Molecular Basis of Colorectal Cancer
Open accessAbstract
This review gives an account of recent advances in our knowledge of the molecular mechanisms in colorectal cancer. Genetic changes in the germ line, combined with somatic mutations, occur in familial syndromes of colorectal cancer, whereas somatic mutations are the outstanding feature of sporadic colorectal cancer. Genetic changes drive the progression from adenoma to carcinoma and probably influence individual susceptibility and response to treatment.
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KRAS mutations are usually progression events in colon cancers that follow a driver mutation in the Wnt signaling pathway.
“In contrast, KRAS mutations are usually progression events in colon cancers that follow a driver mutation in the Wnt signaling pathway [43].”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [43]
In colorectal cancer, KRAS mutation is a progression event that occurs after Wnt pathway mutation.
“In contrast, in colorectal cancer KRAS mutation is a progression event that occurs after the initiation event of mutation in the Wnt pathway (57).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [57]
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- Authors
- Markowitz, S. D., & Bertagnolli, M. M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Brigham and Women's Hospital (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2009-12-17
- Volume
- 361
- Issue
- 25
- Pages
- 2449-2460
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC2843693
- OpenAlex
- W2095692554
- Cited by
- 2,052
- References
- 130
- Citations by year
- 2026: 34 · 2025: 67 · 2024: 96 · 2023: 244 · 2022: 127 · 2021: 145 · 2020: 111 · 2019: 121 · 2018: 120 · 2017: 112 · 2016: 142 · 2015: 149 · 2014: 144 · 2013: 146 · 2012: 127
- FWCI
- 11.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Cancer Institute (R01CA127306)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Oncology › Colorectal Cancer Screening and Detection
- Keywords
- colorectal cancer, molecular mechanisms, somatic mutations, germline mutations, sporadic colorectal cancer, adenoma-carcinoma sequence, cancer susceptibility, treatment response
- MeSH terms
- DNA Repair, Humans, Mutation, Oncogenes, Biomarkers, Tumor, Colorectal Neoplasms, Signal Transduction, Genes, Tumor Suppressor, Genome, DNA Methylation, Genetic Predisposition to Disease
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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