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Pathol Int ; 49(8): 687-94, 1999 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-10504535

RESUMO

In basal cell nevus syndrome (BCNS) patients, mutations of a gene, patched (ptc), which encodes a putative signal transducer of sonic hedgehog protein (SHH), were found and are thought to be one of the major causes of BCNS. The SHH signaling pathway is an important developmental pathway, and ptc protein (PTC) is a suppressive component serving as a receptor for the secreted SHH. Another transmembrane protein, smoothened (SMO), forms a complex with PTC and regulates this signaling pathway. Recent transgenic studies have strengthened the importance of the SHH signaling system in the etiology of basal cell carcinoma (BCC). In this study, we examined the expression patterns of mRNA for ptc and smo in two different BCC subtypes and normal skin. We found that the expressions of ptc and smo mRNA were enhanced in the tumor nests of the nodular BCC, especially at the advancing portions, but were under the detectable level in the superficial BCC cases examined, indicating that ptc and smo mRNA expressions might be associated with BCC tumor progression and divide the BCC histologic types into two subtypes, superficial and nodular types. In addition, no obvious signals for ptc and smo mRNA were detected in the normal human epidermis, appendages, or seborrheic keratosis, indicating that the abnormal proliferation of follicular epithelial cells caused by ptc, smo and/or other genetic changes, which also cause ptc and smo overexpressions, might result in BCC tumor formation.


Assuntos
Carcinoma Basocelular/genética , Expressão Gênica , Proteínas de Membrana/genética , Proteínas/fisiologia , Receptores de Superfície Celular/genética , Receptores Acoplados a Proteínas G , Transdução de Sinais , Neoplasias Cutâneas/genética , Transativadores , Idoso , Idoso de 80 Anos ou mais , Proteínas Hedgehog , Humanos , Hibridização In Situ , Pessoa de Meia-Idade , Receptores Patched , Receptor Patched-1 , RNA Mensageiro/metabolismo , Receptor Smoothened
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