ABO blood groups and pancreatic cancer risk and survival: Results from the PANcreatic Disease ReseArch (PANDoRA) consortium

Abstract

Abstract. There is strong epidemiologic evidence indicating that common genetic variability could be implicated in pancreatic cancer risk and, to date, various loci have been proposed. In particular, there is increasing evidence of the involvement of ABO gene variability and pancreatic cancer risk. In a large multicentric study of 1,028 pancreatic ductal adenocarcinoma cases and 2,257 controls in the context of the PANcreatic Disease ReseArch (PANDoRA) consortium, we investigated the suggested association with increased risk for carriers of single nucleotide polymorphisms (SNPs) determining the A or B allele in comparison with the O allele, which encodes for a non-functional enzyme. Since glycosyltransferase activity, encoded by ABO, is higher for the A1 variant compared with the A2 variant, we investigated the hypothesis that A1 carriers were at an increased risk of pancreatic cancer. In our analysis, carriers of the A1 were indeed at greater risk of developing the disease. In addition, we investigated the possible influence that genetic variability at the ABO locus may have in pancreatic cancer survival, but we observed no effect in our population.

ABO blood types and cancer risk—A cohort study of 339,432 subjects in Taiwan

“…These findings, however, differ from results in a recent European consortium study [30] and a large population-based case-control study in Shanghai, China [27]. Assessing ABO blood type based on genotype, these studies found an increased risk of pancreatic cancer associated only with blood type A, and not type B or AB, when compared with type O.…”

Blood type, ABO genetic variants, and ovarian cancer survival

“…Common variants result in different glycosyltransferases, oligosaccharide antigens, and phenotypes: N-acetylgalactosamine for blood type A, D-galactose for blood type B, both for blood type AB, and neither for an unmodified H antigen in blood type O. Blood type A and B differ predominantly by four amino acid substitutions (R176G, G235S, L266M, and G268A) from four common missense variants (rs7853989, rs8176743, r8176746, and rs8176747), while blood type O is predominantly due to a single nucleotide deletion (rs8176719) which shifts the reading frame and results in early protein termination [2–6]. In addition, multiple alleles, new mutations, and frequent recombination events add complexity to the genetic diversity of the ABO locus [3,4].…”

Evolutionary aspects of ABO blood group in humans

“…In the Nurses' Health Study and Health Professionals Follow-up Study, Wolpin and colleagues [37] found that participants with blood groups A, AB or B were more likely to develop pancreatic cancer compared to those with blood group O (adjusted hazard ratio [aHR] 1.44; 95% CI: 1.14-1.82). Further studies confirmed the protective effect of O group and showed that the A1 allele (which is responsible for an increased glycosyltransferase activity) confers a greater risk of pancreatic cancer than the A2 allele [38]. As regards gastric cancer, the higher prevalence of blood group A in patients with carcinoma of the stomach historically observed by several studies [36] has been recently confirmed in a large prospective population-based study involving more than one million of Scandinavian blood donors, who were followed for up to 35 years (OR 1.20; 95% CI: 1.02-1.42) [39].…”