ArticleVox sanguinis2026
A novel FUT1 variant, c.[35C>T;133_136dupCGCC], underlies a group A para-Bombay phenotype in a Chinese blood donor.
Article in Vox sanguinis, 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
BACKGROUND AND
objectivesThe para-Bombay phenotype is characterized by H antigen deficiency and the natural production of antibody against the I and H antigens (anti-IH), some of which are occasionally clinically significant. It genetically results from the presence of two non-functional FUT1 alleles coupled with at least one functional FUT2 allele. We present the serological and molecular characterization of a para-Bombay phenotype case, which led to the identification of a novel FUT1 allele. MATERIALS AND
methodsA sample from a blood donor was identified as a result of a discrepancy between forward and reverse typing. This sample subsequently underwent serological typing for A, B and H antigens in accordance with the American Association of Blood Banks Technical Manual. Furthermore, Sanger sequencing and nanopore sequencing were employed to analyse the ABO, FUT1 and FUT2 genes.
resultsThe donor was found to have an H-deficient phenotype and the presence of anti-IH. Sanger sequencing identified an ABO*A1.01/ABO*O.01.02 genotype. Nanopore sequencing showed a compound heterozygous state in FUT1, represented by the FUT1*01W.09 allele and a novel FUT1 allele carrying the c.[35C>T;133_136dupCGCC] variant. The FUT2 genotype was determined as FUT2*01/FUT2*01W.02.01.
conclusionThis study identifies a novel FUT1 allele characterized by the c.[35C>T;133_136dupCGCC] variant that impairs H antigen expression on red blood cells, thereby contributing to the understanding of FUT1 allele diversity.
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.