ArticleeLife2013
Global cellular response to chemotherapy-induced apoptosis.
Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 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
50 citing papers in PubMed, 73 citations in OpenAlex.
- Modifying quality and equity of care: emerging roles of genetic disease modifiers in β-hemoglobinopathies.Blood advances · 2026Review
- Highly specific Immunoproteasome inhibitor M3258 induces proteotoxic stress and apoptosis in KMT2A::AFF1 driven acute lymphoblastic leukemia.Scientific reports · 2025Article
- Inhibition of proteolytic and ATPase activities of the proteasome by the BTK inhibitor CGI-1746.iScience · 2024Article
- N-Terminomic Identification of Intracellular MMP-2 Substrates in Cardiac Tissue.Journal of proteome research · 2024Article
- Article
- An N terminomics toolbox combining 2-pyridinecarboxaldehyde probes and click chemistry for profiling protease specificity.Cell chemical biology · 2024Article
- Early recovery of proteasome activity in cells pulse-treated with proteasome inhibitors is independent of DDI2.bioRxiv : the preprint server for biology · 2023Article
- Gene expression flux analysis reveals specific regulatory modalities of gene expression.iScience · 2023Article
- Proteomic characterization of post-translational modifications in drug discovery.Acta pharmacologica Sinica · 2022Review
- Short open reading frame genes in innate immunity: from discovery to characterization.Trends in immunology · 2022Review
- 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
- Effects of Cancer Presence and Therapy on the Platelet Proteome.International journal of molecular sciences · 2021Article
- Proteasome inhibitor-induced modulation reveals the spliceosome as a specific therapeutic vulnerability in multiple myeloma.Nature communications · 2020Article
- In Vivo RNAi-Mediated eIF3m Knockdown Affects Ribosome Biogenesis and Transcription but Has Limited Impact on mRNA-Specific Translation.Molecular therapy. Nucleic acids · 2020Article
- Sensitive Determination of Proteolytic Proteoforms in Limited Microscale Proteome Samples.Molecular & cellular proteomics : MCP · 2019Article
- Multiomics of azacitidine-treated AML cells reveals variable and convergent targets that remodel the cell-surface proteome.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Ribosome elongating footprints denoised by wavelet transform comprehensively characterize dynamic cellular translation events.Nucleic acids research · 2018Article
- Seeking Convergence and Cure with New Myeloma Therapies.Trends in cancer · 2018Review
- Repurposing tofacitinib as an anti-myeloma therapeutic to reverse growth-promoting effects of the bone marrow microenvironment.Haematologica · 2018Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
How cancer cells globally struggle with a chemotherapeutic insult before succumbing to apoptosis is largely unknown. Here we use an integrated systems-level examination of transcription, translation, and proteolysis to understand these events central to cancer treatment. As a model we study myeloma cells exposed to the proteasome inhibitor bortezomib, a first-line therapy. Despite robust transcriptional changes, unbiased quantitative proteomics detects production of only a few critical anti-apoptotic proteins against a background of general translation inhibition. Simultaneous ribosome profiling further reveals potential translational regulation of stress response genes. Once the apoptotic machinery is engaged, degradation by caspases is largely independent of upstream bortezomib effects. Moreover, previously uncharacterized non-caspase proteolytic events also participate in cellular deconstruction. Our systems-level data also support co-targeting the anti-apoptotic regulator HSF1 to promote cell death by bortezomib. This integrated approach offers unique, in-depth insight into apoptotic dynamics that may prove important to preclinical evaluation of any anti-cancer compound. DOI:http://dx.doi.org/10.7554/eLife.01236.001.
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.