Mutant p63 has been found in a wide variety of human ndignaneiea including carcinomas of the lung, breast and colon. Beoaum of the controvermial mutational rate of the pS3 gene in hepatocellular carcinoma, a large series of liver tumors from white patients with different riek factors w a ~ examined immunohistochdcally for expramion of the pS3 mutant to asee%e its prevalence and the relationehipa betwwn p63 overexpdon and clinicopathological data. Nine of 68 epecimene were found to have detectable evidence of pSS gene mutation by virtue of the immunohistochemical detection of mutant pS3 protein. The p63 mutation waa more frequent in @enta with serological hepatitis B and C markers than in patienta without these markers (p = 0.046).
The prevalence of pS3-poeitive tumors was also aignificantly higher in the group of tumors with invaded portal branchthan in the group without (p = 0.02). Our d t s showed that p63-positive hepatowllular carcinoma ie a rare findinn in patients exposed to a low dietary aflatoxin intake and that pS3 mutation seem8 to occur at a late &age of the tumoral procees and could contribute to an aggredve tumoral phenotype. (HEpAT0UK;y 1992;161171-1175.)
TP53 is a tumor-suppressor gene located on the short arm of chromosome 17 (1). Its coded product is a 53-kD nuclear phosphoprotein with probable cell cycleregulatory function and a putative nuclear transcription activity. Understanding of its role or interactions at the molecular level is still incomplete (2). It has been shown that the p53 gene frequently acquires mutations during the development of most malignancies (3). Current data indicate that approximately half of the cancers of the lung (4-71, colon (8-101, breast (11, 121, esophagus (13) and skin ( 14) in adults contain p53 gene mutation. It has been suggested that the loss of wild-type function may