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Record W2044153248 · doi:10.1158/1538-7445.am10-3422

Abstract 3422: Synthetic lethal siRNA screening reveals novel modifiers of insulin-like growth factor-1 receptor (IGF1R) inhibitor activity in childhood sarcomas

2010· article· en· W2044153248 on OpenAlexaff
Jenny Potratz, Darren N. Saunders, Daniel Wai, C. Patrick Reynolds, Jonathan D. Buckley, R.J. Arceci, Gregory H. Reaman, Timothy J. Triche, Heribert Jürgens, Michaël Pollak, Poul H. Sorensen

Bibliographic record

VenueCancer Research · 2010
Typearticle
Languageen
FieldMedicine
TopicSarcoma Diagnosis and Treatment
Canadian institutionsMcGill University
Fundersnot available
KeywordsInsulin-like growth factor 1 receptorInsulin-like growth factorGrowth factorCancer researchReceptorMedicineGrowth factor receptorInternal medicineEndocrinologyBiology

Abstract

fetched live from OpenAlex

Abstract The insulin-like growth factor-1 receptor (IGF1R) is emerging as a therapeutic target in many cancers including Ewing family tumors and other childhood sarcomas, where IGF1R blocking antibodies show promising anti-tumor activity in some but not all patients. A key question remains as to what underlies IGF1R inhibitor sensitivity versus resistance. IGF1R mutations have to date not been found in these tumors. Instead, we hypothesize that compensatory signaling circuits by-passing targeted IGF1R inhibition are involved. We performed synthetic lethal siRNA screens in Ewing family tumor cell lines to study the IGF1R signaling axis and related protein tyrosine kinase networks in the presence and absence of sub-lethal doses of an IGF1R kinase inhibitor, with the goal of identifying siRNAs that restored full inhibitor activity. This strategy revealed (1) that Ewing sarcoma and rhabdomyosarcoma cells are exquisitely sensitive to loss of distal IGF1R signaling components such as the ribosomal protein S6 (RPS6); (2) IGF1R inhibitors fail to block RPS6 activation in resistant cell lines; and (3) that siRNA knock-down of certain protein tyrosine kinases such as the MET family receptor MST1R restores inhibitor efficacy, even in highly drug resistant cell lines. Moreover, we confirmed MST1R expression in childhood sarcomas and found that loss of MST1R blocks downstream RPS6 activation when combined with IGF1R inhibition in vitro. Taken together, we present an approach in principle applicable to any promising drug of interest. We demonstrate that key signaling effectors of the IGF1R axis in childhood sarcomas represent distal pathway proteins such as RPS6, and we identify the MST1R receptor tyrosine kinase as a potential therapeutic target whose knock-down markedly enhances sensitivity to IGF1R inhibition in high-risk sarcoma cell types, including resistant lines. These data underscore the importance of fully understanding protein tyrosine kinase networks for successful implementation of kinase inhibitor strategies. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3422.

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)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.001

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 head0.079
GPT teacher head0.372
Teacher spread0.292 · 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
Published2010
Admission routes1
Has abstractyes

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