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. 2011 Jun 27;61(2):248–254. doi: 10.1136/gut.2011.239772

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© 2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode.

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Models of associations between telomere length and colorectal cancer (CRC) risk. Arrows indicate causality. (1) The current model is based on observation of shorter leucocytes telomeres in CRC cases than controls, assumes that this is mirrored in colorectal crypt stem cells and posits a causal link between shorter telomeres and CRC development, possibly through chromosomal instability. (2) Our model proposes that genetic factors cause longer telomeres, assumes that this is mirrored in colorectal crypt stem cells and proposes that longer telomeres directly influences CRC risk, possibly through effects on stem cell numbers or longevity. The shorter telomeres in retrospectively collected CRC arise as a result of disease or as a sample collection artefact caused by shorter survival in individuals with longer telomeres. (3) A third possibility must be borne in mind, namely that genetic factors cause longer telomeres, but that the genetic factors do not influence risk through telomere length, which is an epiphenomenon with no relevance or even a partially compensatory restraining influence on carcinogenesis; shorter telomeres of other origins may still cause an increased CRC risk.