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

Welsch, Clifford W.; Scieszka, Karen M.; Senn, Eric R.; DeHoog, Jane V.

doi:10.1002/ijc.2910320415

Cited by 27 publications

(18 citation statements)

References 25 publications

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“…Even though animal and cellular studies seem to show either a protective [23][24][25] or harmful [21,22] effect of coffee and tea in relation to breast cancer, we were not able to demonstrate this in humans most probably due to higher doses of coffee/tea constituents used in laboratory studies or due to differences in causal factors of cancer in humans and animals [36]. It may also be possible that the counter effect among various constituents in these beverages leaves no net effect in humans.…”

Section: Discussioncontrasting

confidence: 67%

“…The hypothesis that caffeine may increase the risk of breast cancer was coined in 1970s and 1980s. Caffeine was found to be carcinogenic in animal models [21] possibly caused by an inhibitory effect of caffeine on the repair of UV-damaged DNA, and an enhancing effect on cytotoxic and mutagenic activities of alkylating agents [22]. On the contrary, flavonoids and lignans are members of a diverse group called phytoestrogens, which have similar structural properties with estradiol and may also act as estrogen antagonists [23].…”

Section: Introductionmentioning

confidence: 97%

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Coffee and tea intake and risk of breast cancer

Bhoo-Pathy

Peeters

Gils

et al. 2009

Breast Cancer Res Treat

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Known risk factors account for about 10-15% of breast cancer incidence suggesting that lifestyle exposures are crucial in its etiology. Previous epidemiological studies on the association between coffee and tea consumption and breast cancer risk have been inconsistent. We investigated the association of coffee and tea consumption with the risk of breast cancer among women in EPIC-NL cohort, a population-based prospective cohort in Netherlands with 27,323 participants. Exposure was measured by a validated food frequency questionnaire, and the outcome was verified by direct linkage with the Netherlands Cancer Registry. A total of 681 invasive primary breast cancers were diagnosed in 9.6 years of follow-up. Coffee intake increased the risk of breast cancer by more than twofold as compared to non-consumers (HR; 2.25, 95% CI; 1.30-3.90). This association did not hold after multivariate adjustment which resulted in a HR of 1.17, 95% CI; 0.65-2.12. After adjustment to breast cancer risk factors and lifestyle, no association was observed between intake of coffee or tea and risk of breast cancer across all categories of intake. These results were also not altered by body mass index (BMI). Coffee and tea consumption does not seem to be related to the risk of breast cancer in women.

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Section: Discussioncontrasting

confidence: 67%

Section: Introductionmentioning

confidence: 97%

Coffee and tea intake and risk of breast cancer

Bhoo-Pathy

Peeters

Gils

et al. 2009

Breast Cancer Res Treat

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“…The stimulatory effect of tea, caffeine, or EGCG on apoptosis in tumors of tumor-bearing mice suggests that enhanced apoptosis may be a unifying mechanism by which tea, caffeine, or EGCG inhibit carcinogenesis and tumor growth. Although administration of caffeine inhibits carcinogenesis in several animal models (21)(22)(23)(24)(25)(26)(27)(28)(29), carcinogenesis is stimulated in some animal models (30)(31)(32)(33)(34). The reasons caffeine inhibits carcinogenesis in some animal models and enhances carcinogenesis in other models are not known.…”

Section: Treatment Of Skh-1 Hairless Mice With Uvb (30 Mj͞cmmentioning

confidence: 99%

Topical applications of caffeine or (−)-epigallocatechin gallate (EGCG) inhibit carcinogenesis and selectively increase apoptosis in UVB-induced skin tumors in mice

