ReviewMolecular cancer research : MCR2015
When Cancer Fights Back: Multiple Myeloma, Proteasome Inhibition, and the Heat-Shock Response.
Review in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed.
- Trial
- Comprehensive Bioinformatic Analysis Reveals Survival-Associated Hub Genes and MicroRNAs in Multiple Myeloma Patients.Iranian journal of biotechnology · 2025Article
- Exosome-transmitted HSPA9 facilitates bortezomib resistance by targeting TRIP13/USP1 signaling in multiple myeloma.Cell communication and signaling : CCS · 2025Article
- Synergistic induction of mitotic pyroptosis and tumor remission by inhibiting proteasome and WEE family kinases.Signal transduction and targeted therapy · 2024Article
- Searching for LINCS to Stress: Using Text Mining to Automate Reference Chemical Curation.Chemical research in toxicology · 2024Article
- An Overview of Cancer in Djibouti: Current Status, Therapeutic Approaches, and Promising Endeavors in Local Essential Oil Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Dual inhibition of HSF1 and DYRK2 impedes cancer progression.Bioscience reports · 2023Article
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Allosteric HSP70 inhibitors perturb mitochondrial proteostasis and overcome proteasome inhibitor resistance in multiple myeloma.Cell chemical biology · 2022Article
- The surfaceome of multiple myeloma cells suggests potential immunotherapeutic strategies and protein markers of drug resistance.Nature communications · 2022Article
- The stress-responsive kinase DYRK2 activates heat shock factor 1 promoting resistance to proteotoxic stress.Cell death and differentiation · 2021Article
- The proteostasis guardian HSF1 directs the transcription of its paralog and interactor HSF2 during proteasome dysfunction.Cellular and molecular life sciences : CMLS · 2021Article
- Article
- In vitro and ex vivo gene expression profiling reveals differential kinetic response of HSPs and UPR genes is associated with PI resistance in multiple myeloma.Blood cancer journal · 2020Article
- Proteasome inhibitor-induced modulation reveals the spliceosome as a specific therapeutic vulnerability in multiple myeloma.Nature communications · 2020Article
- BET Inhibitors Synergize with Carfilzomib to Induce Cell Death in Cancer Cells via Impairing Nrf1 Transcriptional Activity and Exacerbating the Unfolded Protein Response.Biomolecules · 2020Article
- Blockade of HSP70 by VER-155008 synergistically enhances bortezomib-induced cytotoxicity in multiple myeloma.Cell stress & chaperones · 2020Article
- Increased expression of miR-27 predicts poor prognosis and promotes tumorigenesis in human multiple myeloma.Bioscience reports · 2019Article
- Article
- Small Molecule Inhibitors of HSF1-Activated Pathways as Potential Next-Generation Anticancer Therapeutics.Molecules (Basel, Switzerland) · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Multiple myeloma is a plasma cell malignancy with an estimated 26,850 new cases and 11,240 deaths in 2015 in the United States. Two main classes of agents are the mainstays of therapy-proteasome inhibitors (PI) and immunomodulatory drugs (IMiD). Other new targets are emerging rapidly, including monoclonal antibodies and histone deacetylase (HDAC) inhibitors. These therapeutic options have greatly improved overall survival, but currently only 15% to 20% of patients experience long-term progression-free survival or are cured. Therefore, improvement in treatment options is needed. One potential means of improving clinical options is to target resistance mechanisms for current agents. For example, eliminating the cytoprotective heat-shock response that protects myeloma cells from proteasome inhibition may enhance PI-based therapies. The transcription factor heat-shock factor 1 (HSF1) is the master regulator of the heat-shock response. HSF1 is vital in the proteotoxic stress response, and its activation is controlled by posttranslational modifications (PTM). This review details the mechanisms of HSF1 regulation and discusses leveraging that regulation to enhance PI activity.
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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.