p73 gene, a new p53 homologue, has been identified: it supposedly acts as t
umour suppressor gene in neuroblastoma. To clarify whether p73 might be inv
olved in lung carcinogenesis, we examined p73 expression in resected lung c
ancer and paired normal lung in 60 cases using semi-quantitative reverse tr
anscription-polymerase chain reaction (RT-PCR). We also examined p73 gene s
tatus in three representative cases using Southern blot, and p53 gene alter
ation in 49 cases using PCR-single-strand conformation polymorphism (PCR-SS
CP) and direct sequence. In 87% of the cases (52/60) p73 expression in tumo
ur was more than twice as high as that in paired normal lung tissues, and t
he difference between p73 expression in tumour and normal lung tissue was s
ignificant (P < 0.0001). However, Southern blot analysis revealed that none
of the cases showed p73 gene amplification. Compared with clinicopathologi
cal characteristics, p73 expression correlates significantly with histologi
cal differences and age of patient, independently (P< 0.05). Concerning p53
gene status, 43% (21/49) showed p53 gene alteration, but there was no corr
elation between p73 overexpression and p53 gene alteration. Our results sug
gest that need for further functional analysis of the role of p73 in lung c
arcinogenesis.