SPONTANEOUS APOPTOSIS IN GALLBLADDER CARCINOMA - RELATIONSHIPS WITH CLINICOPATHOLOGICAL FACTORS, EXPRESSION OF E-CADHERIN, BCL-2 PROTOONCOGENE, AND P53 ONCOSUPPRESSOR GENE
E. Sasatomi et al., SPONTANEOUS APOPTOSIS IN GALLBLADDER CARCINOMA - RELATIONSHIPS WITH CLINICOPATHOLOGICAL FACTORS, EXPRESSION OF E-CADHERIN, BCL-2 PROTOONCOGENE, AND P53 ONCOSUPPRESSOR GENE, Cancer, 78(10), 1996, pp. 2101-2110
BACKGROUND. Although valuable information regarding spontaneous apopto
sis in various human cancers has recently been obtained, spontaneous a
poptosis in carcinoma of the gallbladder has not been studied. METHODS
. Apoptotic cells were visualized using the nick end labeling method i
n 49 cases of gallbladder carcinoma The relationships between frequenc
y of apoptosis, which was expressed as the maximal apoptotic index (MA
I), and clinicopathologic factors, immunoreactivity of E-cadherin (E-C
D), bcl-2 protooncogene, and p53 oncosuppressor gene were investigated
. RESULTS. MAI was significantly correlated with the maximum dimension
of the tumor (P = 0.020) and high T category (P = 0.034). A closer co
rrelation between high MAI and high T category was observed in E-CD po
sitive cases (P = 0.0035), whereas no such correlation was evident in
E-CD negative cases (P = 0.536). No relationship was observed between
MAI and age, sex, histology, grading, stromal volume, venous or lympha
tic permeation, and lymph node status. Overexpression of bcl-2 and p53
was observed in 18.4% (9 of 49) and 34.7% (17 of 49) of the cases, re
spectively, and there was a positive correlation between bcl-2 and p53
(P = 0.035). No notable relationship was observed between apoptosis a
nd overexpression of bcl-2 or p53. CONCLUSIONS. These results indicate
that the frequency of apoptosis may increase with the progression of
gallbladder carcinoma, and in this process, cell-to-cell interaction m
ay affect the cancer's capacity to undergo apoptosis. Oncogenic change
s of bcl-2 and p53 may play a role in tumorigenesis of gallbladder car
cinoma, but such changes were not correlated with spontaneous apoptosi
s. (C) 1996 American Cancer Society.