ArticleBMC pediatrics2025
Causal links between congenital malformations, birth weight, and neuroblastoma: insights from Mendelian randomization.
Article in BMC pediatrics, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhile it is commonly observed that congenital malformations (CM), birth weight and neuroblastoma (NB) often co-occur clinically, there is a scarcity of studies investigating their relationship.
aimTo investigate the causal relationship between CM, birth weight and NB using two-sample mendelian randomization (MR) analysis.
methodsThis study utilized data from the Genome-Wide Association Studies (GWAS) database for CM, birth weight, and NB. We identified and analyzed single nucleotide polymorphisms (SNPs) related to CM from various organ systems, ensuring robust instrumental variables through linkage disequilibrium (LD) and F-statistic testing. SNPs were further validated in GWAS Catalog to exclude weak variables. We employed various MR methods including inverse variance weighted (IVW), MR-Egger regression, weighted median, simple mode and weighted mode to assess the causal relationships. Sensitivity analyses were performed using leave-one-out (LOO) and MR-PRESSO.
resultsThe analysis demonstrated a protective effect of genital organ CM, which were inversely associated with both overall neuroblastoma (OR = 0.71, 95% CI: 0.60-0.85, P = 0.001) and the 11q-deleted subtype (OR = 0.33, 95% CI: 0.13-0.85, P = 0.02). In contrast, urinary system,gallbladder, bile ducts, and liver were positively associated with neuroblastoma harbouring 11q deletion (OR = 2.37, 95% CI: 1.32-4.27, P = 0.01),(OR = 1.47, 95% CI: 1.17-1.84 P = 0.001) but not with NB overall.However, no significant associations were found between other CM types, birth weight, and NB, and no evidence of heterogeneity, horizontal pleiotropy, or outlier SNPs was identified.
conclusionGenital organ malformations confer protection against both overall and 11q-deleted neuroblastoma, whereas urinary system, gallbladder, biliary and liver malformations increase risk exclusively for 11q-deleted disease. However, due to the relaxed p-value threshold used for instrument selection, these findings should be interpreted cautiously and warrant replication with stricter criteria.
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.