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Record W2741422412 · doi:10.1158/1538-7445.am2017-1184

Abstract 1184: Characterization of novel STAT5 inhibitors to interfere with the oncogenic activities of STAT5 in hematopoietic diseases

2017· article· en· W2741422412 on OpenAlexaff
Bettina Wingelhofer, Barbara Maurer, Elizabeth Heyes, Patricia Freund, Abbarna A. Cumaraswamy, Jisung Park, Stefan Kubicek, Peter Valent, Patrick T. Gunning, Richard Moriggl

Bibliographic record

VenueCancer Research · 2017
Typearticle
Languageen
FieldMedicine
TopicCytokine Signaling Pathways and Interactions
Canadian institutionsUniversity of Toronto
Fundersnot available
KeywordsSTAT5Cancer researchMyeloid leukemiaTyrosine kinaseBiologyChemistryCell biologySignal transduction

Abstract

fetched live from OpenAlex

Abstract Activation of the transcription factor STAT5 is essential for the pathogenesis of acute myeloid leukemia (AML) containing the FLT3 internal tandem duplication (ITD). FLT3 ITD is a constitutively active tyrosine kinase (TK) that drives the activation of STAT5 leading to the growth and survival of AML cells. Although there has been some success in identifying TK inhibitors that block the function of FLT3 ITD, treatment options are still limited. This is mainly due to drug resistance development by mutations that allow for the continued activation of STATs. Since STAT5 represents a critical mediator of malignant cellular behavior and sits at the convergence point of many kinase pathways, the direct targeting of STAT5 may be an effective means of overcoming this resistance to TK inhibitors. First, we screened a library of potential STAT5 inhibitors for specific SH2 domain binders using a fluorescent polarization assay. Thereby, we identified small inhibitory molecules, called AC-3-019 and AC-4-130, that bind to the SH2 domain of STAT5, subsequently resulting in the disruption of the reciprocal STAT5-phosphopeptide interactions. They efficiently blocked kinase-mediated phosphorylation, dimer formation, nuclear translocation, DNA binding and STAT5 mediated target gene expression. Further, we observed a time- and dose-dependent impairment of proliferation, blocked cell cycle progression and increased apoptosis. Studies with human AML patient-derived samples similarly showed an induction of apoptotic cell death and decreased colony forming capabilities. A combinatorial drug screen revealed synergistic effects with TK inhibitors, as well as with drugs standardly used in the treatment of AML patients, e.g. Cytarabine. Finally, AC-3-019 and AC-4-130 significantly suppressed tumor growth in vivo without general toxicity in healthy organs. Overall, our findings indicate that AC-3-019 and AC-4-130 are potent and selective inhibitors of STAT5. These compounds provide lead structures for further chemical modifications and clinical development for the identification of compounds to improve existing therapies. Citation Format: Bettina Wingelhofer, Barbara Maurer, Elizabeth C. Heyes, Patricia Freund, Abbarna A. Cumaraswamy, Jisung Park, Stefan Kubicek, Peter Valent, Patrick T. Gunning, Richard Moriggl. Characterization of novel STAT5 inhibitors to interfere with the oncogenic activities of STAT5 in hematopoietic diseases [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1184. doi:10.1158/1538-7445.AM2017-1184

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: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.218
Threshold uncertainty score0.229

Codex and Gemma teacher scores by category

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

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 head0.091
GPT teacher head0.415
Teacher spread0.323 · 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
Published2017
Admission routes1
Has abstractyes

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