ArticleCancer cell international2024
Pathogenic nsSNPs of protein kinase C-eta with hepatocellular carcinoma susceptibility.
Article in Cancer cell international, 2024. 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
backgroundHepatocellular carcinoma (HCC) is a global health concern. Due to late diagnosis and limited therapeutic strategies, HCC based mortality rate is exponentially increasing globally. Genetic predisposition is a non-avoidable intrinsic factor that could alter the genome sequence, ultimately leading to HCC. Protein kinase C eta (PKCη) is involved in key physiological roles, hence alteration in PKCη could aid in cancer progression. Research indicates association between non-synonymous (ns) SNPs and HCC onset. However, effect of nsSNP variants of PKCη on HCC development has not been explored yet. Hence, this study aimed to investigate the association between pathogenic nsSNPs of PKCη with HCC.
methodsNon-synonymous (missense) variants of PKCη were obtained from Ensembl genome browser. These variants were filtered out to obtain pathogenic nsSNPs of PKCη. Genotyping of nsSNPs was done through Tetra ARMS PCR. For that, blood samples of 348 HCC patients and 337 controls were collected. The clinical factors that influence HCC were studied. Relative risk (RR) and Odds Ratio (OR) with 95% confidence interval was calculated by Chi-square test and P-value < 0.05 was deemed significant.
resultsFive nsSNP variants of PKCη including rs1162102190 (T/C), rs868127012 (G/T), rs750830348 (G/T), rs768619375 (T/C), and rs752329416 (T/C) were identified. The retrieved nsSNPs were frequently identified in HCC patients. However, rs752329416 T/C was significantly prevalent in patients having HCC family history. Moreover, all the variants were found in HCC patients manifesting the stage II than the advance stages of HCC.
conclusionThis study can be utilized to identify potential genetic markers for early screening of HCC. Moreover, consideration of further clinical factors, and mechanistic approach would enhance the understanding that how alteration in nsSNPs could impact the HCC onset.
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.