Histologic and biologic patterns of microscopic pancreatic ductal adenocarcinomas detected incidentally at autopsy.
BACKGROUND
The major clinical problems with pancreatic carcinoma are its silent course and late, fatal clinical manifestation. The results of treatments of small pancreatic carcinomas (<2 cm in greatest dimension) have led to the assumption that the detection of these cancers at earlier stages would lead to better survival and possible cure. Currently, there is no information about the histologic and biologic patterns of early stage pancreatic carcinoma, and the available data on incidentally detected tumors are fragmentary. The authors observed two incidental microscopic pancreatic ductal adenocarcinomas in female patients who died of advanced gastric carcinoma (Case 1) and renal carcinoma (Case 2).


METHODS
The pancreatic lesions were examined histologically in serial sections and immunocytochemically for islet cells. Microdissection was performed so that the lesions could be examined for c-Ki-ras mutation.


RESULTS
In Case 1, the pancreatic lesion was composed of cystic and solid components. The cystic component consisted of four small cysts compatible with a mucinous cystic tumor and showed no invasion. The solid component was a well-differentiated adenocarcinoma that occupied a 4 x 2 mm area. In Case 2, the pancreatic lesion contained two small, separate cysts, one of which was surrounded by two apparently separate, invasive adenocarcinomas 2.6 x 0.7 mm and 1.2 x 0.5 mm in greatest dimension. There was invasion of pancreatic islets and perineural spaces in both cases; and in Case 2, there was invasion of peripancreatic fatty tissue. In both cases, the epithelia of the cystic components and tumors showed mutation of the c-Ki-ras oncogene at codon 12, with GGT-to-GAT transition. CONCLUSIONS. Pancreatic carcinoma seems to occur under occult circumstances and maintain a silent course. Even in its early developmental stage, the cancer is invasive, primarily affects islets and nerves, and exhibits mutation of the c-Ki-ras oncogene. These findings call for urgency in the development of preventive modalities.
Kimura
W
W
Department of Surgery, University of Tokyo, Japan.
Morikane
K
K
Esaki
Y
Y
Chan
W C
WC
Pour
P M
PM
D000368:Aged; D000369:Aged, 80 and over; D001344:Autopsy; D002277:Carcinoma / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000473:pathology*; D005260:Female; D006801:Humans; D009378:Neoplasms, Multiple Primary / Q000473:pathology*; D010190:Pancreatic Neoplasms / Q000473:pathology*; D013274:Stomach Neoplasms / Q000473:pathology*