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 hypermethylatio n in a wide variety of human cancers. As a result of deficient p16 pro tein, these cancers lack a critical mechanism for halting G1/S cell cy cle progression. In the current study, 59 cases of nasopharyngeal carc inoma were evaluated for expression of the p16 tumor suppressor protei n by immunohistochemical analysis of paraffin-embedded tissue. There w as no detectable p16 in 38/59 cases (64%), which implies a very high r ate of p16 inactivation in this type of cancer. On the other hand, the retinoblastoma gene product, which also regulates the G1 to S phase t ransition of the cell cycle, was consistently expressed in nasopharyng eal carcinomas by immunohistochemical analysis. These results implicat e p16 inactivation but not Rb alteration in the stepwise progression o f nasopharyngeal carcinogenesis.