ReviewHuman genetics2009
Genetic risk factors for melanoma.
Review in Human genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
- Identification of a melanoma susceptibility locus and somatic mutation in TET2.Carcinogenesis · 2014Pooled it
- Genetic Landscape of Familial Melanoma.Genes · 2025Review
- Time-Dependent Effects of Low-Intensity Pulsed Ultrasound on Apoptosis and Autophagy in Malignant Melanoma Stem Cells.Journal of cellular and molecular medicine · 2025Article
- Non-coding RNAs in BRAF-mutant melanoma: targets, indicators, and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Article
- Review
- Phenotypic and Genetic Features that Differ Between Hereditary and Sporadic Melanoma: Results of a Preliminary Study from a Single Center from Turkey.Dermatology practical & conceptual · 2023Article
- Combination of Optical Biopsy with Patient Data for Improvement of Skin Tumor Identification.Diagnostics (Basel, Switzerland) · 2022Article
- Review
- Targeting CDK4/6 Represents a Therapeutic Vulnerability in Acquired BRAF/MEK Inhibitor-Resistant Melanoma.Molecular cancer therapeutics · 2021Article
- Inducible deletion of CDK4 and CDK6 - deciphering CDK4/6 inhibitor effects in the hematopoietic system.Haematologica · 2021Article
- The role of CDK6 in cancer.International journal of cancer · 2020Review
- Functional annotation of melanoma risk loci identifies novel susceptibility genes.Carcinogenesis · 2020Article
- Sphingolipid/Ceramide Pathways and Autophagy in the Onset and Progression of Melanoma: Novel Therapeutic Targets and Opportunities.International journal of molecular sciences · 2019Review
- The interplay of CDK4 and CDK6 in melanoma.Oncotarget · 2019Article
- From fish bowl to bedside: The power of zebrafish to unravel melanoma pathogenesis and discover new therapeutics.Pigment cell & melanoma research · 2017Review
- Childhood Body Size and the Risk of Malignant Melanoma in Adulthood.American journal of epidemiology · 2017Article
- Associations between childhood height and morphologically different variants of melanoma in adulthood.European journal of cancer (Oxford, England : 1990) · 2016Article
- Conceptual approach to early melanoma detection: models, tools, issues and challenges.Melanoma management · 2015Review
- Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma.Cancers · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetic basis of melanoma is complex and has both inherited and acquired components. Different genomic approaches have been used to identify a number of inherited risk factors, which can be stratified by penetrance and prevalence. Rare high-penetrance factors are expressed in familial clustering of melanoma and include mutations in CDKN2A (encoding p16(INK4a) and p14(ARF)) and CDK4. These genes are involved in cell-cycle arrest and melanocyte senescence and are nearly invariably targeted by somatic mutations during melanoma progression. Low-penetrance factors are common in the general population and include single-nucleotide polymorphisms in or near MC1R, ASIP, TYR and TYRP1. These genes are major determinants of hair and skin pigmentation, but their role in melanoma development remains unclear. This review describes the efforts that have led to the current understanding of melanoma susceptibility as the result of complex gene-gene and gene-environment interactions. Despite the significant advances, the majority of familial cases remain unaccounted for.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.