MétaCan
Menu
← Back to cohort
Record W2443386476 · doi:10.1093/neuonc/now073.72

HG-76SPATIAL AND TEMPORAL HOMOGENEITY OF DRIVER MUTATIONS IN DIFFUSE INTRINSIC PONTINE GLIOMA

2016· article· en· W2443386476 on OpenAlexaff
Eshini Panditharatna, Hamid Nikbakht, Leonie G. Mikael, Rui Li, Tenzin Gayden, Matthew Osmand, Cheng‐Ying Ho, Madhuri Kambhampati, Eugene Hwang, Damien Faury, Alan Siu, Simon Papillon‐Cavanagh, Denise Béchet, Keith L. Ligon, Benjamin Ellezam, Wendy J. Ingram, Caedyn L. Stinson, Andrew S. Moore, Katherine E. Warren, Jason Karamchandani, Roger J. Packer, Nada Jabado, Jacek Majewski, Javad Nazarian

Bibliographic record

VenueNeuro-Oncology · 2016
Typearticle
Languageen
FieldMedicine
TopicGlioma Diagnosis and Treatment
Canadian institutionsMcGill University
Fundersnot available
KeywordsHomogeneity (statistics)GliomaNeuroscienceMedicinePsychologyComputer scienceCancer research

Abstract

fetched live from OpenAlex

Diffuse Intrinsic Pontine Glioma (DIPG) is a deadly pediatric brain tumor where needle biopsies help guide diagnosis and targeted therapies. Up to 80% of DIPGs harbor a de novo lysine 27 to methionine mutation in histone 3 (H3.1-, H3.3-K27M). However, the homogeneity of H3K27M and its partner mutation(s) across tumor mass is unknown. Furthermore, our recent findings indicate frequent tumor spread within the brain; however, the molecular signature of extended tumors is unknown. To address these questions, we molecularly analyzed (WES, MiSeq, ddPCR, RNA-Seq, methylation) 134 samples from various neuroanatomical structures of whole autopsied brains from nine DIPG patients. Comparative molecular characterization of extended and primary lesions was completed to assess spatial and temporal hetero/homogeneity of driver mutations in DIPGs. Mutation based-evolutionary reconstruction indicated H3K27M mutations potentially arise first and are associated with obligate partner mutations throughout the tumor and its spread, from diagnosis to end-stage disease. This data supports the necessity of partner mutations for development of DIPG. We also identified a H3.2K27M mutant DIPG. H3K27M associated partner mutations include alterations in cell cycle (TP53/PPM1D) or specific growth factor pathways (ACVR1/PIK3R1). Later oncogenic alterations arise in sub-clones and often affect the PI3K pathway. Our findings are consistent with early tumor spread outside the brainstem. The spatial and temporal homogeneity of driver mutations in DIPG implies they will be captured by limited biopsies, and emphasizes the need to develop therapies specifically targeting obligate oncohistone partnerships.

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: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.004
Threshold uncertainty score0.008

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)0.0010.000

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 head0.017
GPT teacher head0.285
Teacher spread0.268 · 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".

Quick stats

Citations0
Published2016
Admission routes1
Has abstractyes

Explore more

Same venueNeuro-Oncology→Same topicGlioma Diagnosis and Treatment→French-language works237,207→