Alterations in the expression of type 1 blood group-related antigens (Lewis a and b) were examined immunohistochemically in 371 consecutives gastric biopsy and 80 surgical specimens from patients of gastric carcinoma. The ABH and Lewis phenotype and secretor status of the patients were correlated with histologic findings. An anomalous expression of Lewis a antigen was found in 88 of 249 gastric biopsy specimens of Lewis (a-b+) phenotype patients. The prevalence of this anomaly increased with the evolution of the premalignant process, in agreement with the commonly accepted model of gastric carcinogenesis. Thus, anomalous Lewis a antigen appeared in 66.6% of gastric dysplasia cases, in 64.6% of intestinal metaplasia, in 15.4% of atrophic gastritis, and in 7.4% of superficial gastritis. No alterations were found in subjects with normal gastric mucosa. Fortyseven of the 49 Lewis (a-b+) phenotype gastric carcinoma patients showed antigenic alterations in tumor cells (anomalous Lewis a antigen in 36 and loss of Lewis antigens in 11). In 26 of these gastric specimens an anomalous Lewis a antigen was present in areas of intestinal metaplasia and/or dysplasia away from the area of neoplastic transformation. The expression of Lewis a antigen in Lewis (a-b+) phenotype patients is a frequent phenomenon in gastric neoplastic cells and could result from the blocked synthesis of Lewis b antigen with accumulation of its precursors. These findings suggest that, during gastric carcinogenesis, antigenic alterations may precede neoplastic transformation. An anomalous Lewis a antigen could constitute a significant index of severity of the histologic lesion and contribute to identifying high-risk individuals.

The distribution of the blood group-related antigens type 1 (Lewis(a) [Le(a)], Lewis(b) [Le(b)]) and type 2 (H type 2, Y) has been examined in histologically normal and malignant mucosa of 40 surgical specimens of patients with adenocarcinoma of the stomach, with the use of a panel of monoclonal antibodies. Patients' Lewis phenotype and secretor status are correlated to the authors' findings. The surface epithelium of normal pyloric and fundic mucosa expressed the Lewis isoantigen (Le(a) in Le[a+b-] phenotype and Le(b) in Le[a-b+] phenotype), whereas the deep areas of this mucosa no showed the Le(a), Le(b) antigens and expressed the Y and H type 2 antigens whatever the secretor status of patients. Nineteen of 24 patients with Le(a-b+) phenotype showed anomalous expression of Lea antigen in neoplastic cells. In three of them, this alteration was found in tumor adjacent mucosa. No expression of Le(a) or Le(b) antigens was found in tumors or normal mucosa from Le(a-b-) phenotype patients.

Forty biopsies from 36 patients with bladder tumors were tested for T-antigen (TAg) expression on tumor cells on sections untreated or treated with neuraminidase; a 37.5% of tumors showed abnormal expression of TAg either as an aberrant expression, or absence of this antigen after removing sialic acid. These changes were not well correlated with histologic signs of anaplasia or infiltration, nor with other biologic properties of tumor cells such as the expression of blood group antigens (ABH). However, a practical utility of TAg in the study of bladder tumors, is suggested by the analysis of those biopsies with low-grade low-stage tumors, on which the abnormal expression of TAg was more discriminatory than the ABH changes in defining those patients suffering tumors with a particular aggressiveness. Circulating antibody titer was also investigated in 20 patients but all of them displayed titers in the normal range, with independence of the results observed in their corresponding bladder biopsies.

Expression of type 1 and type 2 chain Lewis antigens was studied in 32 rectal adenocarcinoma specimens; the results were correlated with the patients’ Lewis phenotype and secretor status. In addition, the pattern of expression of these antigens was analyzed in adjacent and distant normal mucosa. We used an indirect immunofluorescence technique with p-phenylenediamine counterstaining (Oriol technique) and a panel of monoclonal antibodies directed against the different antigenic specificities. Normal distal colonic mucosa only expresses monofucosylated structures (Le^a and X) arising from activity of the α1–3,4-fucosyltransferase coded by the Le gene. Rectal adenocarcinomas also show Le^a and X, but also reexpress blood group antigens ABH and exhibit difucosylated determinants (Le^b and Y). The accumulation of mono- and difucosylated type 2 chain in neoplastic processes, independently of the Le and Se genes, could be due to the enzymes coded by reactivation of the H and X genes. Blood group antigens form a complex signal code, genetically regulated, which intervenes in differentiation, growth and cellular recognition processes, and which may undergo important modifications during malignant transformation. These alterations could be useful in the diagnosis and prognosis of some types of carcinoma.

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