Enhancing effect of partial gastrectomy on pancreatic carcinogenesis

Watanapa, P.; Flaks, Bojan; Oztas, Haydar; Deprez, Pierre Henri; Calam, J.; Williamson, R. C. N.

doi:10.1038/bjc.1992.77

Cited by 20 publications

(8 citation statements)

References 25 publications

(3 reference statements)

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“…In our own study rats with 60% distal gastrectomy had more (and larger) acidophilic AACF than controls 15 months after exposure to azaserine. Unlike Malfertheiner, we found higher plasma CCK concentrations, both basal and postprandial (Watanapa et al, 1992e). Thus CCK could act as an intermediary for the stimulatory effects of partial gastrectomy on the pancreas, especially since antral resection would reduce gastrin output.…”

Section: Other Specific Dietary Constituentsmentioning

confidence: 54%

Experimental pancreatic hyperplasia and neoplasia: effects of dietary and surgical manipulation

Watanapa

Williamson²

1993

Br J Cancer

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Summary Several studies carried out during the past two decades have investigated the effect of dietary and surgical manipulation on pancreatic growth and carcinogenesis. Diets high in trypsin inhibitor stimulate pancreatic growth and increase the formation of preneoplastic lesions and carcinomas in the rat pancreas. Cholecystokinin (CCK) is the key intermediary in this response, since both natural and synthetic trypsin inhibitors increase circulating levels of the hormone and CCK antagonists largely prevent these changes. Fatty acids enhance pancreatic carcinogenesis in both rats and hamsters, whereas protein appears to have a protective role in the rat, but to increase tumour yields in the hamster. Several surgical operations affect the pancreas. Pancreatobiliary diversion and partial gastrectomy stimulate pancreatic growth and enhance carcinogenesis, probably by means of increased CCK release. Complete duodenogastric reflux has similar effects on the pancreas but the gut peptide involved is gastrin. Although massive small bowel resection increases pancreatic growth, the marked reduction in caloric absorption probably explains its failure to enhance carcinogenesis. CCK and enteroglucagon might work in concert to modulate the tropic response of the pancreas to small bowel resection. In the pancreas, as in the large intestine, hyperplasia appears to precede and predispose to neoplasia.

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Section: Other Specific Dietary Constituentsmentioning

confidence: 54%

Experimental pancreatic hyperplasia and neoplasia: effects of dietary and surgical manipulation

Watanapa

Williamson²

1993

Br J Cancer

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“…For example, the amount of nitrites and N-nitroso compounds, which are known pancreatic carcinogens, increases in the gastric juice after a gastrectomy, while the reflux of these substances from the duodenum into the pancreatic duct might induce pancreatic cancer. 15,16 However, we found no strong clinical evidence to suggest that a partial gastric resection is associated with the development of pancreatic cancer. There were seven patients in the present study who had Table 4.…”

Section: Discussionmentioning

confidence: 90%

Synchronous or metachronous double cancers of the pancreas and other organs: Report on 12 cases

et al. 2000

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Pancreatic carcinoma carries a poor prognosis, especially invasive ductal carcinoma of the pancreas. This retrospective study describes the results of the treatment and prognosis for double cancers in which cancer of the pancreas was associated with malignancies in other organs in 12 patients who were diagnosed and treated at Kurume University Hospital. The patients included 4 women and 8 men, with an average age of 67 years. Of the 12 tumors, 7 were metachronous pancreatic cancers which occurred after resections of other organ malignancies. Five patients had synchronous double cancers, one of whom was diagnosed to have gastric cancer on admission. Two other patients of this group were diagnosed to have lung cancer, while the remaining 2 patients suffered from colon cancer. By the time pancreatic cancer was diagnosed, gastrectomies had been performed in 7 patients for either gastric cancer or ulcers. In addition, one patient underwent a hysterectomy for uterine carcinoma and another received a low anterior resection for rectal carcinoma. Four of 5 patients in the synchronous group had nonresectable tumors and a palliative bypass operation was performed in 2 of these patients. Six patients who had metachronous double cancers died because of pancreatic cancer recurrence or metastases. We conclude that the prognosis of double cancers, where cancer of the pancreas is associated with other organ malignancies, primarily depends on the prognosis of the pancreatic carcinoma, and the present study suggests the necessity of long-term follow-up examinations for gastrectomy patients in order to make an early diagnosis of pancreatic cancer.

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“…Patients with a remote partial gastrectomy for benign ulcer disease may constitute a high risk group for pancreatic cancer, [3][4][5][6][7][8][9] although reports are conflicting. [10][11][12][13][14] The mechanism by which partial gastrectomy may contribute to the development of pancreatic cancer is unclear, but an increased production of N-nitroso compounds and nitrosamines in the operated stomach is thought to play a role.…”

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confidence: 99%

Pancreatic cancer after remote peptic ulcer surgery

Tascilar

Rees

Sturm

et al. 2002

Journal of Clinical Pathology

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Background: Peptic ulcer surgery may carry an increased risk for pancreatic cancer development. Molecular analysis of K-ras codon 12, frequently mutated in conventional pancreatic cancers, might provide insight into the aetiological mechanisms. Methods: The relative risk of pancreatic cancer was computed by multivariate and person-year analysis in a cohort of 2633 patients who had undergone gastrectomy. Lung cancer risk was analysed as an indirect means of assessing smoking behaviour. K-ras codon 12 mutational analysis was performed on 15 postgastrectomy pancreatic cancers. Results: There was an overall increased risk of pancreatic carcinoma of 1.8 (95% confidence interval, 1.3 to 2.6) five to 59 years postoperatively, which gradually increased to 3.6 at 35 years or more after surgery (χ 2 test for trend, p < 0.05). Multivariate analysis indicated that parameters other than postoperative interval did not influence the risk. Lung cancer risk was significantly increased after surgery, but no time trend was observed. The spectrum and prevalence of K-ras codon 12 mutations were comparable to conventional pancreatic cancer. Conclusions: Remote partial gastrectomy is associated with an increased risk of pancreatic cancer. Postgastrectomy and non-postgastrectomy pancreatic cancers may share similar aetiological factors, such as smoking. However, the neoplastic process in patients who have undergone gastrectomy appears to be accelerated by factors related to the surgery itself.

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Enhancing effect of partial gastrectomy on pancreatic carcinogenesis

Cited by 20 publications

References 25 publications

Experimental pancreatic hyperplasia and neoplasia: effects of dietary and surgical manipulation

Experimental pancreatic hyperplasia and neoplasia: effects of dietary and surgical manipulation

Synchronous or metachronous double cancers of the pancreas and other organs: Report on 12 cases

Pancreatic cancer after remote peptic ulcer surgery

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