Lessons from hereditary colorectal cancer
Open accessAbstract
A large body of evidence supports the idea that accumulated genetic changes underlie the development of neoplasia. This multistep process is well illustrated by colorectal cancers, which typically develop over decades and appear to require at least seven genetic events for completion. Even so, inheritance of a single altered gene can result in a marked predisposition to colorectal cancer in two distinct syndromes, Familial Adenomatous Polyposis (FAP) and Hereditary Nonpolyposis Colorectal Cancer (HNPCC). Recent evidence suggests that the genetic defect in FAP affects the rate of tumor initiation by targeting the gatekeeper function of the APC gene. In contrast, the defect in HNPCC largely affects tumor progression by targeting the genome guardian function of DNA mismatch repair. Studies of these syndromes have provided unique insights into both inherited and sporadic forms of human tumors.
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Loss of heterozygosity of APC is one of the earliest and rate-limiting events in the progression from normal epithelium to adenoma formation and then cancer.
“loss of heterozygosity (LOH) of APC has been shown to be one of the earliest and rate-limiting events in the progression from normal epithelium to adenoma formation and then cancer [3–5].”
From Modeling APC mutagenesis and familial adenomatous polyposis using human iPS cells (2018) · cites this paper as [3]
In “Rate-Limiting Events in Tumorigenesis” (indexed as Abstract; page unavailable), the paper says studies of FAP patients and analogous mice suggest that mutation of the remaining wild-type APC allele is rate-limiting for tumor initiation. It also reports complete APC inactivation in very early lesions that may precede adenomas. The copy does not specifically identify that mutation as loss of heterozygosity, or establish it as rate-limiting for the entire progression through cancer. (LLM, conf=0.88)
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- Authors
- Kinzler, K. W., & Vogelstein, B.
- Affiliations
- Johns Hopkins University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Vogelstein, Bert
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1996-10
- Volume
- 87
- Issue
- 2
- Pages
- 159-170
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2093531978
- Cited by
- 4,919
- References
- 1
- Citations by year
- 2026: 26 · 2025: 40 · 2024: 51 · 2023: 97 · 2022: 59 · 2021: 91 · 2020: 96 · 2019: 106 · 2018: 109 · 2017: 110 · 2016: 152 · 2015: 131 · 2014: 164 · 2013: 173 · 2012: 186
- FWCI
- 40.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA 57345, CA43460, P50CA062924, CA 62924)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Keywords
- hereditary colorectal cancer, familial adenomatous polyposis, Lynch syndrome, APC gene, DNA mismatch repair, tumor initiation, tumor progression, multistep carcinogenesis, genetic susceptibility to cancer, gatekeeper function
- MeSH terms
- Adenoma, Colorectal Neoplasms, Hereditary Nonpolyposis, Humans, Hyperplasia, Oncogenes, Adenomatous Polyposis Coli, Colorectal Neoplasms, Point Mutation, Genes, APC
About these checks
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.
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