ReviewInternational journal of molecular sciences2022
The Apoptosis Paradox in Cancer.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 250 papers, 3 of them syntheses 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
250 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- The Role of Artemisinin and its Derivatives in Cancer Therapy via Ferroptosis: A Systematic Review ofAnti-cancer agents in medicinal chemistry · 2026Pooled it
- Association Aamong Ppolymorphisms in the Aapoptosis-Rrelated NKX3-1, Caspase-3, Caspase-9, and BCL-2 Genes and Prostate Cancer Susceptibility From 9706 Cases and 12,567 Controls.Cancer reports (Hoboken, N.J.) · 2025Pooled it
- Administration sequences in single-day chemotherapy regimens for breast cancer: a comprehensive review from a practical perspective.Frontiers in oncology · 2024Pooled it
- Advances in miR‑200c regulation of apoptosis, pyroptosis and autophagy in disease (Review).Molecular medicine reports · 2026Review
- How optimal control of cellular cost shapes population-level tumor growth dynamics.bioRxiv : the preprint server for biology · 2026Article
- Calcitriol, the active form of vitamin D, induces cell death and purinergic signaling modulation in cutaneous melanoma cells.Medical oncology (Northwood, London, England) · 2026Article
- MicroRNAs in Breast Cancer: Biological Functions and Technologies for Experimental and Therapeutic Applications.Cancers · 2026Review
- MicroRNAs and Other Small RNAs in Liquid Biopsies as Biomarkers for Early Detection of Colorectal Cancer.International journal of molecular sciences · 2026Review
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- Novel Camptothecin-Based Lipid Conjugated with Steroids and Triterpene Acids: Enhanced Cellular Uptake and Topoismerase I Inhibition.Pharmaceutics · 2026Article
- Insights into programmed cell death from multiple imaging modalities.Journal of translational medicine · 2026Review
- Tumor-derived apoptotic extracellular vesicles impede hepatocarcinoma progression by disrupting mitochondrial metabolism.Journal of translational medicine · 2026Article
- Disulfidptosis and its molecular mechanisms in cancer: mechanisms, regulation, and therapeutic potential.Medical oncology (Northwood, London, England) · 2026Review
- Magnesium Ions Promote the Apoptosis of Cervical Cancer Cells through the PI3K/AKT/FoxO1 Pathway.Biological trace element research · 2026Article
- Dual Targeting Strategies in Cancer: Carbonic Anhydrase IX Inhibitors Targeting EGFR or VEGFR-2.Molecules (Basel, Switzerland) · 2026Review
- Radionuclide-labeled oxygen-self-supplying calcium reservoir for high-efficiency radioimmunotherapy via synergistic pyroptosis activation and PD-L1 downregulation.Journal of nanobiotechnology · 2026Article
- Araticum (Annona crassiflora) seed extract as a chemopreventive agent against prostate cancer: activation of extrinsic and intrinsic apoptotic pathways in a preclinical model.Journal of molecular histology · 2026Article
- TRAIL-R2 in the shadows: Epigenetic silencing and clinical implications in breast cancer.Oncotarget · 2026Article
- Synergistic apoptotic and epithelial-mesenchymal transition-inhibitory effects ofVeterinary world · 2026Article
- Design, Synthesis, and Anticancer Evaluation of Febuxostat-Based Triazolyl Derivatives.Archiv der Pharmazie · 2026Article
190 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
No grant is acknowledged in the PubMed record.
Abstract
Cancer growth represents a dysregulated imbalance between cell gain and cell loss, where the rate of proliferating mutant tumour cells exceeds the rate of those that die. Apoptosis, the most renowned form of programmed cell death, operates as a key physiological mechanism that limits cell population expansion, either to maintain tissue homeostasis or to remove potentially harmful cells, such as those that have sustained DNA damage. Paradoxically, high-grade cancers are generally associated with high constitutive levels of apoptosis. In cancer, cell-autonomous apoptosis constitutes a common tumour suppressor mechanism, a property which is exploited in cancer therapy. By contrast, limited apoptosis in the tumour-cell population also has the potential to promote cell survival and resistance to therapy by conditioning the tumour microenvironment (TME)-including phagocytes and viable tumour cells-and engendering pro-oncogenic effects. Notably, the constitutive apoptosis-mediated activation of cells of the innate immune system can help orchestrate a pro-oncogenic TME and may also effect evasion of cancer treatment. Here, we present an overview of the implications of cell death programmes in tumour biology, with particular focus on apoptosis as a process with "double-edged" consequences: on the one hand, being tumour suppressive through deletion of malignant or pre-malignant cells, while, on the other, being tumour progressive through stimulation of reparatory and regenerative responses in the TME.
Indexed as
Identifiers
What Socratic 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 Socratic graph.