TEMPORAL EXPRESSION OF THE GASTRIN (CCK-B) RECEPTOR DURING AZASERINE-INDUCED PANCREATIC CARCINOGENESIS

被引:9
作者
POVOSKI, SP
ZHOU, WG
LONGNECKER, DS
BELL, RH
机构
[1] UNIV CINCINNATI,COLL MED,MED CTR,231 BETHESDA AVE,ML 558,CINCINNATI,OH 45267
[2] DEPT VET AFFAIRS MED CTR,CINCINNATI,OH
[3] DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PATHOL,HANOVER,NH 03756
关键词
AZASERINE; PANCREATIC CARCINOGENESIS; GASTRIN RECEPTOR; CHOLECYSTOKININ RECEPTOR;
D O I
10.1097/00006676-199309000-00014
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Cholecystokinin (CCK-A) and gastrin (CCK-B) receptors have been demonstrated in the azaserine-induced rat pancreatic carcinoma DSL-6. In order to determine at what stage in azaserine-induced pancreatic carcinogenesis gastrin (CCK-B) receptors are first expressed, we examined the binding of [I-125]gastrin-I to normal rat pancreas, azaserine-induced premalignant pancreatic nodules, grossly normal internodular pancreas, and DSL-6 carcinoma. We observed that specific gastrin binding was absent in normal pancreas, premalignant nodules, and internodular pancreas, and also reconfirmed our previous report of marked overexpression of gastrin (CCK-B) receptors in the DSL-6 carcinoma. Specific cholecystokinin (CCK) binding was present in all pancreatic tissue types tested. Therefore, we conclude that the presence of gastrin (CCK-B) receptors in the azaserine-induced pancreatic carcinoma DSL-6, in contrast to their absence in premalignant nodules, suggests that the expression of the gastrin (CCK-B) receptor may be important in the transformation from premalignant nodules to pancreatic cancer.
引用
收藏
页码:615 / 621
页数:7
相关论文
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[21]  
ZHOU WG, 1992, CANCER RES, V52, P6905