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. Author manuscript; available in PMC: 2019 Jul 11.
Published in final edited form as: Curr Gastroenterol Rep. 2019 Jan 30;21(2):5. doi: 10.1007/s11894-019-0674-9

Fig. 1.

Fig. 1

A genetic model for colorectal tumorigenesis. Adapted from Fearon and Vogelstein Cell, Vol. 61, 759–767, 1990. Tumorigenesis progresses through a series of genetic alterations. These alterations include oncogenes (ras) and tumor suppressor genes (particularly those on chromosomes 5q, 17p, and 18q). Early stages involve 5q mutations or familial adenomatous polyposis coli loss. Alterations in DNA methylation may follow and then K-ras mutations. Loss of 18q or deleted in colorectal cancer (DCC) follow and then 17p loss (p53). Other alterations may precede metastasis