MétaCan
Menu
Back to cohort
Record W2120281217 · doi:10.1093/carcin/bgm153

The associated contributions of p53 and the DNA mismatch repair protein Msh6 to spontaneous tumorigenesis

2007· article· en· W2120281217 on OpenAlexafffund
Leah C. Young, Angela M. Keuling, Raymond Lai, Patrick N. Nation, Victor A. Tron, Susan E. Andrew

Bibliographic record

VenueCarcinogenesis · 2007
Typearticle
Languageen
FieldMedicine
TopicGenetic factors in colorectal cancer
Canadian institutionsUniversity of Alberta
FundersNatural Sciences and Engineering Research Council of CanadaCanadian Institutes of Health ResearchAlberta Heritage Foundation for Medical Research
KeywordsMSH6DNA mismatch repairMicrosatellite instabilityCarcinogenesisMSH2BiologyCancer researchDNA repairGenome instabilityDNA damageMutationLoss of heterozygosityGeneticsCancerAlleleDNAGene

Abstract

fetched live from OpenAlex

DNA mismatch repair (MMR) is a highly conserved system that repairs DNA adducts acquired during replication, as well as some forms of exogenous/endogenous DNA damage. Additionally, MMR proteins bind to DNA adducts that are not removed by MMR and influence damage-response mechanisms other than repair. Hereditary non-polyposis colorectal cancer, as well as mouse models for MMR deficiency, illustrate that MMR proteins are required for maintenance of genetic stability and tumor suppression. In both humans and mice, the phenotype associated with Msh6-associated tumorigenesis is distinct from that of Msh2. In this study, we hypothesized that Msh6-/-;p53+/- mice would display earlier tumor onset than their Msh6-/- or p53+/- counterparts, indicating that concomitant loss of these two tumor suppressors contributes to tumorigenesis via mechanisms that are only partially interrelated. We generated a Msh6-/-;p53+/- mouse model which succumbed to malignant disease at an accelerated rate and with a tumor spectrum distinct from both Msh6-/- and p53+/- models. Alteration of tumor phenotype in the Msh6-/-;p53+/- mice included a marked increase in microsatellite instability that was associated with loss of heterozygosity of the remaining p53 allele. Also, genetic instability was inversely correlated with survival. This manuscript marks the first in vivo investigation into the association between Msh6 and p53, and their combined role in the suppression of spontaneous tumorigenesis, cell survival and genomic stability. Our results support the hypothesis that p53 and Msh6 are functionally interrelated and that, with concomitant mutation, these tumor suppressors act together to accelerate tumorigenesis.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.002
metaresearch head score (Gemma)0.002
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.300
Threshold uncertainty score0.463

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0020.002
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.008
GPT teacher head0.257
Teacher spread0.248 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations23
Published2007
Admission routes2
Has abstractyes

Explore more

Same venueCarcinogenesisSame topicGenetic factors in colorectal cancerFrench-language works237,207