ReviewCell communication and signaling : CCS2026
Molecular switches in cell death: the interplay of apoptosis and pyroptosis in cancer.
Review in Cell communication and signaling : CCS, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death in cancer encompasses apoptosis, pyroptosis, necroptosis, ferroptosis, autophagy-dependent cell death and other interconnected programs. Within this broader landscape, apoptosis and pyroptosis are especially important because the same upstream anticancer pressure can generate different biological outputs: non-lytic apoptotic clearance, gasdermin-mediated lytic inflammation, or mixed death phenotypes. Rather than cataloguing these pathways as separate descriptions, this review integrates them as a cancer-specific switching network. It organizes the evidence around a sequence of determinants: the initiating tumor stress, the active caspase repertoire, the availability and cleavage site of gasdermin substrates, the cellular compartment in which death occurs, and the resulting immune or inflammatory output. The review discusses caspase-3-mediated cleavage of gasdermin E (GSDME), caspase-8-mediated regulation or cleavage of GSDMD and GSDMC, canonical and noncanonical inflammasome signaling, cFLIP, granzyme-mediated gasdermin cleavage, and autophagy-dependent removal of inflammasome stimuli. It distinguishes mechanisms shown in infection or myeloid-cell models from evidence demonstrated in tumor cells or tumor microenvironment models. This framework highlights when pyroptosis may overcome apoptotic resistance and enhance antitumor immunity, and when excessive or poorly localized pyroptosis may promote tissue injury, immune suppression or chronic tumor-supportive inflammation. A mechanistic, cancer-specific interpretation of apoptosis-pyroptosis crosstalk may support biomarker-guided therapeutic strategies that exploit immunogenic tumor-cell death while limiting inflammatory toxicity.
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.