ArticleOncogene2016
Resistance to HSP90 inhibition involving loss of MCL1 addiction.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Caspase-9 inhibition triggers Hsp90-based chemotherapy-mediated tumor intrinsic innate sensing and enhances antitumor immunity.Journal for immunotherapy of cancer · 2023Article
- HSP90 Inhibitor PU-H71 in Combination with BH3-Mimetics in the Treatment of Acute Myeloid Leukemia.Current issues in molecular biology · 2023Article
- Dynamic BH3 profiling identifies pro-apoptotic drug combinations for the treatment of malignant pleural mesothelioma.Nature communications · 2023Article
- Functional precision oncology using patient-derived assays: bridging genotype and phenotype.Nature reviews. Clinical oncology · 2023Review
- Article
- Integrin αvβ3 Induces HSP90 Inhibitor Resistance via FAK Activation in KRAS-Mutant Non-Small Cell Lung Cancer.Cancer research and treatment · 2022Article
- A novel C-terminal heat shock protein 90 inhibitor that overcomes STAT3-Wnt-β-catenin signaling-mediated drug resistance and adverse effects.Theranostics · 2022Article
- Transcriptional perturbation of protein arginine methyltransferase-5 exhibits MTAP-selective oncosuppression.Scientific reports · 2021Article
- Prodigiosin/PU-H71 as a novel potential combined therapy for triple negative breast cancer (TNBC): preclinical insights.Scientific reports · 2020Article
- Patient-derived explants (PDEs) as a powerful preclinical platform for anti-cancer drug and biomarker discovery.British journal of cancer · 2020Review
- LAM-003, a new drug for treatment of tyrosine kinase inhibitor-resistant FLT3-ITD-positive AML.Blood advances · 2019Article
- Overcoming acquired resistance to HSP90 inhibition by targeting JAK-STAT signalling in triple-negative breast cancer.BMC cancer · 2019Article
- HSP90 inhibition alters the chemotherapy-driven rearrangement of the oncogenic secretome.Oncogene · 2018Article
- Article
- Predicting effective pro-apoptotic anti-leukaemic drug combinations using co-operative dynamic BH3 profiling.PloS one · 2018Article
- HSP90 inhibition targets autophagy and induces a CASP9-dependent resistance mechanism in NSCLC.Autophagy · 2018Article
- Targeting cell death signalling in cancer: minimising 'Collateral damage'.British journal of cancer · 2016Review
- Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
Inhibition of the chaperone heat-shock protein 90 (HSP90) induces apoptosis, and it is a promising anti-cancer strategy. The mechanisms underpinning apoptosis activation following HSP90 inhibition and how they are modified during acquired drug resistance are unknown. We show for the first time that, to induce apoptosis, HSP90 inhibition requires the cooperation of multi BH3-only proteins (BID, BIK, PUMA) and the reciprocal suppression of the pro-survival BCL-2 family member MCL1, which occurs via inhibition of STAT5A. A subset of tumour cell lines exhibit dependence on MCL1 expression for survival and this dependence is also associated with tumour response to HSP90 inhibition. In the acquired resistance setting, MCL1 suppression in response to HSP90 inhibitors is maintained; however, a switch in MCL1 dependence occurs. This can be exploited by the BH3 peptidomimetic ABT737, through non-BCL-2-dependent synthetic lethality.
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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.