***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Skin cancers pose a significant public health problem in high-risk population s. We have prospect ively monitored basal cell carcinoma ( BCC ) and squamous cell carcinoma ( SCC ) incidence in a Queensl and community over a 10-y period by recording newly treated lesions , supplemented by skin examination surveys . Age-st and ardized incidence rates of people with new histologically confirmed BCC were 2787 per 100,000 person-years at risk ( pyar ) among men and 1567 per 100,000 pyar among women , and corresponding tumor rates were 5821 per 100,000 pyar and 2733 per 100,000 pyar , respectively . Incidence rates for men with new SCC were 944 per 100,000 pyar and for women 675 per 100,000 pyar ; tumor rates were 1754 per 100,000 pyar and 846 per 100,000 pyar , respectively . Incidence rates of BCC tumors but not SCC tumors varied noticeably according to method of surveillance , with BCC incidence rates based on skin examination surveys around three times higher than background treatment rates . This was mostly due to an increase in diagnosis of new BCC on sites other than the head and neck , arms , and h and s associated with skin examination surveys and little to do with advancing the time of diagnosis of BCC on these sites as seen by a return to background rates following the examination surveys . We conclude that BCC that might otherwise go unreported are detected during skin examination surveys and thus that such skin cancer screening can influence the apparent burden of skin cancer Background Human studies of dietary fat as a possible risk factor for cutaneous malignant melanoma ( CMM ) and non-melanoma skin cancer ( NMSC ) – principally basal cell carcinoma ( BCC ) and squamous cell carcinoma ( SCC ) – have produced inconsistent results . We had the opportunity to examine the association concurrently for all three types of skin cancer in a population -based study in Tasmania , Australia , involving 652 cases of CMM , BCC and SCC and a common set of 471 controls . Methods Histopathologically-confirmed cases of CMM , BCC and SCC were ascertained from the Tasmanian Cancer Registry ( TCR ) , and controls were selected at r and om from the state 's electoral roll . We compared subjects categorised by thirds of dietary fat intake score measured by the ' Dobson short fat question naire ' , with logistic regression models that adjusted for age , sex , skin type and usual sun exposure . We then followed all subjects for 56–80 months until 31 August , 2004 for a new NMSC using record linkage with both the TCR and the Births , Deaths , and Marriages registry . Incidence rates were calculated and ratios of rates were estimated using Poisson models . Results Relative to subjects in the lowest fat intake category , the odds ratios ( OR ) comparing cases and controls were OR = 0.76 ( 95 % CI : 0.56–1.03 ) for medium fat intake , and OR = 0.62 ( 95 % CI : 0.45–0.85 ) for high fat intake , with a significant ( p < 0.01 ) trend of reduced odds ratio with higher category dietary fat intake . Among cases , the incidence rate ratio ( IRR ) relative to those with lowest fat score was IRR = 0.72 ( 95 % CI : 0.50–1.03 ) for medium fat intake , and IRR = 0.82 ( 95 % CI : 0.56–1.20 ) for highest fat intake ( linear trend p = 0.30 ) . Conclusion Using the same dietary instrument with two study design s in the same Caucasian population , we found no evidence that high fat intake increases the risk of developing melanoma or non-melanoma skin cancers . Instead , our results suggest a risk reduction for high fat intake We prospect ively investigated whether alcohol intake and smoking affect the risk of basal cell carcinoma ( BCC ) in subjects from the United States Radiological Technologists ( USRT ) cohort study . We evaluated 68,371 radiological technologists certified during 1926 - 1982 who were free of cancer at the time they answered a first question naire ( 1983 - 1989 ) and who completed a second question naire ( 1994 - 1998 ) . The first question naire provided baseline information on numerous risk factors , including smoking and alcohol intake , and the second provided self-reported cancer diagnoses . During 698,190 person-years of follow-up , we identified 1,360 cases of BCC : 1,036 in women and 324 in men . Cox proportional hazards regression indicated that the trend in BCC was significantly associated with increased alcohol intake ( P for trend = 0.001 ) . Compared with those who reported no alcohol consumption , those who drank < 1 - 2 , 3 - 6 , 7 - 14 , and > 14 drinks/week had multivariate risks of 1.1 [ 95 % confidence interval ( CI ) , 0.9 - 1.3 ] , 1.3 ( 95 % CI , 1.1 - 1.5 ) , 1.4 ( 95 % CI , 1.2 - 1.7 ) , and 1.0 ( 95 % CI , 0.7 - 1.6 ) , respectively . We found no clear association between smoking and BCC . This is the second large prospect i ve study to report a significant but nonmonotonic trend in increased risk associated with alcohol consumption The influence of polymorphism in the glutathione S-transferase , GSTM3 gene on susceptibility to cutaneous basal cell carcinoma ( BCC ) has been investigated . We have reported previously two GSTM3 alleles , GSTM3*A and GSTM3*B , distinguished by a recognition motif for the YY1 transcription factor in GSTM3*B. In this study , immunohistochemistry was used to identify GSTM3 expression in the epidermis of skin sample s from 11 controls and 9 patients with BCC . A PCR method was used to identify GSTM3*A and  GSTM3*B  and thereby the GSTM3 AA , GSTM3 AB , and GSTM3 BB genotypes  in 300 controls and 286 Caucasians with 1 - 35 primary BCCs . Genotypes at GSTM1 , GSTT1 , and the cytochrome P450 CYP1A1 and CYP2D6 loci were also determined . Frequencies of GSTM3 , GSTM1 , GSTT1 , CYP2D6 , and CYP1A1 genotypes in the cases and controls were not different . Dividing the BCC cases into groups of 92 patients with 1 lesion and 194 patients with 2 - 35 lesions