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Abstract A08: PARP1-mediated E2F1 regulation of DNA repair capacity

2017· article· en· W2604395271 on OpenAlexaffabout
Matthew J. Schiewer, Amy C. Mandigo, Nicholas Gordon, Sumin Han, Shuang G. Zhao, Joseph R. Evans, Theodore Parsons, Ruth Birbe, Peter A. McCue, Tapio Visakorpi, Ganesh V. Raj, Mark A. Rubin, Johann S. de Bono, Costas D. Lallas, Edouard J. Trabulsi, Leonard G. Gomella, Adam P. Dicker, Wm. Kevin Kelly, Felix Y. Feng, Karen E. Knudsen

Bibliographic record

VenueMolecular Cancer Research · 2017
Typearticle
Languageen
FieldMedicine
TopicPARP inhibition in cancer therapy
Canadian institutionsInstitute of Cancer Research
Fundersnot available
KeywordsPARP1DNA repairBiologyCancer researchDNA damageTranscriptomeChromatinGenome instabilityARID1AContext (archaeology)Synthetic lethalityGeneticsGenePoly ADP ribose polymeraseDNAGene expressionPolymeraseMutation

Abstract

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Abstract PARP1 holds two major functions on chromatin, DNA damage repair and transcriptional regulation, both of which are relevant in the context of cancer. Notably, PARP1 has been found to be a key modulator of androgen receptor (AR) function and AR-dependent phenotypes, which is a driving factor in prostate cancer (PCa) biology and therapeutic management. Recent studies indicate an unanticipated prevalence of DNA repair alterations in advanced PCa and showed that PARP1 inhibitors (PARPi) can effectively manage of a subset of these tumors. Despite the functions of PARP1 in DNA repair having been exploited as a therapeutic target for tumors with BRCA1/2 aberrations, factors beyond DNA repair alterations clearly play a role in the response to PARPi. Notably, in the TO-PARP trial, not all patients with DNA repair aberrations responded to PARPi; conversely, tumors lacking BRCA1/2 or other DNA repair alterations show objective response to PARPi in PCa and other tumor types. These clinical data suggest that the genetic (e.g. BRCA-ness) and pharmacologic interplay is complex in the context of PARPi. Given the preclinical and clinical data, pursuing a deeper understanding of the molecular underpinnings of PARPi action in PCa may yield significant benefit. Genome-wide transcriptional profiling in response to PARPi was performed and the PARP1-regulated transcriptome was identified. Both the PARP1-regulated transcriptome, as well as PARP1 enzymatic activity were found to be elevated as a function of PCa progression. Further interrogation of the PARP1-regulated transcriptome revealed a major impact on E2F1-regulated genes, and chromatin immunoprecipitation analyses indicated that PARP1 functions to regulate the chromatin architecture and E2F1 occupancy at E2F1 target gene loci. Most prominent among the E2F1-regulated genes responsive to PARPi were genes associated with DNA damage repair, with a particular enrichment for genes involved in homologous recombination (HR). In sum, these data indicate PARP1 regulates function of key oncogenic transcription factors (AR and E2F1) in PCa, and part of the effect of PARPi may be through down-regulation of DNA repair factors. Citation Format: Matthew J. Schiewer, Amy C. Mandigo, Nicholas Gordon, Sumin Han, Shuang Zhao, Joseph Evans, Theodore Parsons, Ruth Birbe, Peter McCue, Tapio Visakorpi, Ganesh Raj, Mark Rubin, Johann de Bono, Costas Lallas, Edouard Trabulsi, Leonard G. Gomella, Adam P. Dicker, Wm. Kevin Kelly, Felix Y. Feng, Karen E. Knudsen. PARP1-mediated E2F1 regulation of DNA repair capacity [abstract]. In: Proceedings of the AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; 2016 Nov 2-5; Montreal, QC, Canada. Philadelphia (PA): AACR; Mol Cancer Res 2017;15(4_Suppl):Abstract nr A08.

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)0.001
metaresearch head score (Gemma)0.001
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesInsufficient payload (model declined to judge)
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 score0.233
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.001
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.001
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
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 head0.143
GPT teacher head0.442
Teacher spread0.299 · 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

Citations1
Published2017
Admission routes2
Has abstractyes

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