Primary pancreatic carcinomas were studied histologically and histochemically, to assess the frequency of dutal hyperplasia in tissue adjacent to malignat neoplams. Hyperplaaia waw divided into four types: simple, papillary, atypical and ductular, affecting large, medium and small ducts (ductules). All types of hyperplasia were frequently seen in areas adjacent to carcinomas, including ductal, pleomorphic, mucinous, adenosquamous, small and spindel cell and cystadenocarcinomas. In contrast, acinar cell carcinoma and microadenocarcinoma were less frequently associated with ductal hyperplasia. Mucin histochemistyr revealed differences in types of mucin betwwnd the normal ducts and hyperplastic pancreatic ducts and carcinomas. The former group comtained smal amouts of sulphated mucin while the latter showed a marked increase in neutral and sialomucins. Our study salso suggests that both papillary with the latter showed a marked increse in neutral and sialomucins. Our study salso suggests that both papillary and atypical hyperplasia are precancerous lesions, supporitng and hypothesis of ductal origin of pancreatic carcinomas. And atypical hyperplasia are prcancerous lesions, suporintg and hypothesis of ductal origin of poanereatic carcionmas.

The numbers of immunoreactive gastrin and somatostatin cells in gastric and duodenal mucosal biopsy specimens from dyspeptic patients with duodenal ulcers and dyspeptic controls without ulcers were calculated using a morphometric method. The levels of gastrin and somatiotatin in the tissue were also measured by the radioimmunssay. The results showed no significant difference in the number of G cells and the level of gaslrln in the tisse between the ulcer and nun-ulcer groups. However, the number of D ceils and the level of somaosutin in the tissue in ulcer patlems were remarkably reduced in comparison with those in non-ulcer patients (P<0.01 and P<0.05, respectively). The G: D cells and gastrin : somatostatin rsatios in ulcer patients were much higher than those in the non-ulcer control group It is considered that the reduction of D cells and the relative lack of somatostafin in duodenal ulcer patients might have a role in the mechanism of the duodenal ulceration.

The expression of mRNA for epidermal growth factor (EGF), transforming growth factor-α (TGF-α), EGF receptor (EGFR) and e-erbB-2 genes and the immunoreactivity to these gene products were examined in 3 newly established humand panereatic carcinoma cell lines and their corresponding in vivotumor lines using the Northem blot technique and the immunohistochemical method. All 3 cell lines expressed TGF-α, EGFR and 2 of the 3 lines expressed EGF and c-erbB-2mRNAs. The immunohisochemical study showed immunore-acvitity to EGF, TGF-α and EGFR in all these 3 cell lines and their corresponding vivo tuor lines. These results indicate that the autocrine loop of EGF and /or TGF-α/EGFR in pancreatic carcinoma cells may be one of the important reasons for the uncontrolled growth of the pancreatic carcinoma. The c-erbB-2 overexpression in some of the cell lines may slao contribute to the carcinogenesis or progression of this cancer.

目的研究DPC4（deleted in pancreatic cancer locus 4）基因在胰腺癌中的改变。方法用多聚酶链反应2单链构象多态性分析（PCR2SSCP）银染技术及PCR产物直接测序法检测胰腺癌细胞系P1、P2、P3、P4、P7，11例新鲜冷冻胰腺癌组织中DPC4基因第1，2，3，4，8，11外显子的缺失和突变。结果5株人胰腺癌细胞系中，3株（P1、P2、P3）存在DPC4基因突变,DPC4 基因改变率为3/5。11例新鲜冷冻胰腺癌组织中，3例有DPC4基因的纯合性缺失，2例有基因突变，DPC4基因改变率为5/11(45.5%)。结论DPC4作为一种抑癌基因，其改变在胰腺癌的形成中可能起重要作用。

Gene amplification and enhanced expression of the epidermal growth facor receptor (EGFR) represent the major moiecular genetic alteration in glioblastomas and it may play an essential role in cell growth and in the carcinogenic process, On the other hand, the nuclear suppressor proteins PML and p53 are also known to play critical roles in cancer edveiopment and in suppressing cell growth. Here we report that, in glioblastoma cells with cefectivw EGFR function, the expressions of both promyetocytic leukaernia (PML) and p53 were altered. Cells that were transfected with the antisense-cDNA of EGFR were found to have more cells in G1 and fewer cells in Sphase, In Addition, the transfceted cells were found to be non-responsive to EGF-induced cell growth, Inteerestingly, the expression of the suppressors p53 and PML were found to be signillcantly increased by immunohistochemical assay in the antisense-EGFR cells. Moreover, the PML expression in many of the cells was converted from the nucleal dot pattern imto fine-granulated staining pattern, In contrast, the expressions of other cell cycle regulated geries and proto-oncogene, including the cycli-dependent kinase 4(cocik4), retinblastoma, p16 think and p21bjone, were not altered. These data indicate that there are specific inductions of PML and p53 proteins which may account for the increase in G1 and growth arrest in antisense-EGFR treated cells, It also indicates that the EGF, p53 and PML transduction pathways were liked and they may constifulte arrest in an ntegral part of an alterred growth reguiaory programme .The interactions and cross-talks of these critical molecules may be very importtant in regulating cell growth, differentiation and cellular resporise to treatment in glioblastomas.