ReviewCell death & disease2015
How cell death shapes cancer.
Review in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 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
148 citing papers in PubMed, 1 synthesis or guideline pooled it, 292 citations in OpenAlex.
- Pooled it
- Systemic immunomodulation by irreversible electroporation versus stereotactic ablative body radiotherapy in locally advanced pancreatic cancer: the CROSSFIRE trial.Journal for immunotherapy of cancer · 2025Trial
- Metformin effects on head and neck squamous carcinoma microenvironment: Window of opportunity trial.The Laryngoscope · 2017Trial
- The second mitochondrial activator of caspases (SMAC) regulates growth, inflammation and mitochondrial integrity in cancer cells.Cell death and differentiation · 2026Article
- Why are Some Tissues More Vulnerable? Revisiting Tissue Specificity in Hereditary Cancer Syndromes.Molecular diagnosis & therapy · 2026Review
- Article
- Galangin's Therapeutic Potential in Retinoblastoma: Inducing Apoptosis and Modulating RB Protein and Some MicroRNAs.Advanced pharmaceutical bulletin · 2026Article
- Targeting TYRO3 attenuates apoptotic cell-driven cancer stemness in triple negative breast cancer.Cell communication and signaling : CCS · 2026Article
- Emerging evidence on micro- and nanoplastics carcinogenicity: mechanisms, models, and signaling networks.Molecular cancer · 2026Review
- Shaping death: how the microbiome regulates tumour cell demise and therapy response.Cancer metastasis reviews · 2026Review
- Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate.Molecular cancer research : MCR · 2026Article
- Harnessing photodynamic therapy for programmed cell death: the central role and contributions of metal complexes as next generation photosensitizers.RSC medicinal chemistry · 2025Review
- 5-hydroxymethylcytosine analysis reveals stable epigenomic changes in tumor tissue that enable cancer detection in cell-free DNA.Communications biology · 2025Article
- Clinicopathological insights and prognostic implications of DEK in association with apoptosis-regulating factors in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Hypericin Photodynamic Therapy Induces Cytotoxicity and Modulates Cytokine Secretion in MCF-7 Breast Cancer Cells.Journal of clinical medicine · 2025Article
- Metabolites in the extracellular tumor microenvironment and the shaping of macrophage function.Molecular cell · 2025Review
- Aspirin-Inspired 6-O-Carboxymethyl-N-Acetylglucosamine: A potent antitumor agent with enhanced efficacy.Apoptosis : an international journal on programmed cell death · 2025Article
- Tianma Granules Alleviate AOM/DSS-Induced Colorectal Tumorigenesis by Inhibiting the Wnt/β-Catenin Pathway Activation.Journal of cellular and molecular medicine · 2025Article
- Probiotics and Cancer: Mechanistic Insights and Organ-Specific Impact.Biomolecules · 2025Review
- Targeting kinases that regulate programmed cell death: a new therapeutic strategy for breast cancer.Journal of translational medicine · 2025Review
88 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis has been established as a mechanism of anti-cancer defense. Members of the BCL-2 family are critical mediators of apoptotic cell death in health and disease, often found to be deregulated in cancer and believed to lead to the survival of malignant clones. However, over the years, a number of studies pointed out that a model in which cell death resistance unambiguously acts as a barrier against malignant disease might be too simple. This is based on paradoxical observations made in tumor patients as well as mouse models indicating that apoptosis can indeed drive tumor formation, at least under certain circumstances. One possible explanation for this phenomenon is that apoptosis can promote proliferation critically needed to compensate for cell loss, for example, upon therapy, and to restore tissue homeostasis. However, this, at the same time, can promote tumor development by allowing expansion of selected clones. Usually, tissue resident stem/progenitor cells are a major source for repopulation, some of them potentially carrying (age-, injury- or therapy-induced) genetic aberrations deleterious for the host. Thereby, apoptosis might drive genomic instability by facilitating the emergence of pathologic clones during phases of proliferation and subsequent replication stress-associated DNA damage. Tumorigenesis initiated by repeated cell attrition and repopulation, as confirmed in different genetic models, has parallels in human cancers, exemplified in therapy-induced secondary malignancies and myelodysplastic syndromes in patients with congenital bone marrow failure syndromes. Here, we aim to review evidence in support of the oncogenic role of stress-induced 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.