ReviewCold Spring Harbor perspectives in biology2012
The role of apoptosis-induced proliferation for regeneration and cancer.
Review in Cold Spring Harbor perspectives in biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 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
146 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Loss of alanine-glyoxylate and serine-pyruvate aminotransferase expression accelerated the progression of hepatocellular carcinoma and predicted poor prognosis.Journal of translational medicine · 2019Pooled it
- First structural Elucidation of Bcl-2 functional conversion induced by validated modulators using microsecond-scale molecular dynamics simulations and density functional theory.Molecular diversity · 2026Article
- The paradigm-shifting roles of caspase-3 in cancer: from death towards resuscitation.Cancer cell international · 2026Review
- Radionuclide-stimulated dynamic therapy induces complementary immunogenic necroptosis and apoptosis cancer cell death pathways.Communications biology · 2026Article
- Calcium signaling regulates apoptosis-induced proliferation in Drosophila.PLoS biology · 2026Article
- Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Whole body regeneration deploys a rewired embryonic gene regulatory network logic.Nature communications · 2025Article
- Apoptosis-resistant cells drive compensatory proliferation via cell-autonomous and non-autonomous functions of the initiator caspase Dronc.Nature communications · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Article
- Effects of Microplastics and Nanoplastics Exposure on Neurogenesis: Are Thymidine Analogs a Good Option to Study Such Effects?International journal of molecular sciences · 2025Review
- Targeting Cancer Cell Fate: Apoptosis, Autophagy, and Gold Nanoparticles in Treatment Strategies.Current issues in molecular biology · 2025Review
- Remote ischemia precondition protects against renal IRI through apoptosis associated vesicles carrying MIF protein via modulating DUSP6/JNK signaling axis.Journal of nanobiotechnology · 2025Article
- Spatiotemporal control of cell ablation using Ronidazole with Nitroreductase in Drosophila.Developmental biology · 2025Article
- Article
- Curcumin-Loaded Maltodextrin-Based Proniosomes Potentially Effective against Gemcitabine-Resistant Cholangiocarcinoma.ACS applied bio materials · 2025Article
- Modeling of chemo-radiotherapy targeting growing vascular tumors: A continuum-level approach.PloS one · 2025Article
- Functions ofFrontiers in cell and developmental biology · 2025Review
- Tailored Extracellular Vesicles from Dental Stem Cells: Advances in Specific Modifications for Enhanced Therapeutic Applications.International journal of nanomedicine · 2025Review
- Regeneration following tissue necrosis is mediated by non-apoptotic caspase activity.bioRxiv : the preprint server for biology · 2024Article
86 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.
Funding
Abstract
Genes dedicated to killing cells must have evolved because of their positive effects on organismal survival. Positive functions of apoptotic genes have been well established in a large number of biological contexts, including their role in eliminating damaged and potentially cancerous cells. More recently, evidence has suggested that proapoptotic proteins-mostly caspases-can induce proliferation of neighboring surviving cells to replace dying cells. This process, that we will refer to as "apoptosis-induced proliferation," may be critical for stem cell activity and tissue regeneration. Depending on the caspases involved, at least two distinct types of apoptosis-induced proliferation can be distinguished. One of these types have been studied using a model in which cells have initiated cell death, but are prevented from executing it because of effector caspase inhibition, thereby generating "undead" cells that emit persistent mitogen signaling and overgrowth. Such conditions are likely to contribute to certain forms of cancer. In this review, we summarize the current knowledge of apoptosis-induced proliferation and discuss its relevance for tissue regeneration and cancer.
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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.