Increase in incidence rates of basal cell and squamous cell skin cancer in New Hampshire, USA

Karagas, Margaret R.; Greenberg, E. Robert; Spencer, Steven K.; Stukel, Thérèse A.; Mott, Leila A.

doi:10.1002/(sici)1097-0215(19990517)81:4<555::aid-ijc9>3.0.co;2-r

Cited by 289 publications

(247 citation statements)

References 22 publications

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“…12 Controls, derived from the New Hampshire Department of Transportation and Medicare enrollment lists, were frequency matched to cases on gender and age. Inclusion criteria included residence in New Hampshire, age between 25 and 74, and English speaking with a working telephone number.…”

Section: Study Populationmentioning

confidence: 99%

Cutaneous human papillomavirus infection, the EVER2 gene and incidence of squamous cell carcinoma: A case‐control study

Patel¹,

Pawlita

Waterboer

et al. 2008

Intl Journal of Cancer

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The first evidence of an association between HPV and non-melanoma skin cancer comes from patients with epidermodysplasia verruciformis (EV). EV is a rare heritable disease characterized by cutaneous warts that display not only a high rate of progression to squamous cell carcinoma on sun-exposed sites, but also a strong predisposition to infection by b-HPVs, for which HPV 5 and 8 predominate. Two EV genes (EVER1 and EVER2) have been identified, and we tested the hypothesis that variation in the EVER2 gene (rs7208422) is related to seropositivity to HPV (of the genus b types) and risk of squamous cell carcinoma in a population-based casecontrol study of SCC (n 5 239 cases and 432 controls). Among controls, variant genotype was associated with b-HPV seropositvity (OR 5 2.3, 95%CI 5 1.2-4.3), specifically HPV5 or 8 seropositivity (OR 5 2.4, 95%CI 5 1.1-5.1) and seropositivity for multiple b-HPV types (OR 5 2.7, 95%CI 5 1.1-6.6). Furthermore, variant genotype was also related to SCC risk [adjusted OR for homozygous variant versus homozygous wild type for the EVER2 polymorphism 1.7, 95% CI 1.1-2.7]. These data provide evidence for a role of genetic variation in the EVER2 gene in b-HPV infection and risk of SCC, shedding light on the link between HPVs and skin cancers. ' 2008 Wiley-Liss, Inc.Key words: human papillomavirus; skin cancer; EVER2The initial link between HPV and skin cancers was a rare autosomal inherited disease called Epidermodysplasia Verruciformis (EV) first described nearly a century ago.1 The disease is characterized by cutaneous lesions that display a high rate of progression to squamous cell carcinomas (SCCs) beginning in the second decade of life. Furthermore, EV patients experience diminished cell-mediated immunity possibly resulting in an observed susceptibility to infection by specific HPV types falling into the genus b, with HPV5 and HPV8 the most prevalent infections in this patient population. Genome-wide linkage studies were performed to map two EV loci 3,4 and to identify the EVER genes (EVER1 or EVER2, also referred to as TMC6 and TMC8, respectively) in one of these loci. 5The identification of EVER1 and EVER2 expressed sequence tags and cDNA from lymphoid tissue is consistent with a model in which EV mutations exert their direct effects in the immune system. It was recently discovered that 75% of EV patients studied have rare mutations in either of these adjacent, related, novel genes. To date, 10 truncating, loss of function mutations have been identified, 4 in EVER1 and 6 in EVER2 and were identified in EV patients from Algeria, Columbia, Poland and Japan.5 More recently, 5 additional mutations have been detected in the EVER genes supporting the hypothesis that EVER1 and EVER2 are the molecular basis of EV. [6][7][8] b-HPV DNA has been detected in up to 50% of SCC tumors from immunocompetent individuals and in up to 90% of lesions from immunocompromised individuals, 9,10 further emphasizing the role of host susceptibility in infection with these viruses. Recently, we reported that the ...

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Section: Study Populationmentioning

confidence: 99%

Cutaneous human papillomavirus infection, the EVER2 gene and incidence of squamous cell carcinoma: A case‐control study

Patel¹,

Pawlita

Waterboer

et al. 2008

Intl Journal of Cancer

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“…To identify cases for our study, we enlisted the collaboration of dermatologists and pathology laboratories throughout New Hampshire and bordering regions (Karagas et al, 1999). We selected a random sample of BCC cases (for efficiency) and all cases of invasive SCC diagnosed from July 1, 1993 through June 30, 1995 among New Hampshire residents, aged 25-74 years.…”

