ArticleFunctional & integrative genomics2026
A cross-ancestry genetic atlas of shared susceptibility between infectious diseases and cancer.
Article in Functional & integrative genomics, 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
5 authors.
Funding
Abstract
Extensive epidemiological and mechanistic studies have established links between specific infections and cancer, but the inherited host-genetic contribution to broader infection-cancer relationships remains incompletely characterized. Here, we integrated genome-wide association study summary statistics for multiple infectious diseases and cancers from European- and East Asian-ancestry populations and evaluated shared host genetic architecture across genome-wide and local genetic sharing, tissue- and cell-type enrichment, cross-trait locus discovery, functional gene prioritization, proteome-level integration and exploratory bidirectional Mendelian randomization. In the European ancestry analyses, four complementary genome-wide approaches identified 11, 21, 44 and 11 significant infection-cancer trait pairs, respectively; 11 pairs were supported by at least three approaches, and sepsis-lung cancer, pneumonia-kidney cancer and sepsis-colorectal cancer were supported by all four. In the East Asian-ancestry analyses, tuberculosis-lung cancer showed the most prominent regional shared genetic architecture. Local analyses further showed that genetic overlap was not uniformly distributed across the genome, but was concentrated in specific regions with heterogeneous directions of effect. Tissue- and cell-type enrichment analyses indicated that shared signals were primarily concentrated in mucosal and epithelial barrier-related tissues and immune-cell compartments. Cross-trait analyses identified 396 potential pleiotropic independent risk loci, 14 colocalized variants, and 86 high-confidence pleiotropic genes, while proteome-level analysis identified 83 pleiotropic proteins, including MORF4L1, which was associated with five trait pairs. Exploratory Mendelian randomization provided directional genetic-liability evidence, with the strongest European-ancestry signal linking lung cancer liability to sepsis. Together, these findings support a shared host-genetic component underlying part of the relationship between infections and cancers, involving immune regulation, barrier homeostasis and cellular stress adaptation.
Indexed as
Identifiers
42439983What 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.