ArticleDiscover oncology2026
Mendelian randomization analysis of PKD1 in endometrial cancer and comparative multi-cancer study with renal cell carcinoma.
Article in Discover oncology, 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
Abstract
backgroundPolycystic kidney disease 1 (PKD1) has emerged as a potential oncogene in various malignancies, but its causal relationship with endometrial cancer risk and clinical outcomes remains unclear. This study employed Mendelian randomization (MR) analysis to investigate the causal effects of gene expression on endometrial cancer susceptibility, with comparative analysis to renal cell carcinoma, focusing on PKD1’s functional role.
methodsWe conducted a comprehensive summary-data-based Mendelian randomization (SMR) analysis using expression quantitative trait loci (eQTL) from CAGE sparse tissue dataset as instrumental variables. The analysis examined 30 candidate genes for endometrial cancer and 29 genes for renal cancer risk using UK Biobank GWAS data. Cross-cancer comparative analysis identified shared susceptibility genes between both malignancies. PKD1’s role was further characterized through correlation network analysis, immune cell infiltration profiling, and Cox regression survival analysis in 553 endometrial cancer patients. Experimental validation was performed using qRT-PCR in representative cancer cell lines compared to normal controls.
resultsSMR analysis revealed modest but statistically significant causal effects for multiple genes on both cancer types (p_SMR < 0.05), with odds ratios clustering around 1.0. Comparative analysis between renal cancer (220 genes) and endometrial cancer (196 genes) identified only 12 shared susceptibility genes (2.8% overlap) including EP300, CKB, NME7, and TATDN3, highlighting distinct genetic architectures. PKD1 correlation network analysis in endometrial cancer demonstrated positive associations with PET100, AC093899.1, and PDE4DIPP1. Importantly, PKD1 expression levels significantly influenced tumor immune microenvironment composition, with PKD1-low endometrial tumors showing enhanced infiltration of myeloid dendritic cells, T helper cells, and Th1 cells (p < 0.05). However, Cox regression analysis revealed that PKD1 expression did not impact patient survival outcomes (HR = 1.020, 95% CI: 0.681–1.529, p = 0.923), while clinical stage and primary therapy outcome remained significant prognostic factors.
conclusionsThis multi-cancer Mendelian randomization study provides evidence for largely distinct genetic landscapes between renal and endometrial cancers, with minimal gene overlap. PKD1 demonstrates a novel dual role in endometrial cancer pathogenesis.
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.