ArticleCancer cell international2025
Role of PRKCZ non-synonymous genetic variants in breast cancer development.
Article in Cancer cell international, 2025. 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon- synonymous single nucleotide polymorphisms (nsSNPs) impact disease onset and progression. Protein kinase C zeta (PRKCZ) is involved in oncological, neurological, and diabetes pathogenesis. The goal of the research presented here was to investigate the role of nsSNPs in PRKCZ in breast cancer (BC) pathogenesis.
methodsGenotyping analysis was performed to determine the association of PRKCZ genetic variants rs1236161858 (G/T), rs367917640 (G/A/C), rs202071893(A/G), and rs757469768(G/A) with BC risk and clinicopathological variables through Tetra-ARMS PCR.
resultsrs1236161858(G/T) was linked to higher BC risk in codominant (OR = 5.227, RR = 2.225), allele model, (OR = 4.701, and RR = 2.186) and log additive (OR = 2.564). rs367917640 (G/A) was associated with increased BC risk in codominant model (OR = 6.419, RR = 2.350), recessive model (OR = 12.09 and, RR = 4.772) and log additive (OR = 3.340). rs367917640(G/C) was linked to higher BC risk in dominant (OR = 4.892, RR = 2.208), recessive (OR = 1.859, RR = 1.34), over dominant (OR = 3.675, RR = 2.028) and log additive (1.579) models respectively. For rs202071893(A/G) codominant model (OR = 2.295 RR = 1.547), dominant model (OR = 5.943, and RR = 1.781) and over dominant model (OR = 3.433, and RR = 1.974) showed significantly higher BC association. rs757469768(G/A) was linked to higher BC risk in both dominant (OR = 0.1479, and RR = 0.4688) and over dominant (OR = 2.005, and RR = 1.455) models. However, rs757469768(G/A) was associated with reduced BC risk in log additive model (OR = 0.4956).rs1236161858 correlated with DCIS and IDC. rs367917640(G/A/C) correlated with early cancer stage, LCIS, DCIS, IDC, luminal A and post-menopause. rs202071893 was associated with HER2
conclusionAll five nsSNPs exhibited potential as predictive and prognostic biomarkers for BC. However, the current study findings should be validated by conducting research on large cohorts with representation from diverse population. Furthermore, biological mechanism by which these nsSNPs cause BC pathogenesis could be explored in future studies.
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.