Nasopharyngeal carcinomas frequently lack the p16/MTS1 tumor suppressor protein but consistently express the retinoblastoma gene product.
The p16/MTS1 gene is altered by deletion, mutation, or hypermethylation in a wide variety of human cancers. As a result of deficient p16 protein, these cancers lack a critical mechanism for halting G1/S cell cycle progression. In the current study, 59 cases of nasopharyngeal carcinoma were evaluated for expression of the p16 tumor suppressor protein by immunohistochemical analysis of paraffin-embedded tissue. There was no detectable p16 in 38/59 cases (64%), which implies a very high rate of p16 inactivation in this type of cancer. On the other hand, the retinoblastoma gene product, which also regulates the G1 to S phase transition of the cell cycle, was consistently expressed in nasopharyngeal carcinomas by immunohistochemical analysis. These results implicate p16 inactivation but not Rb alteration in the stepwise progression of nasopharyngeal carcinogenesis.
Gulley
M L
ML
Department of Pathology, University of Texas Health Science Center at San Antonio and The Audie L. Murphy Memorial Veteran's Hospital, 78284-7750, USA. gulleym@uthscsa.edu
Nicholls
J M
JM
Schneider
B G
BG
Amin
M B
MB
Ro
J Y
JY
Geradts
J
J
D002294:Carcinoma, Squamous Cell / Q000378:metabolism*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism*; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D009303:Nasopharyngeal Neoplasms / Q000378:metabolism*; D012367:RNA, Viral / Q000378:metabolism; D016160:Retinoblastoma Protein / Q000378:metabolism*; D012189:Retrospective Studies; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D019941:Cyclin-Dependent Kinase Inhibitor p16; C099537:Epstein-Barr virus encoded RNA 1; D012367:RNA, Viral; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53