Tissue-Predisposition to Cancer Driver Mutations

Driver mutations are considered the cornerstone of cancer initiation. They are defined as mutations that convey a competitive fitness advantage, and hence, their mutation frequency in premalignant tissue is expected to exceed the basal mutation rate. In old terms, that translates to "the surviv...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2024-01, Vol.13 (2), p.106
Main Authors: Peters, Luriano, Venkatachalam, Avanthika, Ben-Neriah, Yinon
Format: Article
Language:English
Subjects:
Adenomatous polyposis coli
Analysis
Cancer
cancer evolution
Care and treatment
Cell division
Chronic myeloid leukemia
Colorectal cancer
Colorectal carcinoma
Diagnosis
Disease Susceptibility
DNA methylation
DNA repair
driver mutations
Epigenetics
Esophagus
Gene expression
Gene mutations
Genetic aspects
Genomes
Health aspects
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Melanoma
Mutation
Mutation - genetics
Mutation Rate
Mutation rates
Myeloid leukemia
Phenotype
Precancerous Conditions
selective pressure
Solid tumors
Transcription factors
Citations: Items that this one cites
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Summary:Driver mutations are considered the cornerstone of cancer initiation. They are defined as mutations that convey a competitive fitness advantage, and hence, their mutation frequency in premalignant tissue is expected to exceed the basal mutation rate. In old terms, that translates to "the survival of the fittest" and implies that a selective process underlies the frequency of cancer driver mutations. In that sense, each tissue is its own niche that creates a molecular selective pressure that may favor the propagation of a mutation or not. At the heart of this stands one of the biggest riddles in cancer biology: the tissue-predisposition to cancer driver mutations. The frequency of cancer driver mutations among tissues is non-uniform: for instance, mutations in are particularly frequent in colorectal cancer, and 99% of chronic myeloid leukemia patients harbor the driver fusion mutation, which is rarely found in solid tumors. Here, we provide a mechanistic framework that aims to explain how tissue-specific features, ranging from epigenetic underpinnings to the expression of viral transposable elements, establish a molecular basis for selecting cancer driver mutations in a tissue-specific manner.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells13020106