x
Filter:
Filters applied
- Melanoma
- CIRemove CI filter
- Open AccessRemove Open Access filter
Publication Date
Please choose a date range between 2018 and 2018.
Author
- Barrett, Jennifer H1
- Berry, Jacqueline L1
- Bishop, D Timothy1
- Brossard, Myriam1
- Brown, Kevin M1
- Bui, Minh1
- Cooke, Marcus S1
- Cust, Anne E1
- Demenais, Florence1
- Drummond, Martin1
- Farrar, Mark D1
- Goldstein, Alisa M1
- Hoggart, Clive1
- Hopper, John L1
- Iles, Mark M1
- Kanetsky, Peter A1
- Kift, Richard1
- Landi, Maria Teresa1
- Langton, Abigail K1
- Law, Matthew H1
- MacGregor, Stuart1
- Mann, Graham J1
- Newton-Bishop, Julia A1
- Osman, Joanne1
- Rhodes, Lesley E1
Keyword
- confidence interval2
- 25(OH)D1
- 25-hydroxyvitamin D1
- area under receiver operating characteristic curves1
- AUC1
- CPD1
- cyclobutane pyrimidine dimer1
- L*1
- MED1
- minimal erythema dose1
- net reclassification improvement1
- NRI1
- odds ratio1
- OR1
- SED1
- SEM1
- single nucleotide polymorphism1
- skin lightness1
- SNP1
- standard error of the mean1
- standard erythema dose1
Melanoma
2 Results
- Original Article Melanocytes/MelanomaOpen Access
Assessing the Incremental Contribution of Common Genomic Variants to Melanoma Risk Prediction in Two Population-Based Studies
Journal of Investigative DermatologyVol. 138Issue 12p2617–2624Published online: June 8, 2018- Anne E. Cust
- Martin Drummond
- Peter A. Kanetsky
- Australian Melanoma Family Study Investigators
- Leeds Case-Control Study Investigators
- Alisa M. Goldstein
- and others
Cited in Scopus: 34It is unclear to what degree genomic and traditional (phenotypic and environmental) risk factors overlap in their prediction of melanoma risk. We evaluated the incremental contribution of common genomic variants (in pigmentation, nevus, and other pathways) and their overlap with traditional risk factors, using data from two population-based case-control studies from Australia (n = 1,035) and the United Kingdom (n = 1,460) that used the same questionnaires. Polygenic risk scores were derived from 21 gene regions associated with melanoma and odds ratios from published meta-analyses. - Original Article PhotobiologyOpen Access
Fractional Sunburn Threshold UVR Doses Generate Equivalent Vitamin D and DNA Damage in Skin Types I–VI but with Epidermal DNA Damage Gradient Correlated to Skin Darkness
Journal of Investigative DermatologyVol. 138Issue 10p2244–2252Published online: May 3, 2018- Barbara B. Shih
- Mark D. Farrar
- Marcus S. Cooke
- Joanne Osman
- Abigail K. Langton
- Richard Kift
- and others
Cited in Scopus: 37Public health guidance recommends limiting sun exposure to sub-sunburn levels, but it is unknown whether these can gain vitamin D (for musculoskeletal health) while avoiding epidermal DNA damage (initiates skin cancer). Well-characterized healthy humans of all skin types (I–VI, lightest to darkest skin) were exposed to a low-dose series of solar simulated UVR of 20%–80% their individual sunburn threshold dose (minimal erythema dose). Significant UVR dose responses were seen for serum 25-hydroxyvitamin D and whole epidermal cyclobutane pyrimidine dimers (CPDs), with as little as 0.2 minimal erythema dose concurrently producing 25-hydroxyvitamin D and CPD.