Table A1.
Author (Year) | Study Design | Size of Study Sample | Year(s) of Data Collection | Country | Analytic Model | Risk Measure | Variables in Final Model (1) |
---|---|---|---|---|---|---|---|
English and Armstrong (1988) [20] | Case-control study | 511 cases, 511 controls |
1980–1981 | Australia | Logistic regression | Risk score | Number of raised nevi on arms, age on arrival in Australia, mean time spent outdoors in summer aged 10–24, family history, personal history of non-melanoma skin cancer |
Garbe et al. (1989) [25] | Case-control study | 200 cases, 200 cases |
1987 | Germany | Logistic regression | Relative risks | Number of melanocytic common nevi, number of atypical nevi, actinic lentigines, occupational sun exposure, skin type |
MacKie et al. (1989) [30] | Case-control study | 280 cases, 280 controls |
1987 | Scotland | Logistic regression | Relative risk (risk groups) | Benign nevi >2 mm, freckling, atypical nevi >5 mm, episodes of severe sunburn |
Augustsson et al. (1991) [40] | Case-control study | 121 cases, 379 controls |
1986–1988 | Sweden | Logistic regression | Relative risks | Skin type, hair color, eye color, total body nevus ≥2 mm count, number of dysplastic nevi |
Marret et al. (1992) [32] | Case-control study | 583 cases, 608 controls |
1984–1986 | Canada | Logistic regression | Relative risk | Hair color, skin reaction to repeated sun exposure, freckle density, nevi density |
Garbe et al. (1994) [24] | Case-control study | 513 cases, 498 controls |
1990–1991 | Germany | Logistic regression | Relative risk estimates (risk groups) | Number of melanocytic common nevi, actinic lentigines, atypical nevi, skin type |
Barbini et al. (1998) [17] | Case-control study | 150 cases, 546 controls |
1992–1995 | Italy | Linear discriminant analysis | Risk score (negative score → low risk) | Colorimetric variables, Fitzpatrick |
Landi et al. (2001) [29] | Case-control study | 183 cases, 179 controls |
1994–1999 | Italy | Logistic regression | Odds ratios | Dysplastic nevi, skin color, tanning ability, eye color |
Harbauer e al. (2003) [28] | Case-control study | 202 cases, 202 controls |
2001 | Austria | Logistic regression | Odds ratios | Skin type, UV damage, number of nevi |
Dwyer et al. (2004) [19] | Case-control study | 244 cases, 483 controls |
1998–1999 | Australia | Logistic regression | Odds ratios | MC1R genotype, melanin density |
Fargnoli et al. (2004) [21] | Case-control study | 100 cases, 200 controls |
2000–2001 | Italy | Logistic regression | Relative risk estimates (high risk: ≥ 2 (3) risk factors in model 3 (1)) |
Model 1: Hair color, eye color, skin type Model 2: Hair color, eye color, skin type, occupational sun exposure, atypical nevi Model 3: Skin type, sun exposure, nevi, atypical nevi Model 4: Skin type, occupational sun exposure, nevi, atypical nevi |
Cho et al. (2005) [18] | Cohort study | 535 cases, total 178,155 |
1976, 1986, 1989 | United States | Gail method | Risk score and 10-years-absolute risk | Sex, age, family history, sunburns, number of nevi on arms, hair color |
Whiteman and Green (2005) [35] | Published case-control studies | NA | NA | Several countries | Not reported | 10-years absolute risk | Age, place of residence, number of melanocytic nevi, skin color, MC1R genotype |
Fears et al. (2006) [22] | Case-control study | 718 cases, 945 controls |
1991–1992 | United States | Gail method | 5-year-absolute risk (high risk: p ≥ 0.15%) | Sex, skin color, sunburns, number of moles >5 mm (only men), number of moles ≥2 mm, freckling, severe sun damage (only men), tanning ability (only women) |
Goldberg et al. (2007) [26] | Cohort study | 3329 cases, total 362,804 |
2001–2005 | United States | Logistic regression | Risk score (high risk: score 4–5) | Sex, regular dermatologist, history of previous melanoma, mole changing, age |
Fortes et al. (2010) [23] | Case-control study | 304 cases, 305 controls |
2001–2003 | Italy | Risk score was calculated using effect estimates from meta-analysis | Individual risk score (high risk: risk score ≥ 3) | Freckles in childhood, skin color, number of common nevi, hair color, sunburns in childhood |
