The purpose of this study was to analyse multi-detector row CT (MDCT) signs of peripancreatic arterial and venous invasion in pancreatic carcinoma. Among 101 patients with pancreatic carcinoma examined by MDCT, 54 candidates for surgery were pre-operatively evaluated for vascular invasion based on MDCT signs. The peripancreatic major vessels (including superior mesenteric artery, coeliac artery, common hepatic artery, superior mesenteric vein and portal vein) were examined carefully by surgeons during the operation. At surgical exploration, 78 of 224 vessels were invaded by tumour. The invaded peripancreatic major arteries (n = 29) and veins (n = 49) presented different MDCT signs: 43% of invaded veins (18/42, except for 7 occluded veins) were surrounded by tumour less than 50% of the vessel circumference compared with 97% (28/29) of the invaded arteries, which were surrounded by tumour more than 50% of the vessel circumference or were embedded in tumour (p<0.001). 69% (34/49) of the invaded veins had vascular stenosis or obliteration, compared with 41% (12/29) of the invaded arteries (p<0.05). Irregularity of the vein wall, 74% (31/42, except for 7 occluded veins); occurred more often than that of the artery wall, 45% (13/29) (p<0.05). In conclusion, the MDCT signs of peripancreatic arterial and venous invasion have different characteristics, which should be considered in pre-operative evaluation.

Collision cancers of the pancreas and periampullary region are difficult to diagnose preoperatively. Their prognosis is poor even after radical resection and adjuvant chemotherapy were given.

Cisplatin is an efficient anticancer agent. Cisplatin-based chemotherapy is believed to involve different signal transduction pathways, among which calpain activation has been proposed as an important factor in the induced apoptosis. In our study, based on real-time single cell analysis, we investigated the molecular involvement of calpain in cisplatin-induced apoptosis in living human lung adenocarcinoma cells. After cisplatin treatment, calpain was activated, resulting in Bid cleavage at 4-5 hr, followed by Bid translocation and cytochrome c release, leading to cell death. Calpeptin and PD150606, specific inhibitors of calpain, blocked Bid activation completely; however, cytochrome c release was delayed by more than 2 hr, which was associated with the delay of caspase-3 activation and cell death. Remarkably, calpainmediated release of cytochrome c and cell death was significantly compromised in the Bid knockdown cells. Z-IETD-fmk and Z-VDVAD-fmk were used to block the activation of caspase-8 and caspase-2, respectively; however, the progression of apoptosis were not affected, suggesting that caspase-8 and caspase-2 were not involved in this experimental model. Taken together, the data demonstrate that calpain mediated cisplatin-induced apoptosis in human lung adenocarcinoma cells through activating Bid, which then regulated the mitochondrial apoptotic pathway. The delays of cytochrome c release, caspase-3 activation and subsequent cell death by inactivating calpain or silencing Bid exclude other earlier or parallel pathways, strongly suggesting that the calpain-mediated pathway is the kinetically earliest one, which dominates the cisplatin-induced apoptosis. '

OBJECTIVE:  To investigate the relationship between pancreatic cancer (PC) and diabetes mellitus. METHODS:  All PC patients diagnosed and treated at Zhongshan hospital from January 1991 to December 2007 were retrospectively analyzed. During this period, 770 non‐digestive tract, non‐neoplastic and non‐hormone‐related patients matched for sex and age were collected as controls. The incidence of diabetes mellitus between the two groups was compared. RESULTS:  Between the PC group and the control group, sex and age of the patients were well matched. The incidence of diabetes mellitus was 34.63% in the PC group and 8.83% in the control group (P < 0.001, RR = 5.19). In the PC group there was no correlation between age, sex, site of the cancer, tumor differentiation, lymph node metastasis, TNM staging and the incidence of diabetes mellitus. In this group with diabetes, 74.56% experienced onset within two years of cancer diagnosis. Of the control patients, 57.35% had had diabetes for under 2 years (P = 0.009, RR = 2.18). In the PC group with diabetes, 5.9% had had diabetes for more than 10 years while compared with 8.8% of the controls (P = 0.42). CONCLUSION:  Whether diabetes mellitus is a result of or a risk factor for PC is still unclear. The incidence of diabetes mellitus is much higher in the PC patients. The onset of diabetes mellitus in adults might be an alerting factor that could lead to an early diagnosis of pancreatic cancer.