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Abstract LB-307: Translational and mechanistic implications of osteosarcoma genomics: A TARGET report

2020· article· en· W3083579627 on OpenAlexaff
Paul S. Meltzer, Sean Davis, Jack Zhu, Yonghong Wang, Sven Bilke, Joshua J. Waterfall, Robert Walker, Marbin Pineda, Yuan Jiang, Sharon A. Savage, Tsz‐Kwong Man, Aaron Taylor, Monika J. Sun, Jay S. Wunder, Irene L. Andrulis, Nalan Gökgöz, Shintaro Iwata, Miki Ohira, Mark Krailo, Don Barkauskas, Lisa A. Teot, Timothy J. Triche, Silvia de Toledo, Antônio Sérgio Petrilli, Jaime M. Guidry Auvil, Richard Görlick, Malcolm A. Smith, Daniela S. Gerhard, Ching C. Lau

Bibliographic record

VenueCancer Research · 2020
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer Genomics and Diagnostics
Canadian institutionsMount Sinai Hospital
Fundersnot available
KeywordsCDKN2APDGFRABiologyPTENTranscriptomeCancer researchCopy-number variationSynthetic lethalityCancerGenome instabilityDNA methylationARID1ATargeted therapyGeneticsGeneMutationGenomeDNA repairGene expressionDNA damageDNAPI3K/AKT/mTOR pathwayStromal cell

Abstract

fetched live from OpenAlex

Abstract Osteosarcoma (OS) is the most common malignant bone tumor of children and young adults. Although the optimization of combination chemotherapy has led to significantly improved prognosis, survival remains poor for patients with recurrent tumor or metastatic disease at diagnosis. The international TARGET (Therapeutically Applicable Research to Generate Effective Therapy) OS project team collected 285 clinically annotated samples (age <40 years) for integrative genomics analyses. Eighty-nine cases, the discovery set, were characterized with paired tumor and normal DNA sequencing as well as profiling of transcriptomes, DNA methylation, and miRNA. An additional 196 validation cases were used for copy number analysis and targeted DNA sequencing guided by results from the discovery set. The most frequent recurrent somatic mutations cause loss of function in the tumor suppressors TP53, RB1, CDKN2A, PTEN, and NF1 as well as the chromatin remodeler ATRX. Structural rearrangements are an important mechanism of inactivation for all of these genes. In the discovery set, every case carried at least one mutation of a cell cycle regulator, with TP53 somatically altered in 87/89 cases. Analysis of TP53 mutations suggests that these are often truncal. OS genomes are strikingly complex and contain copy number aberrations (CNA) arising from aneuploidy and extensive structural rearrangements. Transcriptome analysis revealed profound remodeling of gene expression with statistically significant correlation of CNA and gene expression of 3340 genes (FDR<0.001). Regions of high copy number amplification include known therapeutically relevant cancer drivers (e.g. PDGFRA, MYC, CDK4, MDM2, IGF1R, and CCNE1). In contrast, activating mutations of signal transduction genes were rare. With few exceptions (e.g. MYC amplification), mutations or CNA of individual genes were not predictive of outcome. The pattern of significant co-occurrence or mutual exclusion of frequent mutations and amplifications allowed partitioning of 240 cases into four distinct genomic groups. One of these, characterized by relatively simple genomes lacking high copy number amplification, had a more favorable outcome. Unsupervised transcriptome analysis by NMF separated the discovery set into two groups with significantly different outcomes. A pathway-based approach identified a high-risk bone differentiation signature comprised of genes highly correlated with the expression of the osteogenic transcription factors. NMF analysis of DNA methylation and miRNA data also partitioned the discovery set into two groups with the methylation groups significantly correlated with clinical outcome. Our results provide a detailed picture of the genomic complexity and heterogeneity of these tumors that suggests a model wherein most OS are initiated by TP53 loss in a proliferative cell of the osteoblast lineage. TP53 deficiency leads directly to impairment of cell cycle control, DNA repair, and terminal differentiation, a state permissive for the development of secondary CNA and epigenetic changes. The TARGET OS data are publicly available (phs000218) and of immediate relevance to future investigations of the molecular mechanisms driving osteosarcoma. Findings suggest a path forward to improved assessment of risk for individual patients and support a precision medicine approach to future clinical trial development. Citation Format: Paul S. Meltzer, Sean Davis, Jack Zhu, Yonghong Wang, Sven Bilke, Joshua Waterfall, Robert Walker, Marbin Pineda, Yuan Jiang, Sharon Savage, Lisa Mirabello, Tsz-Kwong Man, Aaron Taylor, Monika J. Sun, Jay Wunder, Irene Andrulis, Nalan Gokgoz, Shintaro Iwata, Miki Ohira, Mark Krailo, Don Barkauskas, Lisa Teot, Timothy Triche, Silvia de Toledo, Antonio S. Petrilli, Jaime M. Guidry Auvil, Richard Gorlick, Malcolm A. Smith, Daniela Gerhard, Ching C. Lau. Translational and mechanistic implications of osteosarcoma genomics: A TARGET report [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr LB-307.

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)0.001
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 score0.005
Threshold uncertainty score0.018

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0010.001
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0050.002

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 head0.059
GPT teacher head0.366
Teacher spread0.307 · 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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Citations3
Published2020
Admission routes1
Has abstractyes

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