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Record W3153049780 · doi:10.1101/2021.04.14.437578

Life without mismatch repair

2021· preprint· en· W3153049780 on OpenAlexaff
Mathijs A. Sanders, Harald Vöhringer, Victoria J. Forster, Luiza Moore, Brittany Campbell, Yvette Hooks, Melissa Edwards, Vanessa Bianchi, Tim Coorens, Timothy Butler, Henry Lee-Six, Philip S. Robinson, Christoffer Flensburg, Rebecca A. Bilardi, Ian J. Majewski, Agnes Reschke, Elizabeth Cairney, Bruce Crooks, Scott Lindhorst, Duncan Stearns, Patrick Tomboc, Ultan McDermott, Michael R. Stratton, Adam Shlien, Moritz Gerstung, Uri Tabori, Peter J. Campbell

Bibliographic record

VenuebioRxiv (Cold Spring Harbor Laboratory) · 2021
Typepreprint
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer Genomics and Diagnostics
Canadian institutionsUniversity of TorontoLondon Health Sciences CentreSickKids FoundationIzaak Walton Killam Health CentreHospital for Sick Children
FundersKWF KankerbestrijdingNederlandse Organisatie voor Wetenschappelijk OnderzoekCancer Research UKWellcome Trust
KeywordsDNA mismatch repairBiologyMSH2Somatic hypermutationGeneticsMSH6PMS2DNA replicationNeoplastic transformationIndelDNA repairCancer researchCarcinogenesisGenotypeDNASingle-nucleotide polymorphismGene

Abstract

fetched live from OpenAlex

Abstract Mismatch repair (MMR) is a critical defence against mutation, but we lack quantification of its activity on different DNA lesions during human life. We performed whole-genome sequencing of normal and neoplastic tissues from individuals with constitutional MMR deficiency to establish the roles of MMR components, tissue type and disease state in somatic mutation rates. Mutational signatures varied extensively across genotypes, some coupled to leading-strand replication, some to lagging-strand replication and some independent of replication, implying that the various MMR components engage different forms of DNA damage. Loss of MSH2 or MSH6 (MutSα), but not MLH1 or PMS2 (MutLα), caused 5-methylcytosine-dependent hypermutation, indicating that MutSα is the pivotal complex for repairing spontaneous deamination of methylated cytosines in humans. Neoplastic change altered the distribution of mutational signatures, particularly accelerating replication-coupled indel signatures. Each component of MMR repairs 1-10 lesions/day per normal human cell, and many thousands of additional events during neoplastic transformation. Highlights MMR repairs 1-10 lesions/day in every normal cell and thousands more in tumor cells MMR patterns and rates are shaped by genotype, tissue type and malignant transformation MSH2 and MSH6 are pivotal for repairing spontaneous deamination of methylated cytosine Replication indels and substitutions vary by leading versus lagging strand and genotype

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)0.000
metaresearch head score (Gemma)0.001
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
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 score0.137
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0010.001
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0010.001
Research integrity0.0010.000
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 head0.010
GPT teacher head0.220
Teacher spread0.210 · 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.

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

Citations24
Published2021
Admission routes1
Has abstractyes

Explore more

Same venuebioRxiv (Cold Spring Harbor Laboratory)Same topicCancer Genomics and DiagnosticsFrench-language works237,207