)
Colorectal cancer (CRC) is a heterogeneous disease that is common in both men and women.
In addition to lifestyle and environmental risk factors, gene defects can contribute to an inherited predisposition to CRC. CRC is caused by changes in different molecular pathogenic pathways, such as chromosomal instability, CpG island methylator phenotype, and microsatellite instability. Chromosome instability is the most common alteration and is present in almost 85% of all cases (review by Schweiger et al., 2013; pubmed:23325509). Mutations in a single gene result in a marked predisposition to colorectal cancer in 2 distinct syndromes: familial adenomatous polyposis (FAP; MIM:175100) and hereditary nonpolyposis colorectal cancer (HNPCC; MIM:120435). [from MIM:114500; 2016.02.16]
