Surprisingly, with increased Gb4 availability, the original human AT with the methionine residue at codon 69 was also demonstrated to synthesize FORS1, providing another molecular mechanism of FORS1 appearance in cancer of ordinary FORS1-negative individuals.
In addition to a shift from high sialylation in the cancer area towards blood group ABO in the normal area, we also detected that the LacdiNAc epitope (N,N'-diacetyllactosamine) was significantly decreased in cancer samples.
Several studies have reported a link between the distribution of ABO blood group antigens and a risk of developing specific types of cancer, although no consensus has been reached.
Several studies have evaluated the association between ABO blood group and the prognosis of various types of cancer; however, little is known about the relationship between ABO blood group and esophageal squamous cell carcinoma (SCC).
We evaluated the effect of H. pylori infection status incorporated with H. pylori eradication history and ABO genotype on GC development according to cancer location and histologic type.
We found no association between ABO blood type and risk of aggressive prostate cancer (Type A: OR = 0.97, 95%CI = 0.87-1.08; Type B: OR = 0.92, 95%CI =n0.77-1.09; Type AB: OR = 1.25, 95%CI = 0.98-1.59, compared to Type O, respectively).
Associations between ABO blood groups and risk of several malignancies have been reported, although there are limited data regarding hepatocellular carcinoma (HCC).
Recently, one single nucleotide polymorphism (SNP) rs505922 in ABO gene has been implicated in susceptibility to pancreatic cancer across different populations, but different results were found in other types of cancer.
ABO blood type has been associated with risk and survival for several malignancies; however, data for an association with breast cancer are inconsistent.
It is noteworthy that 2 recent genome-wide association studies of pancreatic cancer have reported that variants in ABO blood type and in 3 other chromosomal regions are associated with risk for this cancer, thus providing new insight into pancreatic cancer etiology.
To explain the molecular basis of how the ABO genes are controlled in cell type-specific expression, during normal cell differentiation, and in cancer cells with invasive and metastatic potential that lack A/B antigens, it is essential to understand the regulatory mechanism of ABO gene transcription.
Deletion of A-antigen in a human cancer cell line is associated with reduced promoter activity of CBF/NF-Y binding region, and possibly with enhanced DNA methylation of A transferase promoter.
In an attempt to verify the ABO mRNA expression in hemopoietic precursor cells, mRNAs were isolated from human chronic myeloid leukemia (CML) cell lines which are believed to be at the most immature level of hemopoietic differentiation among hemopoietic malignancies.