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Record W2314860898 · doi:10.1158/1538-7445.am2013-617

Abstract 617: High-throughput screens identify PARP inhibition as being synthetically lethal with ERCC1 deficiency in non-small cell lung cancer cell lines.

2013· article· en· W2314860898 on OpenAlexaff
Sophie Postel‐Vinay, Ilirjana Bajrami, Luc Friboulet, Marieke Aarts, Yari Fontebasso, Fabrice André, Ken A. Olaussen, Jean‐Charles Soria, Chris Lord, Alan Ashworth

Bibliographic record

VenueCancer Research · 2013
Typearticle
Languageen
FieldMedicine
TopicPARP inhibition in cancer therapy
Canadian institutionsInstitute of Cancer Research
Fundersnot available
KeywordsERCC1Synthetic lethalityBiologyPARP inhibitorCancer researchDNA repairIn vivoDNA damageCell culturePoly ADP ribose polymeraseNucleotide excision repairDNAGenetics

Abstract

fetched live from OpenAlex

Abstract Background: Non-small cell lung cancer (NSCLC) harbors frequent DNA-repair defects that represent therapeutic opportunities. Notably, Excision Repair Cross-Complementation group 1 (ERCC1) deficiency has been described in a subset of tumors and correlated with platinum sensitivity. The use of mechanism-based approaches, such as synthetic lethality, could allow targeting more selectively such DNA repair defects, with reduced systemic toxicity. Methods: To identify ERCC1-selective synthetic lethal interactions, we adopted an integrated functional and molecular profiling approach. An isogenic model of ERCC1-deficient NSCLC cells, consisting of one parental ERCC1-proficient cell line and 3 ERCC1-deficient clones, was functionally profiled by high throughput drug sensitivity screening using a library containing commonly used oncology agents as well as a large number of in-development targeted agents. This was integrated with data from molecular profiling, including high throughput siRNA screens. Results: The comparison of functional viability profiles for ERCC1-deficient models enabled the identification of synthetic lethal effects that could represent therapeutic opportunities for ERCC1-deficient tumors. Notably, ERCC1-deficient cells showed increased sensitivity to several PARP inhibitors, representing promising preliminary results that could be translated in the clinical setting. Mechanistic studies revealed a significant delay in double-strand break repair associated with a G2/M arrest following PARP inhibitor treatment in the ERCC1-deficient population only. Further in vitro work is providing deeper insight into the mechanisms underlying this PARP inhibitors sensitivity and in vivo work is underway. Conclusions: ERCC1-deficiency sensitizes human NSCLC cell lines to PARP inhibitors. In vitro and in vivo revalidations of these results and now underway to further dissect the molecular mechanisms responsible for these ERCC1-deficient selective effects, which could represent therapeutic opportunities. Citation Format: Sophie C. Postel-Vinay, Ilirjana Bajrami, Luc Friboulet, Marieke Aarts, Yari Fontebasso, Fabrice Andre, Ken Olaussen, Jean-Charles Soria, Chris Lord, Alan Ashworth. High-throughput screens identify PARP inhibition as being synthetically lethal with ERCC1 deficiency in non-small cell lung cancer cell lines. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 617. doi:10.1158/1538-7445.AM2013-617

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: Bench or experimental
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)0.0010.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0010.001
Science and technology studies0.0000.000
Scholarly communication0.0010.000
Open science0.0010.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0020.001

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 head0.043
GPT teacher head0.388
Teacher spread0.345 · 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".

Quick stats

Citations0
Published2013
Admission routes1
Has abstractyes

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