ReviewCell communication and signaling : CCS2026
Sex differences in non-reproductive cancers: mechanistic roles of sex-hormone signaling.
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
8 authors.
Funding
Abstract
Sex differences in the incidence and outcomes of non-reproductive cancers persist across many tumor types, even after adjustment for major exposure- and care-related factors. This review examines how sex-hormone signaling may contribute to these patterns through tumor-intrinsic mechanisms and regulation of the tumor microenvironment. In tumor cells, ER, AR and PR mediate classical nuclear transcriptional programs, whereas membrane-associated or cytoplasmic receptor pools, together with GPER, support rapid non-genomic signaling through PI3K/AKT, MAPK/ERK and related kinase or second-messenger pathways. Intratumoral steroid handling can create local ligand conditions that differ from circulating hormone levels and modify context-specific receptor activity. Hormonal context may also influence vascular, stromal and immune phenotypes. Clinically, sex-hormone-related tumor states may be better captured by integrated activity-based readouts, including receptor status, pathway activation, local steroid availability and immune context, rather than receptor immunostaining alone. Overall, sex-hormone signaling offers a hypothesis-generating framework for understanding sex-biased tumor biology beyond traditional hormone-driven cancers, but its clinical relevance requires further mechanistic and prospective validation.
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.