Effects of caffeine on pancreatic tumorigenesis by 4-hydroxyamino-quinoline 1-oxide in partially pancreatectomized rats

Denda, Ayumi; Yokose, Yoshihiko; Emi, Yohko; Murata, Yoji; Ohara, T.; Sunagawa, Masaoki; Mikami, S; Takahashi, Seiichi; Konishi, Yoichi

doi:10.1093/carcin/4.1.17

Cited by 12 publications

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“…In this respect, it is perhaps relevant that caffeine has been reported to enhance the induction of acinar cell tumors in rats. 53 The present observations, therefore, suggest that in the human pancreas atypical acinar cell lesions are involved in the pathogenesis of acinar cell carcinoma. An epidemiologic study in the Japanese population on the degree of association between these lesions and lifestyle factors could yield useful information on the etiology of cancer in the pancreas.…”

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confidence: 51%

Atypical and neoplastic acinar cell lesions of the pancreas in an autopsy study of Japanese patients

Tanaka

Mori

Williams

1988

Cancer

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A histopathologic examination of the pancreas was performed on a series of adult Japanese autopsies. In ten of 162 pancreases (6%) with adequate tissue available, two types of focal atypical acinar cell lesions, composed of acidophilic or basophilic cells, were found. Acidophilic atypical acinar cell lesions were more frequent than basophilic ones, although the one case of acinar cell adenoma and two cases of acinar cell carcinomas showed high incidences of basophilic atypical acinar cell lesions. The findings are concluded to support the possibility that atypical acinar cell lesions are precursors for acinar cell carcinomas. Cancer 61:2278-2285,1988. HE INCIDENCE OF PANCREATIC cancer has in-T creased somewhat in recent including cases in J a ~ a n. ~-~ In pancreatic exocrine cancers duct cell adenocarcinoma is the most common type, representing more than 75% of The incidence of carcinoma in situ in the duct epithelium is 24% in patients with pancreatic ~ a n c e r. ~ In addition, atypical or dysplastic epithelial lesions in the pancreatic ducts have been found in association with pancreatic carcinoma more frequently than in noncancerous pancreases. It has therefore been assumed that these cancers arise from ductal epithelium. lo The other principal type of pancreatic cancer, which represents up to 15% of pancreatic carcinomas, is acinar cell carcinoma, which is assumed to originate from the acinar cell^.^,^^'^ This interpretation is supported by findings from experimental pancreatic carcinogenesis in which carcinogen-induced atypical acinar cell foci (AACF) or atypical acinar cell nodules (AACN) have been identified as possible precursor lesions of acinar cell car~inoma.~-'~ Atypical acinar cell lesions resembling those of experimentally induced pancreatic lesions in rats also have been reported in the human pan-creas. I4-l7 To determine the frequency of human atypical acinar cell lesions in a low-risk population, we studied a series of autopsies performed at a university medical center in Gifu prefecture in western Japan. This article describes the morphologic characteristics of the pancreatic lesions and the clinical information on the patients. Materials and Methods Pancreas tissue sections from 22 1 autopsies performed from 1974 to 1983 at the Gifu University School of Medicine in Gifu prefecture, Japan were studied. To be selected for review, a postmortem interval of no longer than 6 hours from death until fixation of the pancreas was required. This would ensure adequate tissue quality for study. All pancreases were fixed in 10% formalin and stained with hematoxylin and eosin. Of the 174 cases, 162 pancreases without autolysis were found to be suitable for quantitative histopathologic study. The 162 patients with adequate pancreatic tissue ranged in age from 30 to 89 years. Ninety-nine (61%) were men and 63 (39%) were women. The mean age of males was 60 for men, 6 1 for women. Eighty-five of the patients from which adequate pancreatic tissue was obtained had died in the following numbers of the following c...

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confidence: 51%

Atypical and neoplastic acinar cell lesions of the pancreas in an autopsy study of Japanese patients

Tanaka

Mori

Williams

1988

Cancer

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“…Caffeine is well known to inhibit urethane or 4-nitrosoquinoline-1 -oxide induced tumorigenesis in mice [22]. The inhibitory effect of caffeine on tumorigenesis is considered to be due to a potentiation of the lethal effects of chemical carcinogens by inhibition of error-prone repair, leading to the death of cells that would have produced tumor if they had survived [23,24].…”

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confidence: 99%

Suppressive effects of two bioresponse modifiers, Krestin and Levamisole, on 5‐azacytidine‐induced digital defects in rats

Kurishita

1990

Teratog Carcinog Mutagen

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The effects of two bioresponse modifiers, krestin (PSK) and levamisole hydrochloride (levamisole), on 5‐azacytidine (5‐AC)‐induced syndactyly, brachydactyly, and ectrodac‐tyly were investigated. Both PSK and levamisole suppressed 5‐AC‐induced digital malformations in the rat. The effect of PSK was significant when given 24 h before to 1 h after 5‐AC treatment, and levamisole when given 12 h before to 3 h after treatment. Both agents showed an immune‐stimulating effect and have been used as cancer chemotherapeutic drugs. However, as the contribution of fetal or maternal immune functions or the alleviation action is unknown, further investigations are required to clarify the mechanism.

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Caffeine (1,3,7‐trimethylxanthine), a temperate promoter of DMBA‐induced rat mammary gland carcinogenesis

Welsch

Scieszka

Senn

et al. 1983

Intl Journal of Cancer

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The administration of caffeine to the drinking water (250 mg/l and 500 mg/l) of female Sprague-Dawley rats after treatment with 7,12-dimethylbenzanthracene (DMBA) (5 mg i.g.) resulted in an increase in mammary carcinoma incidence. The confidence levels of statistical significance for the groups of rats receiving the 250-mg and 500-mg doses of caffeine were greater than 0.70 and greater than 0.99, respectively. This increase in mammary carcinoma incidence was observed when caffeine treatment was initiated commencing 3 days after DMBA treatment and continued for 21 weeks. This effect was also observed when caffeine treatment was initiated commencing 20 weeks after DMBA treatment and continued for 6 weeks in rats relatively refractory to carcinogen treatment (mammary tumor-free at onset of treatment) and in rats relatively sensitive to the carcinogen (mammary tumor bearing at onset of caffeine treatment). Caffeine treatment of rats prior to and during carcinogen treatment did not significantly affect mammary carcinoma incidence. Thus caffeine consumption has been shown to significantly enhance the promoting phase but is without effect on the initiating phase of this carcinogenic process.

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Effects of caffeine on pancreatic tumorigenesis by 4-hydroxyamino-quinoline 1-oxide in partially pancreatectomized rats

Cited by 12 publications

References 0 publications

Atypical and neoplastic acinar cell lesions of the pancreas in an autopsy study of Japanese patients

Atypical and neoplastic acinar cell lesions of the pancreas in an autopsy study of Japanese patients

Suppressive effects of two bioresponse modifiers, Krestin and Levamisole, on 5‐azacytidine‐induced digital defects in rats

Caffeine (1,3,7‐trimethylxanthine), a temperate promoter of DMBA‐induced rat mammary gland carcinogenesis

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