ArticleCancer cell2017
Developmental Regulation of Mitochondrial Apoptosis by c-Myc Governs Age- and Tissue-Specific Sensitivity to Cancer Therapeutics.
Article in Cancer cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
163 citing papers in PubMed, 1 synthesis or guideline pooled it, 227 citations in OpenAlex.
- Chemotherapy cardiotoxicity research in cancer patients: a bibliometric and visual analysis (1994-2024).Frontiers in oncology · 2025Pooled it
- Intratumoral T cell activation kills tumors regardless of T cell specificity.Nature immunology · 2026Article
- Advances in Somatostatin Receptor-Targeting Peptide Receptor Radionuclide Therapy for Neuroendocrine Tumors: Biological Rationale, Combination Strategies, and Clinical Perspectives.International journal of molecular sciences · 2026Review
- Dying for Clarity: Common Pitfalls in Cardiac Cell Death Research.Cardiovascular drugs and therapy · 2026Article
- The myeloid cell leukaemia-1 inhibitor MIK665 is a potent therapy in preclinical models of paediatric acute myeloid leukaemia.British journal of haematology · 2026Article
- BH3 profiling analyses for functional precision medicine.Oncogenesis · 2026Review
- Targeting CIC::DUX4 sarcoma with Minnelide in a dual recombinase-initiated genetically engineered mouse model.The Journal of clinical investigation · 2026Article
- A peptide-based screen for cell death inhibitors identifies the cytoprotective compound CDL36.bioRxiv : the preprint server for biology · 2026Article
- Induction of caspase-mediated suppression of interferon signaling potentiates viral oncolysis of resistant tumor cells.Cell communication and signaling : CCS · 2026Article
- Residuals of Chemical Cleaning Agents Impair Peri-Implant Cell Viability: An in Vitro Study.ACS biomaterials science & engineering · 2026Article
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- Of Barriers and Loops-How Evolution Limits Most Cancer Risks to Older Ages.Cancer discovery · 2026Review
- Platelet aging and desialylation increase apoptotic priming and BCL-XCell death & disease · 2026Article
- Article
- Allosteric regulation of BH3-in-groove interactions by tail anchors of BCL-xL complexes limits BH3 mimetic antagonism.Nature communications · 2025Article
- Efficacy of Minnelide in a Next-Generation Dual-Recombinase Regulated Genetically Engineered Mouse Model of CIC::DUX4 Sarcoma.bioRxiv : the preprint server for biology · 2025Article
- Mutational analysis of the mitochondrial tRNA genes and flanking regions in lymphocytes from long-term pediatric cancer survivors given doxorubicin chemotherapy for acute lymphoblastic leukemia.Cardio-oncology (London, England) · 2025Article
- A molecular circuit regulates fate plasticity in emerging and adult AT2 cells.Nature communications · 2025Article
- BCL-xL dependency in chromophobe renal cell carcinoma.Cancer gene therapy · 2025Article
- Dual Modes of Gene Regulation by CDK12.bioRxiv : the preprint server for biology · 2025Article
103 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 2 countries.
Funding
Abstract
It is not understood why healthy tissues can exhibit varying levels of sensitivity to the same toxic stimuli. Using BH3 profiling, we find that mitochondria of many adult somatic tissues, including brain, heart, and kidneys, are profoundly refractory to pro-apoptotic signaling, leading to cellular resistance to cytotoxic chemotherapies and ionizing radiation. In contrast, mitochondria from these tissues in young mice and humans are primed for apoptosis, predisposing them to undergo cell death in response to genotoxic damage. While expression of the apoptotic protein machinery is nearly absent by adulthood, in young tissues its expression is driven by c-Myc, linking developmental growth to cell death. These differences may explain why pediatric cancer patients have a higher risk of developing treatment-associated toxicities.
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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.