SynthesisBMC cancer2026
PDCD1 gene polymorphisms linked with altered risk of female-specific hormone-dependent cancers: a systematic review and meta-analysis.
Synthesis in BMC cancer, 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
backgroundThe programmed cell death-1 (PDCD1) gene plays a critical role in immune regulation and tumor immune evasion, making it a key target in cancer immunotherapy. Genetic variants in PDCD1, including rs2227981, rs2227982, rs7421861, and rs11568821, may influence susceptibility to female-specific cancers. This systematic review and meta-analysis aimed to evaluate the association of these variants with the risk of breast, cervical, ovarian, and endometrial cancers across ethnic populations.
methodsA systematic literature search was conducted in PubMed, Scopus, Web of Science, and Google Scholar for studies published up to January 2025. Eligible studies were case-control in design and reported genotypic or allelic frequencies. Risk of bias was assessed using the Newcastle-Ottawa Scale. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated under dominant, recessive, and allelic genetic models. Heterogeneity was evaluated using the I² statistic. Publication bias was assessed using funnel plots, Egger's test, and Begg's test. Sensitivity analyses were performed to evaluate the robustness of the results.
resultsEleven case-control studies were included, comprising 3534 breast cancer, 1468 cervical cancer, 1160 ovarian cancer, and 873 endometrial cancer cases, each with corresponding controls. The rs2227981 C allele and rs2227982 T allele were significantly associated with increased risk of female-specific cancers (p < 0.0001). Similarly, rs7421861 and rs11568821 showed significant associations across multiple genetic models. Heterogeneity ranged from low to high (I² = 19.5%-84%). No significant publication bias was detected (Egger's test p = 0.586; Begg's test p = 0.548). However, variability between studies and limited sample sizes should be considered when interpreting the findings.
conclusionsPDCD1 gene polymorphisms are associated with susceptibility to female-specific cancers, underscoring the importance of genetic variability in immune regulation and oncogenesis. Further large-scale and functional studies are needed to validate these findings and to explore gene-environment interactions.
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.