ReviewJournal of oral biology and craniofacial research
Targeting compensatory proliferation signals in oral cancer.
Review in Journal of oral biology and craniofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
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 is an orchestrated phenomenon that regulates cell populations in physiological and pathological conditions. Carcinogenesis involves a state of disequilibrium between cell proliferation and cell death. The resistance to conventional therapeutic modalities of cancer, including surgery, radiotherapy, and chemotherapy, can be explained by the compensatory repair and regeneration that occurs in the tumor microenvironment following apoptosis through the apoptotic compensatory proliferation signaling microvesicles (ACPSVs) or apoptotic extracellular microvesicles (ApoEVs). These microvesicles provide proliferative signals and act as mutagens, triggering cell proliferation, angiogenesis, immune evasion, metastasis, and invasion. This review discusses the phenomenon of apoptosis-induced proliferation and the role of ApoEVs in establishing an oncoregenerative niche, resulting in therapeutic resistance and recurrence of malignancies.
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.