ArticleeLife2017
Tumor-promoting function of apoptotic caspases by an amplification loop involving ROS, macrophages and JNK in
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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
62 citing papers in PubMed, 100 citations in OpenAlex.
- Macrophage restriction inScience advances · 2026Article
- Electron transport chain complex I and mitochondrial fusion regulate ROS for differentiation in Drosophila neural stem cells.Stem cell reports · 2026Article
- Systemic Propagation of STING Signalling via Generation of Large Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- Fatty acid synthesis supports tumor progression through facilitating the activity of TORC1 signaling.Cell death & disease · 2026Article
- Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.Cell communication and signaling : CCS · 2026Review
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- Single-cell RNA analysis reveals unexpected hemocyte plasticity and immune cell specialization in abioRxiv : the preprint server for biology · 2026Article
- 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
- Medicine on the menu: When illness informs appetite.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hemocytes facilitate interclonal cooperation-induced tumor malignancy by hijacking the innate immune system in Drosophila.The EMBO journal · 2025Article
- PINK1 functions in mitophagy and mitochondrial homeostasis during mice oocyte maturation.Cell & bioscience · 2025Article
- Decoding the divide: what distinguishes apoptosis-induced proliferation from compensatory proliferation?Cell communication and signaling : CCS · 2025Review
- Epithelial cell competition is promoted by signaling from immune cells.Nature communications · 2025Article
- Messages from Beyond the Grave: How Can Drosophila Help Us Understand the Consequences of Apoptosis?Advances in experimental medicine and biology · 2025Review
- Article
- Review
- Xeroderma pigmentosum protein XPD controls caspase-mediated stress responses.Nature communications · 2024Article
- Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration.The EMBO journal · 2024Article
- Article
2 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 at 1 institution in 1 country.
Funding
Abstract
Apoptosis and its molecular mediators, the caspases, have long been regarded as tumor suppressors and one hallmark of cancer is 'Evading Apoptosis'. However, recent work has suggested that apoptotic caspases can also promote proliferation and tumor growth under certain conditions. How caspases promote proliferation and how cells are protected from the potentially harmful action of apoptotic caspases is largely unknown. Here, we show that although caspases are activated in a well-studied neoplastic tumor model in
Indexed as
Identifiers
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.