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Abstract A189: Expression of fusion proteins in acute myeloid leukemia cells increases sensitivity to histone deacetylase inhibitors

2009· article· en· W1995058453 on OpenAlexaff
Luca A. Petruccelli, Filippa Pettersson, Daphné Dupéré-Richer, Kim L. Rice, Jonathan D. Licht, Wilson H. Miller

Bibliographic record

VenueMolecular Cancer Therapeutics · 2009
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicProtein Degradation and Inhibitors
Canadian institutionsMcGill University
Fundersnot available
KeywordsBiologyDNA damageDNA repairVorinostatCancer researchCell biologyFusion proteinHistoneGene silencingMyeloid leukemiaHistone deacetylaseMolecular biologyGeneticsGeneDNA

Abstract

fetched live from OpenAlex

Abstract Acute Myeloid Leukemias (AMLs) are often characterized by chromosomal rearrangements that result in fusion proteins with aberrant transcriptional regulatory activities. These fusion proteins bind to gene promoters and recruit corepressors such as histone deacetylases (HDACs), which remodel chromatin into a closed conformation thereby silencing genes and contributing to a malignant phenotype. Aberrantly silenced genes include tumor suppressor and pro-differentiation genes. In addition, multiple groups have reported a DNA repair deficient phenotype concurrent with the expression of different fusion proteins in leukemia. Small molecule HDAC inhibitors (HDACi) were devised as a strategy to reverse transcriptional repression. Indeed, many studies have demonstrated the ability of HDACi to re-sensitize leukemic cells to differentiating stimuli. However, other studies have revealed alternate methods by which HDACi exert anti-tumor activity, including induction of apoptosis that may be dependent on induction of ROS, MAPK signaling etc. We find that low doses of HDACi, including Vorinostat and LBH589, induce cell death in the AML cell line U937 in a dose and time-dependant manner. Further, Vorinostat induced cell death in U937 cells is preceded by DNA damage and a G2/M arrest. This correlates with reports that HDACi repress DNA repair, by down-regulating DNA repair genes and by acetylating repair proteins thereby impairing their repair function. Due to the inhibitory effect of leukemic fusion proteins on DNA repair, we predicted that DNA damage induced by HDACi, and thus cell death, would be amplified in AML cells expressing PML-RARα and PLZF-RARα fusion proteins. Sensitivity to Vorinostat and LBH589 was tested in three U937 derived cell lines: PR9 (PML-RARα inducible), B412 (PLZF-RARα inducible) and SN4 (mock transfected control). Indeed, induction of PLZF-RARα increased sensitivity of B412 cells to both Vorinostat- and LBH-mediated cell death. Assaying for DNA damage using alkaline comet assay, PR9 and B412 cells displayed an increase in DNA damage when their respective fusion protein is expressed. Nonetheless, the contribution of DNA damage to HDACi-mediated cell death remains unclear and further study is necessary. These findings are significant as they point to fusion protein expressing AMLs as a target group that may respond better to HDACi-based therapies. Citation Information: Mol Cancer Ther 2009;8(12 Suppl):A189.

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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 score0.003
Threshold uncertainty score0.008

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 integrity0.0000.001
Insufficient payload (model declined to judge)0.0030.001

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 head0.010
GPT teacher head0.271
Teacher spread0.260 · 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".

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Citations0
Published2009
Admission routes1
Has abstractyes

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