A genetic model for colorectal tumorigenesis

Fearon, Eric R.; Vogelstein, Bert

doi:10.1016/0092-8674(90)90186-i

Cited by 12,132Genetic factors in colorectal cancerColorectal Cancer Treatments and StudiesColorectal Cancer Screening and Detection

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A genetic model for colorectal tumorigenesis

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Fearon, Eric R., Vogelstein, Bert·1990·Cell

DOI 10.1016/0092-8674(90)90186-i

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More than 50% of hypermutated colorectal tumors and more than 80% of non-hypermutated colorectal tumors have mutations in APC.
“more than 50% of hypermutated tumors and more than 80% of non-hypermutated tumors have mutations in APC [1, 2].”
From Modeling APC mutagenesis and familial adenomatous polyposis using human iPS cells (2018) · cites this paper as [1]
APCmin/+ mice harbor a point mutation in the APC gene, resulting in APC deletion and constitutive activation of Wnt signaling.
“APCmin/+ mice that harbored a point mutation in the APC gene, resulting in APC deletion and constitutive activation of Wnt signaling25”
From A PROTAC peptide induces durable β-catenin degradation and suppresses Wnt-dependent intestinal cancer (2020) · cites this paper as [25]
Colorectal cancer follows a relatively ordered mutational process and can be efficiently modeled through progressive loss of niche factors in ASC-derived colon organoids.
“We again focused on colorectal cancer which follows a relatively ordered mutational process55 and can be efficiently modeled through progressive loss of niche factors in ASC-derived colon organoids13,14.”
From One-step generation of tumor models by base editor multiplexing in adult stem cell-derived organoids (2023) · cites this paper as [55]
GTP binding to KRAS shifts the active site from an open to a closed conformation, allowing multiple downstream effector pathways including MAPK and PI3K to interact and activate.
“GTP binding to KRAS shifts the active site from an open to a closed conformation, allowing multiple downstream effector pathways to interact and activate, including the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways [12, 13].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [13]

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Authors: Fearon, E. R., & Vogelstein, B.
Affiliations: Johns Hopkins University (US)
ORCID: Fearon, Eric R.
Vogelstein, Bert
Venue: Cell
Publisher: Elsevier BV
Published: 1990-06
Volume: 61
Issue: 5
Pages: 759-767
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/0092-8674(90)90186-i
OpenAlex: W2001258296
Cited by: 12,132
References: 76
Citations by year: 2026: 199 · 2025: 247 · 2024: 300 · 2023: 321 · 2022: 367 · 2021: 387 · 2020: 320 · 2019: 339 · 2018: 358 · 2017: 394 · 2016: 374 · 2015: 392 · 2014: 411 · 2013: 395 · 2012: 376
FWCI: 48.49
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor, 5431 d)
Locations: Cell (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Funders: National Institutes of Health
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 carcinogenesis, colorectal cancer, genetic models, tumor progression, colorectal adenoma
MeSH terms: Alleles, Chromosome Deletion, Heterozygote, Humans, Models, Genetic, Mutation, Oncogenes, Suppression, Genetic, Colorectal Neoplasms

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