Section: Study Groupmentioning

confidence: 99%

Non-melanoma skin cancers and glucocorticoid therapy

et al. 2001

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Organ transplant recipients taking immunosuppressive drugs are at an estimated 65-fold greater risk of squamous cell carcinoma (SCC) and a 10-fold higher risk of basal cell carcinoma (BCC) (McCann, 1999). Agents used to prevent allograft rejection include cyclosporine or azathioprine, often combined with glucocorticoids. Systemic glucocorticoids alone (e.g., prednisone, prednisolone, dexamethasone and cortisone) are widely used for a variety of medical conditions including connective tissue diseases, musculoskeletal disorders and allergies. However, it is presently unknown whether these patients are at an increased risk of NMSC. Therefore, we examined the potential risks of SCC and BCC associated with glucocorticoid use in non-transplant recipients, as part of a population-based case-control study of NMSC conducted in New Hampshire, USA. MATERIALS AND METHODS Study groupTo identify cases for our study, we enlisted the collaboration of dermatologists and pathology laboratories throughout New Hampshire and bordering regions (Karagas et al, 1999). We selected a random sample of BCC cases (for efficiency) and all cases of invasive SCC diagnosed from July 1, 1993 through June 30, 1995 among New Hampshire residents, aged 25-74 years. The sample of BCC cases was drawn concomitantly with the SCC cases and controls, and stratified on anatomic site, age and gender to ensure representation of the entire group of BCC diagnoses. As of March 1996, we identified 1143 potential participants. One patient was not contacted at the physician's request, 31 (3%) were reported as deceased by a household member or physician, 10 (1%) lived in households in which no one answered after 40 attempts to telephone distributed over days, evenings and weekends, 178 (16%) declined participation and 27 (2%) were deemed mentally incompetent or too ill to take part. We interviewed a total of 603 BCC and 293 SCC cases.We chose controls from New Hampshire residents aged 25-74 years who were frequency-matched on age (25-34, 35-44, 45-54, 55-64, 65-69, 70-74 years) and gender to represent the combined distribution of the SCC and BCC cases. We selected controls (roughly equal in number to the number of BCC cases) from lists of New Hampshire residents provided by the New Hampshire Department of Transportation (for those less than 65 years old) and Health Care Financing Administration's Medicare Program (for those 65 years and older). For interviewing purposes, controls were randomly assigned reference dates comparable to the cases' diagnosis dates. Of the 820 potential controls, 12 (2%) were reported as deceased by a member of the household, for 12 (2%), no one answered in the household after 40 attempts to telephone distributed over days, evenings and weekends, 228 (28%) declined participation and 28 (3%) were deemed mentally incompetent or too ill to take part. We thus interviewed 540 controls for the study. Personal interviewAll participants provided informed consent in accordance with the Committee for the Protection of Human Subjects at Dartmouth ...

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“…NMSC cases were identified from an incident survey of all newly diagnosed BCC and SCC in New Hampshire (Karagas et al, 1999). Bladder cancer cases were identified by a rapid reporting system of the New Hampshire State Cancer Registry (Karagas et al, 1998).…”

Section: Study Populationmentioning

confidence: 99%

Microsatellite instability at tetranucleotide repeats in skin and bladder cancer

et al. 2002

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Recently, a novel form of MSI has been described that occurs only at tetranucleotide repeat markers. This has been termed elevated microsatellite instability at selected tetranucleotide repeats (EMAST). EMAST has been related to alterations of the p53 gene, and to the nature of the repeat sequence. We initially tested whether loss of heterozygosity (LOH) at the p53 and the patched (ptch) genes was related to EMAST in a series of 61 non-melanoma skin cancer (NMSC) tumors. We then analysed a series of 57 primary bladder cancers for the presence of EMAST, testing whether this was related to mutation or expression of the p53 gene. In both NMSC and bladder tumors we found a high prevalence of EMAST (75.4 and 43.9%). In NMSC the prevalence of EMAST was higher in tumors that had either p53 or ptch LOH, although the difference was not statistically significant. There was a significant association of extensive EMAST (three or more loci) with mutations in p53 among the bladder cancer tumors, but no indication of elevated EMAST in tumors with abnormal p53 staining without mutation. The association of EMAST with p53 mutation was confined to non-invasive disease. Hence, EMAST likely reflects a particular pattern of somatic events that are interactive with p53 mutation, particularly common in skin cancer and limited to non-invasive disease in bladder cancer.

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Increase in incidence rates of basal cell and squamous cell skin cancer in New Hampshire, USA

Cited by 289 publications

References 22 publications

Cutaneous human papillomavirus infection, the EVER2 gene and incidence of squamous cell carcinoma: A case‐control study

Cutaneous human papillomavirus infection, the EVER2 gene and incidence of squamous cell carcinoma: A case‐control study

Non-melanoma skin cancers and glucocorticoid therapy

Microsatellite instability at tetranucleotide repeats in skin and bladder cancer

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