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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
Published on: December 19, 2019
Sun-related factors, betapapillomavirus, and actinic keratoses: a prospective study
Penelope McBride1, Rachel Neale, Nirmala Pandeya
1Cancer and Population Studies Unit, Queensland Institute of Medical Research, PO Royal Brisbane Hospital, Brisbane, Queensland, Australia 4029. penelope.mcbride@qimr.edu.au
Objective:
To examine prospectively the relationship among sun exposure, Betapapillomavirus, and development of actinic keratoses.
Design:
Prospective, community-based cohort study.
Setting:
Township of Nambour in Southeast Queensland, Australia.
Participants:
A total of 291 randomly selected adults aged 36 to 86 years with the presence or absence of Betapapillomavirus DNA in eyebrow hair follicle cells known at baseline in August 1996 and with subsequently documented sun exposure histories.
Main Outcome Measures:
Prevalence of actinic keratoses in March 2003 after 7 years of follow-up.
Results:
Beyond the known determinants of multiple actinic keratoses, namely, advanced age, male sex, fair skin, and lifetime occupational sun exposure, Betapapillomavirus infection was associated with having more than 10 actinic keratoses (odds ratio, 1.8; 95% confidence interval, 0.7-4.4). However, Betapapillomavirus positivity led to a significant 13-fold increase in the risk of actinic keratoses among those 60 years or older, a nearly 6-fold increase in risk when combined with fair skin color, and a doubling in risk of actinic keratoses when combined with high sun exposure, recent or cumulative, compared with those who had neither Betapapillomavirus infection nor the respective risk factor of interest.
Conclusions:
Although the presence of Betapapillomavirus DNA in eyebrow hair follicle cells had only a small independent association with actinic keratoses, Betapapillomavirus infection in combination with key risk factors increased the risk of actinic keratoses, which is consistent with a potentiation by Betapapillomavirus of the effect of established causal factors.
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