ReviewCancers2019
Cancer Metabolism and the Evasion of Apoptotic Cell Death.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Angiosarcoma: a systematic review of biomarkers in diagnosis, prognosis, and therapeutic strategies.Frontiers in oncology · 2025Pooled it
- Time-resolved simultaneous imaging of mitochondrial reactive oxygen species and lysosomal permeabilization to determine organelle-centred cell death.Redox report : communications in free radical research · 2026Article
- Deciphering the Medicinal Chemistry Aspects of Akt Inhibitors for the Management of Cancer: Structure-Activity Relationship Frameworks, Landscapes, and Optimization Approaches.Chemistry & biodiversity · 2026Review
- Liposomal honokiol attenuates dimethylhydrazine-induced colon carcinogenesis in rats through modulation of oxidative stress, inflammation, apoptosis, autophagy, and lipid metabolism pathways.Medical oncology (Northwood, London, England) · 2026Article
- In Vitro Evaluation of Combination Therapy with Doxorubicin and Quercetin for Uveal Melanoma.Current issues in molecular biology · 2026Article
- Flavonoids as Modulators of the p53-Bcl-2 Axis in Cancer: Molecular Mechanisms and Therapeutic Implications.Pharmaceutics · 2026Review
- mCell death & disease · 2026Article
- M. canadensis and its active component salvianolic acid B overcome paclitaxel resistance in gastric cancer via ROS-ER stress signaling.Cancer cell international · 2026Article
- Unlocking the Secrets of Regulated Cell Death in Large B-Cell Lymphoma Beyond Apoptosis: Signaling Pathways and Therapeutic Options.International journal of molecular sciences · 2026Review
- Higher order synthetic lethals are keys to minimize cancer treatment effects on non-tumor cells.PloS one · 2026Article
- Harnessing ferroptosis for cancer therapy: Mechanisms and therapeutic strategies (Review).Oncology reports · 2026Review
- AMP-activated protein kinase-driven lipid droplet dynamics govern melanoma sensitivity to polyunsaturated fatty acid and iron-induced ferroptosis.Nature communications · 2025Article
- Pioglitazone-Based Combination Approaches for Non-Small-Cell Lung Cancer.Pharmaceutics · 2025Review
- Anti-cancer effects of carnosol in DMBA-induced oral experimental carcinogenesis by oncogenic signaling pathways on in vivo and in silico study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Functions and mechanisms of long non-coding RNA in esophageal squamous cell carcinoma (Review).Oncology letters · 2025Review
- Stilbenes from Vine Extracts: Therapeutic Potential and Mechanisms.International journal of molecular sciences · 2025Review
- Article
- Potential Active Compounds ofFood science & nutrition · 2025Review
- Metabolic reprogramming promotes apoptosis resistance in acute lymphoblastic leukemia through CASP3 lactylation.Molecular cancer · 2025Article
- Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025Review
26 more citing papers are in PubMed but not listed here.
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
Cellular growth and proliferation depend upon the acquisition and synthesis of specific metabolites. These metabolites fuel the bioenergy, biosynthesis, and redox potential required for duplication of cellular biomass. Multicellular organisms maintain tissue homeostasis by balancing signals promoting proliferation and removal of cells via apoptosis. While apoptosis is in itself an energy dependent process activated by intrinsic and extrinsic signals, whether specific nutrient acquisition (elevated or suppressed) and their metabolism regulates apoptosis is less well investigated. Normal cellular metabolism is regulated by lineage specific intrinsic features and microenvironment driven extrinsic features. In the context of cancer, genetic abnormalities, unconventional microenvironments and/or therapy engage constitutive pro-survival signaling to re-program and rewire metabolism to maintain survival, growth, and proliferation. It thus becomes particularly relevant to understand whether altered nutrient acquisition and metabolism in cancer can also contribute to the evasion of apoptosis and consequently therapy resistance. Our review attempts to dissect a causal relationship between two cancer hallmarks, i.e., deregulated cellular energetics and the evasion of programmed cell death with primary focus on the intrinsic pathway of apoptosis.
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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.