Plasma gastrin and cholecystokinin (CCK) responses were measured after a pancreatoduodenectomy (PD) using the Billroth-I type reconstruction combined with distal partial gastrectomy (standard PD) and combined with preservation of the pylorus and the duodenal bulb (PPPD). Six unoperated patients, 4 men and 2 women, were studied as control subjects. Basal plasma levels of gastrin were significantly higher in controls than in patients who had a standard PD (p less than 0.05) and gastrin responses to a meal were also blunted in these patients. In contrast basal and postprandial levels of gastrin after PPPD were significantly higher than these found in patients with standard PD (p less than 0.05). Postprandial gastrin response after PPPD were similar in pattern to these found in controls. Integrated gastrin release after PPPD was less than that of the control but was significantly greater than that in patients with standard PD. Basal plasma levels of CCK in the patients after the standard PD were significantly lower than in controls and significantly higher postprandial levels of CCK were found after PPPD compared to standard PD (p less than 0.05). However integrated CCK from 0 to 120 minutes were not significantly different between PPPD and standard PD groups. Based on these observations concerning hormonal release of gastrin and CCK, preservation of the stomach and the duodenal bulb appears to be a more physiologic reconstructive procedure than the standard PD. In addition the operation probably has more beneficial effect on the injured pancreas in time.

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Abstract. We analyzed DNA copy number aberrations (DCNAs) by chromosomal comparative genomic hybridization (CGH) in 93 consecutive sporadic gastric adenocarcinomas. In addition, numerical aberrations in chromosomes 7, 11, 17, and 18 were evaluated by fluorescence in situ hybridization (FISH). Gastric cancers were divided on the basis of nuclear DNA content measured by laser scanning cytometry (LSC) into two groups, 36 DNA diploid (1.0 ≤ DNA index (DI) < 1.2) and 57 aneuploid (DI ≥ 1.2) cancers. The most frequent gain and loss of DNA copy number were found at 8q21-23 and 19p13.3, respectively, in both diploid and aneuploid cancers. Diploid cancers were further divided on the basis of genetic aberrations into major type and subtype cancers. The diploid cancer group included nine subtype cancers that showed large numbers of DCNAs; the mean number of DCNAs detected by CGH was 26.7 per tumor. This value was much larger in these diploid subtype cancers than diploid major type cancers (mean, 5.2 per tumor, p<0.0001). These nine cancers were also characterized by large intercellular variations in chromosome copy numbers that were not detected in the 27 major diploid type cancers. The aneuploid cancer group included only three subtype tumors that showed only a small number of DCNAs (mean, 3 per tumor) and minimal intercellular variations in chromosomal copy number. These data indicate that gastric adenocarcinomas can be divided into three types; aneuploid, major diploid type and diploid subtype cancers. Large-scale studies are necessary to clarify the differences in biological characteristics and underlying genetic mechanisms between these types.

Background: The treatment strategy usually depends on the disease state in the individual patient. However, it is difficult to estimate the disease state before treatment in many patients. The purpose of this study was to develop a BAC (bacterial artificial chromosome) mini-array allowing for the estimation of node metastasis, liver metastasis, peritoneal dissemination and the depth of tumor invasion in gastric cancers.

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