IBR   13079
INSTITUTO DE BIOLOGIA MOLECULAR Y CELULAR DE ROSARIO
Unidad Ejecutora - UE
artículos
Título:
DLG1 polarity protein expression associates with the disease progress of low-grade cervical intraepithelial lesions
Autor/es:
BUGNON VALDANO, MARINA; DI GREGORIO, ALEJANDRA; BOTTAI, HEBE; CABRAL, MARIELA; GARDIOL, DANIELA; NOCITO, ANA LIA; BUGNON VALDANO, MARINA; DI GREGORIO, ALEJANDRA; BOTTAI, HEBE; CABRAL, MARIELA; GARDIOL, DANIELA; CAVATORTA, ANA LAURA; NOCITO, ANA LIA; MARZIALI, FEDERICO; CITTADINI, JORGE; CAVATORTA, ANA LAURA; MARZIALI, FEDERICO; CITTADINI, JORGE
Revista:
EXPERIMENTAL AND MOLECULAR PATHOLOGY.
Editorial:
ACADEMIC PRESS INC ELSEVIER SCIENCE
Referencias:
Lugar: Amsterdam; Año: 2017 vol. 102 p. 65 - 69
ISSN:
0014-4800
Resumen:
Human Discs large tumour suppressor (DLG1) participates in regulating cell polarity and proliferation, suggesting an important connection between epithelial organization and cellular growth control. However, it was demonstrated that DLG1 could acquire oncogenic attributes in some specific contexts. In this work, we evaluated the expression of DLG1 and its contribution to the progress of cervical lesions in order to investigate a potential role of this polarity protein in human oncogenic processes. We analyzed cervical biopsies from women with low-grade squamous intraepithelial lesion (LSIL) diagnosis (n = 30), for DLG1 expression by immunohistochemistry. These results were correlated with the clinical monitoring of the patients during a 24-month follow-up period. Our data indicate that while all LSIL patients with a DLG1 staining pattern similar to normal tissues are significantly more likely to regress (n = 23, Pattern I), all LSIL biopsy specimens showing a diffuse and intense DLG1 staining likely progress to high-grade lesions (n = 4, Pattern II). Finally, all persistent LSIL analyzed showed an undetermined DLG1 staining, with a diffuse distribution without a strong intensity (n = 3, Pattern III). We found a significant association between the expression pattern of DLG1 and the evolution of the lesion (p