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Mechanisms of Caffeine-Induced Inhibition of UVB Carcinogenesis

Overview of attention for article published in Frontiers in oncology, January 2013
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  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (98th percentile)
  • High Attention Score compared to outputs of the same age and source (99th percentile)

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9 news outlets
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21 X users
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1 Facebook page

Citations

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31 Dimensions

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68 Mendeley
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Title
Mechanisms of Caffeine-Induced Inhibition of UVB Carcinogenesis
Published in
Frontiers in oncology, January 2013
DOI 10.3389/fonc.2013.00144
Pubmed ID
Authors

Allan H. Conney, Yao-Ping Lu, You-Rong Lou, Masaoki Kawasumi, Paul Nghiem

Abstract

Sunlight-induced non-melanoma skin cancer is the most prevalent cancer in the United States with more than two million cases per year. Several studies have shown an inhibitory effect of caffeine administration on UVB-induced skin cancer in mice, and these studies are paralleled by epidemiology studies that indicate an inhibitory effect of coffee drinking on non-melanoma skin cancer in humans. Strikingly, decaffeinated coffee consumption had no such inhibitory effect. Mechanism studies indicate that caffeine has a sunscreen effect that inhibits UVB-induced formation of thymine dimers and sunburn lesions in the epidermis of mice. In addition, caffeine administration has a biological effect that enhances UVB-induced apoptosis thereby enhancing the elimination of damaged precancerous cells, and caffeine administration also enhances apoptosis in tumors. Caffeine administration enhances UVB-induced apoptosis by p53-dependent and p53-independent mechanisms. Exploration of the p53-independent effect indicated that caffeine administration enhanced UVB-induced apoptosis by inhibiting the UVB-induced increase in ATR-mediated formation of phospho-Chk1 (Ser345) and abolishing the UVB-induced decrease in cyclin B1 which resulted in caffeine-induced premature and lethal mitosis in mouse skin. In studies with cultured primary human keratinocytes, inhibition of ATR with siRNA against ATR inhibited Chk1 phosphorylation and enhanced UVB-induced apoptosis. Transgenic mice with decreased epidermal ATR function that were irradiated chronically with UVB had 69% fewer tumors at the end of the study compared with irradiated littermate controls with normal ATR function. These results, which indicate that genetic inhibition of ATR (like pharmacologic inhibition of ATR via caffeine) inhibits UVB-induced carcinogenesis support the concept that ATR-mediated phosphorylation of Chk1 is an important target for caffeine's inhibitory effect on UVB-induced carcinogenesis.

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X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 68 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 68 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 13 19%
Student > Bachelor 13 19%
Researcher 9 13%
Other 5 7%
Student > Ph. D. Student 3 4%
Other 12 18%
Unknown 13 19%
Readers by discipline Count As %
Medicine and Dentistry 12 18%
Biochemistry, Genetics and Molecular Biology 10 15%
Agricultural and Biological Sciences 9 13%
Pharmacology, Toxicology and Pharmaceutical Science 7 10%
Chemistry 4 6%
Other 11 16%
Unknown 15 22%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 93. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 06 July 2024.
All research outputs
#488,773
of 26,561,164 outputs
Outputs from Frontiers in oncology
#75
of 23,272 outputs
Outputs of similar age
#3,296
of 294,835 outputs
Outputs of similar age from Frontiers in oncology
#1
of 327 outputs
Altmetric has tracked 26,561,164 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 98th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 23,272 research outputs from this source. They receive a mean Attention Score of 3.2. This one has done particularly well, scoring higher than 99% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 294,835 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 98% of its contemporaries.
We're also able to compare this research output to 327 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 99% of its contemporaries.