ArticleCell reports2015
A Hyperactive Signalosome in Acute Myeloid Leukemia Drives Addiction to a Tumor-Specific Hsp90 Species.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 63 citations in OpenAlex.
- Targeting HSP90 in cancer: advances in the development of inhibitors, mechanisms of action, and therapeutic applications.Molecular cancer · 2026Review
- eIF4E and Ezrin cooperate in pseudopods to drive a localized migratory translation program in acute myeloid leukemia.bioRxiv : the preprint server for biology · 2026Article
- Directed discovery of high-loading nanoaggregates enabled by drug-matched oligo-peptide excipients.Chem · 2025Article
- Review
- In Vitro Purging of Acute Lymphoblastic Leukemia (B-ALL) Cells with the Use of PTL, DMAPT, or PU-H71.International journal of molecular sciences · 2024Article
- RNA sequestration in P-bodies sustains myeloid leukaemia.Nature cell biology · 2024Article
- Pharmacological p38 MAPK inhibitor SB203580 enhances AML stem cell line KG1a chemosensitivity to daunorubicin by promoting late apoptosis, cell growth arrest in S-phase, and miR-328-3p upregulation.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Phosphorylation-Driven Epichaperome Assembly: A Critical Regulator of Cellular Adaptability and Proliferation.Research square · 2024Article
- Co-targeting HSP90 alpha and CDK7 overcomes resistance against HSP90 inhibitors in BCR-ABL1+ leukemia cells.Cell death & disease · 2023Article
- Structural and functional complexity of HSP90 in cellular homeostasis and disease.Nature reviews. Molecular cell biology · 2023Review
- Article
- HSP90 Inhibitor PU-H71 in Combination with BH3-Mimetics in the Treatment of Acute Myeloid Leukemia.Current issues in molecular biology · 2023Article
- A Coumarin-Imidazothiadiazole Derivative, SP11 Abrogates Tumor Growth by Targeting HSP90 and Its Client Proteins.Molecules (Basel, Switzerland) · 2023Article
- Targeting stressor-induced dysfunctions in protein-protein interaction networks via epichaperomes.Trends in pharmacological sciences · 2023Review
- HSF1 is a driver of leukemia stem cell self-renewal in acute myeloid leukemia.Nature communications · 2022Article
- TRAP1 Chaperones the Metabolic Switch in Cancer.Biomolecules · 2022Review
- Allogeneic TCRαβ deficient CAR T-cells targeting CD123 in acute myeloid leukemia.Nature communications · 2022Article
- The penalty of stress - Epichaperomes negatively reshaping the brain in neurodegenerative disorders.Journal of neurochemistry · 2021Review
- Pharmacologically controlling protein-protein interactions through epichaperomes for therapeutic vulnerability in cancer.Communications biology · 2021Article
- Chemical tools for epichaperome-mediated interactome dysfunctions of the central nervous system.Nature communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is a heterogeneous and fatal disease with an urgent need for improved therapeutic regimens given that most patients die from relapsed disease. Irrespective of mutation status, the development of aggressive leukemias is enabled by increasing dependence on signaling networks. We demonstrate that a hyperactive signalosome drives addiction of AML cells to a tumor-specific Hsp90 species (teHsp90). Through genetic, environmental, and pharmacologic perturbations, we demonstrate a direct and quantitative link between hyperactivated signaling pathways and apoptotic sensitivity of AML to teHsp90 inhibition. Specifically, we find that hyperactive JAK-STAT and PI3K-AKT signaling networks are maintained by teHsp90 and, in fact, gradual activation of these networks drives tumors increasingly dependent on teHsp90. Thus, although clinically aggressive AML survives via signalosome activation, this addiction creates a vulnerability that can be exploited with Hsp90-directed therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.