The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Colorectal Cancer: Molecules and Populations
Abstract
The epidemiology and molecular biology of colorectal cancer are reviewed with a view to understanding their interrelationship. Risk factors for colorectal neoplasia include a positive family history, meat consumption, smoking, and alcohol consumption. Important inverse associations exist with vegetables, nonsteroidal anti-inflammatory drugs (NSAIDs), hormone replacement therapy, and physical activity. There are several molecular pathways to colorectal cancer, especially the APC (adenomatous polyposis coli)-beta-catenin-Tcf (T-cell factor; a transcriptional activator) pathway and the pathway involving abnormalities of DNA mismatch repair. These are important, both in inherited syndromes (familial adenomatous polyposis [FAP] and hereditary nonpolyposis colorectal cancer [HNPCC], respectively) and in sporadic cancers. Other less well defined pathways exist. Expression of key genes in any of these pathways may be lost by inherited or acquired mutation or by hypermethylation. The roles of several of the environmental exposures in the molecular pathways either are established (e.g., inhibition of cyclooxygenase-2 by NSAIDs) or are suggested (e.g., meat and tobacco smoke as sources of specific blood-borne carcinogens; vegetables as a source of folate, antioxidants, and inducers of detoxifying enzymes). The roles of other factors (e.g., physical activity) remain obscure even when the epidemiology is quite consistent. There is also evidence that some metabolic pathways, e.g., those involving folate and heterocyclic amines, may be modified by polymorphisms in relevant genes, e.g., MTHFR (methylenetetrahydrofolate reductase) and NAT1 (N-acetyltransferase 1) and NAT2. There is at least some evidence that the general host metabolic state can provide a milieu that enhances or reduces the likelihood of cancer progression. Understanding the roles of environmental exposures and host susceptibilities in molecular pathways has implications for screening, treatment, surveillance, and prevention.
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Cites
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DPC4 , A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1
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Vegetables, Fruit, and Cancer Prevention
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Self-citationMethylation of the oestrogen receptor CpG island links ageing and neoplasia in human colon
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Molecular Genetics of Colorectal Cancer
Fearon, E. R. (2011) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-011110-130235 · Cited by 1,805
A prospective study of obesity and cancer risk (Sweden)
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Novel trends in development of dietary fiber rich meat products—a critical review
Mehta, N., Ahlawat, S. S., Sharma, D. P., & Dabur, R. S. (2015) · Journal of Food Science and Technology · doi:10.1007/s13197-013-1010-2 · Cited by 268
Influence of Sex Hormones on Cancer Progression
Folkerd, E. J., & Dowsett, M. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2009.27.4290 · Cited by 229
Risk for cancer in a cohort of patients hospitalized for schizophrenia in Denmark, 1969–1993
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Cancer risk among users of neuroleptic medication: a population-based cohort study
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Decreased intestinal polyp multiplicity is related to exercise mode and gender in ApcMin/+ mice
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Dietary fibre and the risk of colorectal cancer: A case—Control study
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Eating Frequency and the Risk of Colon Cancer
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Metadata
- Authors
- Potter, J. D.
- Venue
- JNCI Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-06-02
- Volume
- 91
- Issue
- 11
- Pages
- 916-932
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2121245276
- Cited by
- 881
- References
- 6
- FWCI
- 34.79
- Type
- journal article
- Language
- en
- Open access
- closed
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