Mar et al. (2011) [31] | Published meta-analysis and registry data | NA | NA | Australia | Gail method | 5-year-absolute risk | Common nevi, atypical nevi, freckles, hair color, family history, non-melanoma skin cancer, personal melanoma history |
Nielsen et al. (2011) [33] | Cohort study | 215 cases, total 29,520 |
1990–1992 (Followup: –2007) |
Sweden | Cox regression | Hazard ratios for each risk factor | Family history, number of nevi, hair color, sunbathing vacations, sunbed use |
Quéreux et al. (2011) [37] | Case-control study | 171 cases, 1390 controls |
2007 | France | Gail method, logistic regression and combinatorial analysis | Risk Score | Gail method: Sunburn in childhood, family history, number of common nevi on arms, density of freckles, skin type, recalled total sun exposure Logistic regression and combinatorial analysis: Sex, age, skin type, presence of freckles, number of nevi on arms, severe blistering sunburn in childhood, life in a country at low latitude, family history |
Williams et al. (2011) [36] | Case-control study | 386 cases, 727 controls |
1997 | United States | Logistic regression | Risk score (high risk: top 15%) | Sex, age, number of severe sunburns, hair color, freckles, number of raised moles, non-melanoma skin cancer history |
Guther et al. (2012) [27] | Cohort study | 250 cases, total 108,281 |
2005–2006 | Germany | Logistic regression | Risk score (high risk: >0.0034) | Age, hair color, personal history of melanoma, suspicious melanocytic lesions |
Smith et al. (2012) [39] | Case-control study | 923 cases, 813 controls |
Not reported | United States | Not reported | Not reported | Model A: Sex, age, hair color, eye color, mole count, freckling, family melanoma history Model B: Model A + outdoor UV, indoor UV, MC1R |
Bakos et al. (2013) [16] | Case-control study | 53 cases, 66 controls |
2005–2008 | Brazil | Risk score calculated using effect estimates from meta-analysis | Risk score (high risk: >3) |
Presence of freckles in childhood, skin color, eye color, hair color, sunburn episodes throughout life |
Cust et al. (2013) [45] | Case-control study | 413 cases, 263 controls |
2000–2002 | Australia | Logistic regression | Odds ratios | Base model: Age, sex, city Self-reported model: MC1R genotype, nevi, pigmentation score (2), sun and sunbed exposure (3), family history, non-melanoma skin cancer Physician-measured model: Nevi, MC1R genotype, non-melanoma skin cancer, solar lentigines, family history, pigmentation score (4) |
Fang et al. (2013) [59] | Multiple case-control studies | 2298 cases, 6652 controls |
NA | United States | Logistic regression | Odds ratios | Model 1: Single SNP Model 2: PRS (5) Model 3: Sex + age Model 4: Sex + age + pigmentation Model 5: Sex + age + pigmentation + PRS |
Stefanaki et al. (2013) [34] | Case-control study | 284 cases, 284 controls |
NA | Greece | Logistic regression | Odds ratios | Model A: Eye color, hair color, skin color, skin type, tanning, sunburns Model B: All predictors in model A + 3 strongest SNPs Model C: All predictors in model A + all SNPs |
Nikolic et al. (2014) [57] | Case-control study | 341 cases, 356 controls |
2001–2012 | Serbia | Logistic regression + decision tree | Absolute risk | Level of education, intermitted exposure, use of sunbeds, HCT, solar damage of skin, Fitzpatrick, hair color, eye color, number of common nevi, number of dysplastic nevi, congenital nevi |
Penn et al. (2014) [56] | Case-control study | 875 cases, 765 controls |
2004–2007 | United States | Logistic regression | Odds ratios | Base model: Age, sex, hair color, eye color, skin color, freckles, mole phenotype Full model: Base model + sun burns, indoors tanning, MC1R genotype |
Sneyd et al. (2014) [61] | Case-control study | 368 cases, 270 controls |
1992–1994 | New Zealand | Logistic regression + Gail method | 5-year-absolute risk |
Women: Skin color, 1st degree relative with large or unusual moles, number of moles, personal history of nonmelanoma skin cancer Men: Number of moles, personal history, age at diagnosis, occupation, birthplace |
