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Record W1587087382

Abstract #5543: Lovastatin induces apoptosis of ovarian cancer cells and modulates the efficacy of chemotherapeutics: Implications for patient treatment

2009· article· en· W1587087382 on OpenAlexaff
Աննա Մարտիրոսյան, James W. Clendening, Carolyn A. Goard, Linda Z. Penn

Bibliographic record

VenueCancer Research · 2009
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer, Lipids, and Metabolism
Canadian institutionsUniversity of TorontoOntario Institute for Cancer Research
Fundersnot available
KeywordsLovastatinDoxorubicinApoptosisStatinOvarian cancerCancer researchHMG-CoA reductasePharmacologyCancerCancer cellMedicineChemotherapyBiologyCholesterolReductaseInternal medicineBiochemistryEnzyme
DOInot available

Abstract

fetched live from OpenAlex

AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO The statin family of cholesterol control agents have recently been shown to have promise as anticancer therapeutics. By inhibiting HMG CoA reductase (HMGCR) and the mevalonate pathway, statins can trigger cells from certain tumor types to undergo apoptosis, in the absence of damage to normal, non-transformed cells. To maximally exploit these readily available agents for patient care, it is important to both identify statin-sensitive tumor types and delineate the mechanisms of statin-induced apoptosis. In this report we show that lovastatin can trigger ovarian cancer cells to undergo apoptosis by two complementary anticancer mechanisms. We first demonstrate that human ovarian cancer cells are sensitive to lovastatin-induced apoptosis via inhibition of HMGCR, independently of p53 mutation status. Second, we show that lovastatin synergizes with doxorubicin, a chemotherapeutic used to treat drug-resistant disease, by a mechanism that increases intracellular doxorubicin within drug-resistant cells. This activity does not depend upon HMGCR inhibition, but instead inhibits P-glycoprotein-mediated drug efflux. Elevated doxorubicin retention is accompanied by enhanced DNA damage and apoptosis, arguing for the combination of lovastatin and doxorubicin to treat drug-resistant cancers, including ovarian cancer. While previous studies exploring the effect of lovastatin on P-gp were limited, our results are made distinctly more relevant to the clinic. To achieve this, we used human cell systems selected to overexpress human P-glycoprotein as well as physiologically attainable concentrations of both doxorubicin and lovastatin in its biologically relevant acid form. This work should serve as evidence that chemotherapeutics combined with statins may have profound, synergistic effects. Whether these effects are positive or negative may depend on several variables which need to be explored. Ultimately, exploiting the ability of statins to both trigger apoptosis and block P-glycoprotein should be done in such a way to maximize anticancer activity without increasing toxicity. Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 5543.

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 score0.021
Threshold uncertainty score0.070

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 communication0.0010.000
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0210.008

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 head0.054
GPT teacher head0.381
Teacher spread0.327 · 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
Published2009
Admission routes1
Has abstractyes

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