INVESTIGADORES
COTORRUELO carlos miguel
artículos
Título:
Expression of the gene encoding secretor type galactoside 2 alfa fucosyltransferase (FUT2) and ABH antigens in patients with oral lesions
Autor/es:
CAMPI C; ESCOVICH L; MORENO A; RACCA L; RACCA A; COTORRUELO C; BIONDI C
Revista:
MEDICINA ORAL PATOLOGIA ORAL Y CIRUGIA BUCAL
Editorial:
MEDICINA ORAL S L
Referencias:
Año: 2012 vol. 17 p. 63 - 68
ISSN:
1698-4447
Resumen:
Objective: The aim of this work was to evaluate the expression of FUT2 gene in saliva and histo ABH antigens of patients with oral lesions. Study Design: In total 178 subjects were examined, half of whom suffered from oral pre-cancerous and cancerous lesions, while the other half were the healthy control group We analyzed the FUT 2 polymorphism by ASO-PCR (allele specific oligonucleotid ? polymerase chain reaction) with specific primers for G428 allele and the wild type allele of FUT2 gene. To reveal A, B and H antigens in tissue sections of the patients (n= 89) we used a modified specific red cell adherence technique. Results: We found a high intensity of oral disease in the non-secretor group (OR = 2.43). A total of 58% of the patients with oral pre-cancerous and cancerous lesions was non secretors (se_/_), in contrast with the healthy population (21.5%). A strongly positive reaction was defined as a sheet of indicator erythrocytes adhered to the epithelial cells. In 31 of the 54 samples analyzed the test showed slightly positive results on atypical areas, and there was a complete antigen deletion in areas affected by neoplasia. Nineteen samples showed a total absence of ABH antigens in both histologically normal and pathological areas. Blood group antigens were expressed at a high level in benign and highly differentiated malignant tumors. In poorly differentiated malignant tumors, they were mostly absent. Conclusion: Considering these results we suggest the use of this method to monitor probable preneoplastic lesions in risk population, especially in those with no secretor status (absence of FUT2 gene).