Lü

Lou

Xie

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

273

216

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SKH-1 hairless mice were irradiated with ultraviolet B (UVB) twice weekly for 20 weeks. These tumor-free mice, which had a high risk of developing skin tumors during the next several months, were then treated topically with caffeine (6.2 mol) or (؊)-epigallocatechin gallate (EGCG; 6.5 mol) once a day 5 days a week for 18 weeks in the absence of further treatment with UVB. Topical applications of caffeine to these mice decreased the number of nonmalignant and malignant skin tumors per mouse by 44% and 72%, respectively. Topical applications of EGCG decreased the number of nonmalignant and malignant tumors per mouse by 55% and 66%, respectively. Immunohistochemical analysis showed that topical applications of caffeine or EGCG increased apoptosis as measured by the number of caspase 3-positive cells in nonmalignant skin tumors by 87% or 72%, respectively, and in squamous cell carcinomas by 92% or 56%, respectively, but there was no effect on apoptosis in nontumor areas of the epidermis. Topical applications of caffeine or EGCG had a small inhibitory effect on proliferation in nonmalignant tumors as measured by BrdUrd labeling (16 -22%), and there was also a similar, but nonsignificant, inhibitory effect on proliferation in malignant tumors. The results suggest a need for further studies to determine whether topical applications of caffeine or EGCG can inhibit sunlight-induced skin cancer in humans.tea constituents ͉ programmed cell death ͉ caspase 3 S kin cancer is a major cancer in the United States, and its incidence is expected to increase substantially because of increased recreational exposure to sunlight and depletion of the ozone layer (1, 2). The identification and use of protective agents should have an important impact on the formation of these cancers. Although the use of sunscreens is an approach that has decreased the risk of skin cancers (3, 4), there is also a need to identify additional approaches for skin cancer prevention in individuals previously exposed to high-dose levels of sunlight (high-risk individuals). Treatment of SKH-1 hairless mice with ultraviolet B (UVB) (30 mJ͞cm 2 ) twice a week for 20 weeks resulted in mice without tumors but with epidermal hyperplasia and a high risk of developing skin tumors during the next several months in the absence of further UVB treatment (initiated high-risk mice) (5). This animal model resembles humans who are heavily exposed to sunlight early in life and then have reduced exposure later in life. We have used UVB-pretreated high-risk mice for evaluating the effects of potential chemopreventive agents on skin tumor formation in the absence of further exposure to UVB. Oral administration of green tea, black tea, or caffeine to UVBpretreated high-risk mice inhibited tumorigenesis, but the decaffeinated teas had little or no activity, and reconstitution of the decaffeinated teas with caffeine restored biological activity (5). These observations indicate that caffeine is a major cancer chemopreventive constituent in tea. Potential antitumor mechanisms include...

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“…In addition, treatment of rats with caffeine in the drinking water enhanced DMBA-induced breast carcinogenesis [Minton et al, 1983;Welsch et al, 1983] and PhIP-induced colon carcinogenesis [Hagiwara et al, 1999]. It was also observed that multiple topical applications Female SKH-1 mice (30/group) were treated topically with 200 nmol of DMBA.…”

Section: Inhibitors Of Carcinogenesis In One Experimental Model May Smentioning

confidence: 88%

“…Although many studies indicated inhibitory effects of caffeine administration on carcinogenesis in animals [Rothwell, 1974;Nomura, 1976Nomura, , 1980Nomura, , 1983Theiss and Shimkin, 1978;Zajdela and Latarjet, 1978;Perchellet and Boutwell, 1981;VanderPloeg and Welsch, 1991;Huang et al, 1997;Hagiwara et al, 1999;Lou et al, 1999;Lu et al, 2002], some studies showed a stimulatory effect of caffeine administration on carcinogenesis [Hiroshino and Tanooka, 1979;Minton et al, 1983;Welsch et al, 1983Welsch et al, , 1988Nagasawa and Konishi, 1988;Hagiwara et al, 1999]. It was found that topical applications of caffeine inhibited TPA-induced tumor promotion and cigarette smoke condensate-induced tumorigenesis in mouse skin [Rothwell, 1974;Perchellet and Boutwell, 1981], and that oral or topical administration of caffeine also inhibited UVB-induced carcinogenesis in mouse skin [Zajdela and Latarjet, 1978;Huang et al, 1997;Lou et al, 1999;Lu et al, 2002].…”

Section: Inhibitors Of Carcinogenesis In One Experimental Model May Smentioning

confidence: 97%

Tailoring cancer chemoprevention regimens to the individual

Conney

2004

J of Cellular Biochemistry

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The present article, which is a tribute to the memory of Dr. Edward Bresnick, emphasizes the importance of environmental and life-style factors for cancer causation in the human population and points out approaches to cancer prevention. These approaches include vaccinations for the prevention of cancers that are caused by infectious agents as well as the use of cancer chemopreventive agents. The use of tamoxifen and letrozole to prevent breast cancer, finasteride to prevent prostate cancer, sunscreens or topical applications of 5-fluorouracil to prevent sunlight-induced skin cancer, and aspirin or calcium to prevent colon cancer are a few examples of cancer chemoprevention in high risk individuals and in the general population. An underdeveloped area of cancer chemoprevention is the use of combinations of agents that work by different mechanisms. It was pointed out that animal studies indicate that many cancer chemopreventive agents inhibit carcinogenesis under one set of experimental conditions but enhance carcinogenesis under another set of experimental conditions. These observations suggest that tailoring the chemopreventive regimen to the individual or to groups of individuals living under different environmental conditions or with different mechanisms of carcinogenesis may be an important aspect of cancer chemoprevention in human populations. How to tailor cancer chemoprevention regimens to the individual is an important challenge for the future.

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

Cited by 27 publications

References 25 publications

Coffee and tea intake and risk of breast cancer

Coffee and tea intake and risk of breast cancer

Topical applications of caffeine or (−)-epigallocatechin gallate (EGCG) inhibit carcinogenesis and selectively increase apoptosis in UVB-induced skin tumors in mice

Tailoring cancer chemoprevention regimens to the individual

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