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The Fanconi Pathway in Pediatric T-Cell Acute Lymphoblastic Leukemia

2017· article· en· W2786335525 on OpenAlexaff
Gayle P. Pouliot, Melissa Burns, James Degar, Chau D Vo, Lisa A. Moreau, Justine E. Roderick, Bose Kochupurakkal, Sofie Peirs, Björn Menten, Mignon L. Loh, Stephen P. Hunger, Lewis B. Silverman, Stephen E. Sallan, Marian H. Harris, Kristen E. Stevenson, Donna Neuberg, David M. Weinstock, Andrew P. Weng, Michelle A. Kelliher, Pieter Van Vlierberghe, Alan D. D’Andrea, Alejandro Gutiérrez

Bibliographic record

VenueBlood · 2017
Typearticle
Languageen
FieldMedicine
TopicAcute Lymphoblastic Leukemia research
Canadian institutionsBC Cancer Agency
Fundersnot available
KeywordsFanconi anemiaBiologyCancer researchGeneticsGermline mutationMutationFANCD2DNA repairMolecular biologyGene

Abstract

fetched live from OpenAlex

BRCA2 (also known as FANCD1), a core component of the Fanconi pathway, suppresses transformation of immature T-cell progenitors in mice. However, whether the Fanconi pathway contributes to human T-cell acute lymphoblastic leukemia (T-ALL) pathogenesis is unknown. Using targeted exon sequencing of childhood T-ALL diagnostic specimens, we found heterozygous mutations of Fanconi pathway genes in 23% of 40 cases analyzed. Array comparative genomic hybridization (CGH) analysis revealed that an additional 15% of these cases harbored large heterozygous deletions involving Fanconi pathway genes. The majority of these mutations appear to be somatic although in 2 of 8 available remission samples, the mutations were present, suggestive that these mutations are likely to be germline. Fanconi genes are typically considered two-hit tumor suppressors, where breast or ovarian cancers arising in heterozygous carriers often lose activity of the wild-type allele, leading to genomic instability. However, T-ALL cases with heterozygous Fanconi mutations lacked evidence of increased genomic instability based on array CGH analysis, were not hypersensitive to the PARP inhibitor olaparib, and did not demonstrate increased radial chromosome formation in response to mitomycin C (MMC), indicating that these cases retained activity of the wild-type allele. Complementation studies of Fanconi mutant cells revealed that most of the identified Fanconi mutations encoded pathogenic alleles, as evidenced by their impaired ability to rescue Fanconi-deficient cells from mitomycin C-induced radial chromosome formation and cytotoxicity. Treatment of a patient-derived xenograft sample harboring a heterozygous BRCA2 mutation with mitomycin C revealed that these cells had an intermediate increase in sensitivity to mitomycin C-induced cytotoxicity compared to Fanconi wild-type T-ALLs, suggesting that Fanconi haploinsufficiency is pathogenic in T-ALL. Together, these findings implicate a tumor suppressor role for Fanconi pathway haploinsufficiency in childhood T-ALL. Disclosures Hunger: Jazz Pharmaceuticals: Honoraria; Novartis: Consultancy; Amgen: Consultancy, Equity Ownership; Erytech Pharmaceuticals: Consultancy. Neuberg: Synta Pharmaceuticals: Other: Stock shares.

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: Bench or experimental · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.004

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.001
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 head0.012
GPT teacher head0.265
Teacher spread0.252 · 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 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".

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Citations0
Published2017
Admission routes1
Has abstractyes

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