Davies et al. (2015) [51] | Multiple case-control studies | NA | NA | Several countries | Logistic regression | Risk score (with risk categories) | Hair color, skin type, freckles, family history, nevi distribution, number of large nevi, sunburn |
Kypreou et al. (2016) [54] | Case-control study | 800 cases, 800 controls |
2000–2014 | Greece | Logistic regression | Odds ratios | Genetic risk score (6), age, sex, eye color, hair color, skin color, phototype, tanning ability |
Vuong et al. (2016) [49] | Case-control study | 629 cases, 535 controls |
2000–2002 | Australia | Gail method | 20-year-absolute risk | Hair color, nevi density, family history, personal history of non-melanoma skin cancer, sunbed use |
Cho et al. (2018) [58] | Cohort study | 422/289 cases (lifetime/incident melanoma); total 19,102 |
NA–2015 | United States | Logistic regression + Cox regression | Odds ratios and hazard ratios | Genetic risk score (7) |
Cust et al. (2018) [62] | Case-control study | 629 cases, 535 controls |
2000–2002 | Australia | Logistic regression | Odds ratios | Base model: Family history, hair color, nevi, personal history of non-melanoma skin cancer, sunburns in childhood, sunbed sessions, freckles, eye color, sun exposure Full model: Base model + PRS (8) |
Gu et al. (2018) [60] | Case-control study | 15,976 cases, 25,504 controls |
NA | Several countries | Logistic regression | 10- and 20-year-absolute risk | Model 1: Age, sex, country Model 2: (1) + eye color, hair color, skin type, common nevi Model 3: (1) + PRS (9) Model 4: (2) + PRS |
Hübner et al. (2018) [53] | Cohort study based on data from SCREEN project | 585 cases, total 354,635 |
2003–2004 | Germany | Logistic regression | Odds ratios | Sex, age, personal melanoma history, family history, multiple common nevi, atypical nevi, congenital nevi |
Olsen et al. (2018) [52] | Cohort study | 655 cases, total 41,954 |
2011–2014 | Australia | Cox regression | Hazard ratios |
Model 1 (invasive melanoma): Age, sex, tanning ability, moles at age 21, hair color, number of previous skin lesions treated destructively, sunscreen use Model 2 (all melanoma): (1) + ethnicity, private health insurance, family history, past history of excisions for skin cancer, skin checks in past 3 years |
Richter and Khoshgoftaar (2018) [55] | Cohort study based on EHR data | 17,246 cases, total 9,531,408 |
2011–2017 | United States | Logistic regression, decision tree + random forest | Risk score | Not reported |
Tagliabue et al. (2018) [46] | Case-control study | 3830 cases, 2619 controls |
NA | Several countries | Logistic regression | Odds ratios | Base model: Age, sex, sunburns, number of common nevi, RH-phenotype Base model + MC1R genotype |
Vuong et al. (2019) [50] | Case-control study | 461 cases, 329 controls |
2000–2002 | Australia | Logistic regression | Relative risks | Number of nevi, solar lentigines, hair color, personal history of keratinocytic cancer |
Abbreviations: UV = ultraviolet, MC1R = melanocortin 1 receptor, SNP = Single Nucleotide Polymorphism, PRS = Polygenic Risk Score, HCT = Hormonal Contraceptive Therapy, SCREEN = Skin Cancer Research to provide Evidence for Effectiveness of Screening in Northern Germany, EHR = Electronic Health Records, RH-Phenotype = Red Hair-Phenotype. (1) For studies with multiple models: Models included in analysis are highlighted in bold. (2) Score calculated from the variables: tanning ability, propensity to sunburn, skin color, eye color, hair color and freckles. (3) Term for the individual variables total childhood sun exposure, blistering sunburns and lifetime sunbed sessions. (4) Score was calculated from the following variables: hair color, eye color, skin reflectance, tanning ability, propensity to sunburn and freckles. (5) Comprised of 11 SNPs that demonstrated association with melanoma risk in previous studies. (6) Based on SNPs that showed genome-wide significant association with melanoma in previous studies. (7) Calculated using 21 genome-wide association study—significant SNPs. (8) Derived from 21 gene regions associated with melanoma. (9) Combines 204 common SNPs.