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Record W1996349796 · doi:10.1158/1538-7445.am10-3487

Abstract 3487: Synergy with combined inhibition of upstream EGFR-HER2 and downstream RAF-MEK nodes in breast cancer cells with activating RAS and RAF mutations

2010· article· en· W1996349796 on OpenAlexaff
Teddy S. Nagaria, Peter A. Greer, Waheed Sangrar

Bibliographic record

VenueCancer Research · 2010
Typearticle
Languageen
FieldMedicine
TopicAdvanced Breast Cancer Therapies
Canadian institutionsQueen's University
Fundersnot available
KeywordsLapatinibMAPK/ERK pathwayCancer researchMEK inhibitorEpidermal growth factor receptorEGFR inhibitorsKinaseReceptor tyrosine kinaseChemistryCancerBiologyMedicineBreast cancerCell biologyInternal medicineTrastuzumab

Abstract

fetched live from OpenAlex

Abstract Targeted therapies have been developed to target a variety of oncogenic proteins implicated in breast cancer. These include epidermal growth factor receptor (EGFR), epidermal growth factor receptor type-2 (HER-2), as well as RAS, RAF and MEK, which together comprise the mitogen activated protein kinase (MAPK) cascade. Herein, we explored the therapeutic efficacy of tyrosine kinase inhibitors of EGFR and HER-2 by testing these inhibitors on a human metastatic breast cancer cell line MDA-MB-231. We also determined whether inhibiting tyrosine kinase receptors correlated with the activity of downstream nodes such as MEK and ERK. We report that EGFR inhibitors potently inhibited the phosphorylation of EGFR, but had no effect on MEK and ERK activity, which were observed to be constitutively active in this cell line. Interestingly, MEK/ERK insensitivity correlated with cytotoxic resistance of MDA-MB-231 cells to EGFR inhibitor treatment. In contrast, targeting both EGFR and HER-2 with a dual EGFR/HER-2 inhibitor Lapatinib resulted in significantly improved cytotoxic effects and a partial reduction in MEK and ERK activity. In comparison to the effects of Lapatinib, targeting RAF with Sorafenib resulted in almost complete abrogation of MEK/ERK signaling activity and enhanced cytotoxicity. Our results are consistent with earlier reports suggesting that MAPK signaling is required for MDA-MB-231 cell survival, consistent with the reported presence of activating RAS and RAF mutations in this cell line. Our data highlight the role of RAS and RAF mutations in the uncoupling of downstream nodes (MEK and ERK) from upstream receptor activation. Lastly, the MEK inhibitor U1026 fully inhibited ERK activity but exhibited poor cytotoxicity. This suggests that MDA-MB-231 cells may circumvent MEK inhibition through upstream survival pathways mediated by activated RAS or RAF. An apparent synergistic cytotoxic effect was noted when combining Sorafenib and U1026. Cytotoxic synergy was also observed when Sorafenib was combined with Lapatinib. These putative synergistic drug combinations show promise in that they could deliver significant cytotoxic effects with reduced doses. We find there is merit in targeting multiple oncogenic nodes concurrently to promote additional therapeutic benefits. This also shows potential use in targeting a broader variety of cancer cells that harbor constitutive MAPK signaling associated with oncogenic RAS or RAF mutations. 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 3487.

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)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.413
Threshold uncertainty score0.999

Codex and Gemma teacher scores by category

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

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 head0.019
GPT teacher head0.341
Teacher spread0.322 · 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.

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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