A novel gene, termed p73, encodes a protein with a significant homolog
y to p53 and has been mapped at chromosome 1p36.3, which is a locus of
multiple suppressor genes for tumors including neuroblastoma and othe
r cancers. Since the 1p36 locus is reported to be deleted and p53 is f
requently mutated in esophageal carcinomas, we examined loss of hetero
zygosity (LOH) and mutation of the p73 gene in 48 untreated esophageal
tumors, as well as mRNA expression in 8 tumors. We screened the pi ge
nomic library to obtain a pi clone containing the p73 gene and found a
polymorphic short tandem CT repeat site at intron 9, Intragenic seque
nces for 14 PCR primer sets and a primer pair flanking the repeat were
also determined for the analysis of PCR single-strand conformation po
lymorphism (SSCP) and LOH studies, respectively, Expression of p73 mRN
A was detectable but at low levels in all 8 tumor tissues by reverse t
ranscriptase PCR, We did not find any type of mutation other than poly
morphisms in the 48 esophageal carcinomas, though aberration of the p5
3 gene on the PCR-SSCP gels was observed in 15 of 38 (39%) tumors of t
he same set. In addition, LOH for p73 was found in only 2 of 25 (8%) t
umors. These results suggest that, at least in esophageal carcinomas,
allelic loss or mutation of p73 may not be a main genetic event for th
e tumorigenesis as it is with P53. (C) 1998 Wiley-Liss, Inc.