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Record W2404348945 · doi:10.1158/1538-7445.brain15-b09

Abstract B09: DNA polymerase mutations trigger rapid onset of ultra-hypermutant malignant brain tumors in children with biallelic mismatch repair deficiency

2015· article· en· W2404348945 on OpenAlexaff
Adam Shlien, Brittany Campbell, Richard de Borja, Ludmil B. Alexandrov, Daniele Merico, David C. Wedge, Peter Van Loo, Patrick Tarpey, Paul Coupland, Aaron Pollett, Tatiana Lipman, Abolfazl Heidari, Shriya Deshmukh, Moritz Gerstung, Diana M. Merino, Manasa Ramakrishna, Marc Remke, Roland Arnold, Gagan B. Panigrahi, Samina Afzal, Valérie Larouche, Harriet Druker, Jordan Lerner‐Ellis, Matthew Mistry, Rina Dvir, Ronald Grant, Ronit Elhasid, Roula Farah, Glenn Taylor, Paul C. Nathan, Sarah Alexander, Shay Ben‐Shachar, Nada Jabado, Steven Gallinger, Shlohmi Constantini, Peter B. Dirks, Annie Huang, Steven W. Scherer, Richard G. Grundy, Carol Durno, Melyssa Aronson, M. Stephen Meyn, Michael D. Taylor, Zachary F. Pursell, Christopher E. Pearson, David Malkin, P. Andrew Futreal, Cynthia Hawkins, Éric Bouffet, Peter J. Campbell, Uri Tabori

Bibliographic record

VenueCancer Research · 2015
Typearticle
Languageen
FieldMedicine
TopicGenetic factors in colorectal cancer
Canadian institutionsConcordia UniversityMcGill UniversityMount Sinai HospitalIzaak Walton Killam Health CentreHospital for Sick Children
Fundersnot available
KeywordsCancer researchPMS2MutationDNA mismatch repairGermline mutationBiologyMLH1Microsatellite instabilityMSH2MSH6Malignant transformationCancerCarcinogenesisATRXExome sequencingGeneticsDNA repairGeneAlleleMicrosatellite

Abstract

fetched live from OpenAlex

Abstract Background: Biallelic Mismatch Repair Deficiency (bMMRD) is a childhood cancer predisposition syndrome caused by germline mutations in MSH2, MSH6, MLH1, and PMS2. The leading cause of death is malignant brain tumors. The genomic landscape and secondary somatic mutations of bMMRD brain tumors are unknown. Methods: We analyzed 27 cancers and corresponding normal tissues from bMMRD patients using genome, exome sequencing and SNP-arrays. Additionally, we performed sequential sequencing from five primary and recurrent tumor pairs. Results: BMMRD malignant brain tumors harbored massive numbers of substitution mutations (>250/Mb), greater than all childhood and most adult cancers (>7,000 analyzed). These cancers lacked copy number alterations (p<0.01) and microsatellite instability as seen in sporadic glioblastoma and adult deficient MMR cancers respectively. All ultra-hypermutated bMMRD brain cancers acquired early and conserved somatic mutations in DNA polymerases ε or δ. We examined a panel of eight genes involved in brain tumor pathogenesis (TP53, EGFR,NF1, RB1, ATRX, PDGFRA, BRAF, ACVR1) and found that 80% of ultra-hypermutant tumors carried a mutation in five or more of these genes, with 70% of the mutations fitting the bMMRD/POL signature. Sequential tumor analysis revealed that brain tumors acquired over 20,000 mutations in less than 6 months during malignant transformation. However, recurrent glioblastomas did not display a higher mutation load than ultra-hypermutant primary tumors with a polymerase mutation. Conclusions/Significance: Early-onset brain tumors from bMMRD patients have a unique mechanism of malignant progression through secondary mutations in DNA polymerases. During transformation, brain tumors quickly reach a threshold of mutations developed in a rapid burst once a mutation in a DNA polymerase is acquired. The high mutation load and threshold of bMMRD cancers may be its Achilles' heel, exploitable for diagnosis and therapeutic intervention. Note: This abstract was not presented at the conference. Citation Format: Adam Shlien, Brittany B. Campbell, Richard de Borja, Ludmil B. Alexandrov, Daniele Merico, David Wedge, Peter Van Loo, Patrick S. Tarpey, Paul Coupland, Aaron Pollett, Tatiana Lipman, Abolfazl Heidari, Shriya Deshmukh, Moritz Gerstung, Diana Merino, Manasa Ramakrishna, Marc Remke, Roland Arnold, Gagan B. Panigrahi, Samina Afzal, Valerie Larouche, Harriet Druker, Jordan Lerner-Ellis, Matthew Mistry, Rina Dvir, Ronald Grant, Ronit Elhasid, Roula Farah, Glenn P. Taylor, Paul C. Nathan, Sarah Alexander, Shay Ben-Shachar, Nada Jabado, Steven Gallinger, Shlohmi Constantini, Peter Dirks, Annie Huang, Steven W. Scherer, Richard G. Grundy, Carol Durno, Melyssa Aronson, M Stephen Meyn, Michael D. Taylor, Zachary F. Pursell, Christopher E. Pearson, David Malkin, P Andrew Futreal, Cynthia Hawkins, Eric Bouffet, Michael D. Taylor, Peter J. Campbell, Uri Tabori. DNA polymerase mutations trigger rapid onset of ultra-hypermutant malignant brain tumors in children with biallelic mismatch repair deficiency. [abstract]. In: Proceedings of the AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2015;75(23 Suppl):Abstract nr B09.

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 machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.007

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.000

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 head0.070
GPT teacher head0.370
Teacher spread0.300 · 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 source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
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".

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Citations0
Published2015
Admission routes1
Has abstractyes

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