Beta-catenin and the morphogenesis of colorectal cancer.
Tumor growth and progression are morphogenetic processes that are characterized by ongoing changes in tumor structure and differentiation. These processes show similarities to morphogenesis in embryonic development, as supported by the fact that the main pathways regulating morphogenesis in early embryogenesis and organogenesis are directly or indirectly altered in most neoplasms. In colorectal adenocarcinomas, different morphogenetic areas can be clearly defined. The focus of this review is on combining morphology-based aspects and recent molecular and genetic data on the progression of colorectal carcinomas. The decisive genetic alteration in most colorectal cancers is the loss of function mutation in the adenomatous polyposis coli tumor suppressor gene, leading to an accumulation of the oncoprotein beta-catenin, the main effector of the embryonic Wnt/wingless pathway. The possibility is discussed that, on the basis of this genetic alteration, the tumor microenvironment is an additional driving force of tumor progression.
Institute of Pathology, University of Erlangen-Nürnberg, Krankenhausstrasse 8-10, 91054 Erlangen, Germany. thomas.brabletz@patho.med.uni-erlangen.de
Thomas
T
Brabletz
Andreas
A
Jung
Thomas
T
Kirchner
D015179:Colorectal Neoplasms / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D003598:Cytoskeletal Proteins / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D009154:Mutation; D015534:Trans-Activators / Q000235:genetics* / Q000378:metabolism; D051176:beta Catenin
C495270:CTNNB1 protein, human; D003598:Cytoskeletal Proteins; D015534:Trans-Activators; D051176:beta Catenin