showed that the frequencies of GSTM3 BB ( 2.6 % ) and GSTM1 A/B ( 1.3 % ) in the group with 2 - 35 tumors were almost significantly lower than in the group with 1 lesion ( 7.6 % , exact P = 0.0601 , chi 2(1 ) = 3.390 ; 6.5 % , exact P = 0.055 , chi 2(1 ) = 4.946 , respectively ) . Within the cases with 2 - 35 tumors , a Poisson regression model was used to identify genotypes , characteristics such as skin type , and interactions between genotypes and characteristics associated with increasing numbers of tumors . This showed , after correction for male gender and age , that GSTM3 AA was not associated with risk of increased numbers of tumors , although in combination with skin type 1 , GSTM1 null , and CYP1A1 m1m1 , the genotype did confer increased risk ( P < 0.001 , rate ratio , 2.058 ; P < 0.001 , rate ratio , 1.606 ; P < 0.001 , rate ratio , 1.470 respectively ) . The data suggest that , like other allelic GST , GSTM3 influences cancer risk . As GSTM3 AA was associated with increased tumor numbers , it appears that YY1 acts as an activator of the recognition motif in Objective To investigate the relationship between basal cell carcinoma ( BCC ) and antioxidant nutrients , specifically carotenoids , vitamin E and selenium . Methods The Nambour Skin Cancer Study is an ongoing , community-based study of r and omly selected adult residents of a township in sub-tropical Queensl and , Australia . Using a nested case – control design , incident cases of BCC ( n=90 ) were compared with age and sex matched controls ( n=90 ) .  Dietary exposure was measured using food frequency question naire estimates of intake as well as serum biomarkers . Other determinants of skin cancer including sun exposure were also considered . Dietary intakes were adjusted for energy intake , and serum carotenoids and vitamin E were adjusted for serum cholesterol . Odds ratios were calculated across quartiles of dietary intake and serum biomarkers and linear trends were assessed using logistic regression , adjusting for age , sex and supplement use . Results and conclusions In this prospect i ve study no significant associations were found between BCC and  carotenoids , vitamin E or selenium  , as measured by serum biomarkers or dietary intake , although there was a suggestion of a positive association with lutein intake Cutaneous basal cell carcinoma ( BCC ) risk is mediated by interactions between ultraviolet radiation ( UVR ) and host factors , including DNA repair efficiency . We investigated the association between BCC risk and SNPs in exon 6 ( c.466C > A , dbSNP238406:g . C > A ; design ated C/A156 ) , exon 10 ( c.932G > A , dbSNP1799793:g . G > A ; design ated G/A312 ) , and exon 23 ( c.2251A > C , dbSNP13181:g . A > C ; design ated A/C751 ) of the nucleotide excision repair gene , XPD ( ERCC2 ; excision repair cross‐complementing repair deficiency , complementation 2 [ xeroderma pigmentosum D ] ) . XPD genotype frequencies were not significantly different in 509 cases and 379 controls , although AA156 ( odds ratio [OR]=0.61 , 95 % confidence interval [CI]=0.37–1.01 , P=0.052 ) and AA312 ( OR=0.65 , 95 % CI=0.40–1.05 , P=0.08 ) were linked with reduced risk . A156–A312 and A156–A312–A751 haplotype frequencies however , were significantly lower in cases than controls ( OR=0.12 , 95 % CI=0.05–0.31 , P<0.001 ; OR=0.10 , 95 % CI=0.03–0.33 , P<0.001 ) . We confirmed the robustness of these findings by showing significant associations of the haplotypes with risk in two r and omly selected equal sized groups of cases and controls and , using the false positive report probability ( FPRP ) approach ( FPRP values<0.001 and < 0.004 , respectively ) . A156–A312 was similarly associated with reduced risk in subgroups , including cases with no family history of skin cancer , with only BCC on the head/neck , and those with a high rate of increase in BCC numbers . The association was not dependent on gender , age , or extent of UVR exposure . A156–A312 was found in 6.3 % of controls and the corresponding risk haplotype , C156–G312 ( OR=1.65 , 95 % CI=1.21–2.26 , P=0.002 ) in 35.4 % of controls . We interpret these data as showing that XPD SNP mediate susceptibility to BCC . Hum Mutat 25:353–359 , 2005 . © 2005 Wiley‐Liss , Experimental studies have consistently shown a protective effect of nonsteroidal antiinflammatory drugs ( NSAIDs ) against nonmelanoma skin cancers ( NMSC ) . However , little human epidemiological research has been done in this regard . We used data from the Skin Cancer Chemoprevention Study to explore the association of NSAID use and with the risk of basal‐cell carcinoma ( BCC ) and squamous‐cell carcinoma ( SCC ) . 1,805 subjects with a recent history of NMSC were r and omized to placebo or 50 mg of daily β‐carotene . Participants were asked about their use of over‐the‐counter and prescription medications at baseline and every 4 months during the trial . Skin follow‐up examinations were scheduled annually with a study dermatologist ; confirmed lesions were the endpoints in the study . We used a risk set approach to the analysis of grouped times survival data and unconditional logistic regression to compute odds ratios [ ORs ] for various exposures to NSAIDs . The use of NSAIDs was reported in over 50 % of question naires . For BCC , NSAIDs exhibited a weak protective effect in crude analyses , which attenuated markedly after adjustment . For SCC , the use of NSAIDs in the year previous to diagnosis reduced the odds by almost 30 % ( adjusted OR= 0.71 , 95 % CI 0.48–1.04 ) . When we accounted 
    Output:
    
Certain genomic alterations have been associated with increased or reduced risk for BCC development , with a second primary BCC or with recurrence of BCC .
Information review ed suggests that these predictors are of higher predictive value compared with biomarkers whilst they are indisputably cheaper and easier to monitor even in developing countries .