ReviewCells2026
ASK1 in Cancer Cell Death: Insights from In Vitro and In Vivo Studies.
Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase (MAP3K) involved in stress-induced apoptosis. Increasing evidence indicates that ASK1 activation contributes to the anticancer activity of numerous compounds, particularly those that induce oxidative or endoplasmic reticulum stress. This review summarizes studies demonstrating ASK1-dependent apoptosis in models of lung, breast and gynecologic, or gastrointestinal cancers following treatment with natural products, phytochemicals, and synthetic agents, focusing on mechanistic evidence linking ASK1 to downstream activation of the JNK and p38 MAPK pathways, mitochondrial dysfunction, and caspase-dependent cell death. Studies were selected based on direct experimental validation of ASK1 activation and involvement in the observed anticancer effects. Overall, this review supports ASK1 as a promising molecular target for the development of novel cancer treatment strategies.
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.