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ABO Blood-group Antigens in Oral Cancer

Department of Oral Diagnostics, School of Dentistry, University of Copenhagen, Nørre Alle 20, DK-2200 Copenhagen N, Denmark;

View larger version (10K): [in a new window]   Figure 1. The ABH determinants are composed of L-fucose, D-galactose, and D-N-acetylgalactosamine, with a minimal determinant structure and the synthetic pathway as described in the text (Yamamoto et al., 1990).

View larger version (20K): [in a new window]   Figure 2. Genotyping by diagnostic restriction enzyme digestion. The single-based deletion associated with O alleles (position 258) creates a Kpnl site (O allele) and eliminates the BstEII site (A/B allele). Three or 4 nucleotide substitutions between A and B allelic cDNA can also be identified by diagnostic enzymes. For genotyping, polymerase chain-reaction (PCR)-amplified DNA was analyzed by diagnostic enzyme digestion (Yamamoto et al., 1990).

View larger version (117K): [in a new window]   Figure 3. Blood group AB patient. (A) A antigen staining is strong in normal epithelium (Nor), but absent in dysplastic (Dys) and in tumor (Tum) tissue. (B,C) Antigen B staining is weak in normal, but positive in dysplastic epithelium. (D) Three-day wound stained with antibodies to blood-group antigen A precursor (Ley). The outgrowth of the epithelium shows loss of A and B antigens and up-regulation of the precursor Ley (see also Fig. 5). (E,F) Oral carcinoma from a blood-group AO person. A antigen staining is positive in a part of the tumor (E) and in normal epithelium (not shown), but negative in the remaining part of the tumor (F). (G) Agarose gel of the ABO gene-specific products in the above AO person. Lanes 1, 4, 7, and 10 show undigested PCR products; lanes 2, 5, 8, and 11 show Kpn I digested, revealing O allele; lanes 3, 6, 9, and 12 show BstE II digested, revealing A allele. Blood-group type O control and a negative control are included. In the normal epithelium, both A and O alleles are present; the positive-stained tumor (Tumor+) shows O allele loss, whereas the negative-stained tumor (Tumor-) shows A allele loss.

View larger version (12K): [in a new window]   Figure 4. Examples of methylation status of the genes at chromosome 9q33-34. (A) MS-PCR (methylation-specific PCR) shows the hypermethylation status of ABO, TSC1, DAPK1, and DBCCR1, all of which are located at chromosome 9q33-34 in 2 tumor samples (T1 and T2). M, methylated allele; U, unmethylated allele. For both the DAPK1 and DBCCR1, hypermethylation occurs at the same time as hypermethylation of the ABO gene promoter. There is no hypermethylation of the TSC1 gene promoter, which is close to the ABO gene. (B) Methylation-specific melting curve analysis (MS-MCA) of a tumor and normal adjacent tissue. The curve pattern of the tumor demonstrates that, in the tumor, both methylated and unmethylated alleles are found; in normal epithelium, only an unmethylated allele is present.

View larger version (12K): [in a new window]   Figure 5. The synthetic pathway of Ley involves the formation of H from a precursor by the action of 1-2 fucosyltransferase and then the transformation of this structure to Ley by the action of 1-3 fucosyltransferase.