ArticleThe Journal of investigative dermatology2015
KIT is a frequent target for epigenetic silencing in cutaneous melanoma.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
29 citing papers in PubMed, 46 citations in OpenAlex.
- Nilotinib in KIT-driven advanced melanoma: Results from the phase II single-arm NICAM trial.Cell reports. Medicine · 2024Trial
- Studies on the Critical Therapeutic Role of Artemisinin and its Derivatives in Melanoma: a Review of Preclinical Evidence.Current treatment options in oncology · 2025Review
- The Role of Tyrosine Kinase in Beauty and Skincare: A Comprehensive Review.Journal of cosmetic dermatology · 2025Review
- Review
- Gene Regulations upon Hydrogel-Mediated Drug Delivery Systems in Skin Cancers-An Overview.Gels (Basel, Switzerland) · 2022Review
- BRD9 inhibition promotes PUMA-dependent apoptosis and augments the effect of imatinib in gastrointestinal stromal tumors.Cell death & disease · 2021Article
- Article
- Transcriptional signatures underlying dynamic phenotypic switching and novel disease biomarkers in a linear cellular model of melanoma progression.Neoplasia (New York, N.Y.) · 2021Article
- Methylation multiplicity and its clinical values in cancer.Expert reviews in molecular medicine · 2021Review
- Identification of the EMT-Related Genes Signature for Predicting Occurrence and Progression in Thyroid Cancer.OncoTargets and therapy · 2021Article
- Overcoming Immune Evasion in Melanoma.International journal of molecular sciences · 2020Review
- Higher methylation subtype of malignant melanoma and its correlation with thicker progression and worse prognosis.Cancer medicine · 2020Article
- KIT and Melanoma: Biological Insights and Clinical Implications.Yonsei medical journal · 2020Review
- Identification ofG3 (Bethesda, Md.) · 2020Article
- Silencing of microRNA-517a induces oxidative stress injury in melanoma cells via inactivation of the JNK signaling pathway by upregulating CDKN1C.Cancer cell international · 2020Article
- Highly sensitive detection of DNA hypermethylation in melanoma cancer cells.Biosensors & bioelectronics · 2019Article
- miFAST: A novel and rapid microRNA target capture method.Molecular carcinogenesis · 2018Article
- Melanoma: Genetic Abnormalities, Tumor Progression, Clonal Evolution and Tumor Initiating Cells.Medical sciences (Basel, Switzerland) · 2017Review
- KIT Suppresses BRAFCancer research · 2017Article
- Simultaneous Profiling of DNA Mutation and Methylation by Melting Analysis Using Magnetoresistive Biosensor Array.ACS nano · 2017Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor tyrosine kinase KIT and its ligand, stem cell factor (SCF), are essential for the proliferation and survival of normal melanocytes. In melanomas arising on mucosal, acral, and chronically sun-damaged skin, activating KIT mutations have been identified as oncogenic drivers and potent therapeutic targets. Through an initial whole-genome screen for aberrant promoter methylation in melanoma, we identified the KIT promoter as a target for hypermethylation in 43/110 melanoma cell lines, and in 3/12 primary and 11/29 metastatic cutaneous melanomas. Methylation density at the KIT promoter correlated inversely with promoter activity in vitro and in vivo, and the expression of KIT was restored after treatment with the demethylating agent 5-aza-2'-deoxycytidine. Hypermethylation of KIT showed no direct or inverse correlations with well-documented melanoma drivers. Growth of melanoma cells in the presence of SCF led to reduced KIT expression and increased methylation density at the KIT promoter, suggesting that SCF may exert a selection pressure for the loss of KIT. The frequent loss of KIT in cutaneous melanoma by promoter hypermethylation suggests that distinct KIT signaling pathways have opposing roles in the pathogenesis of melanoma subtypes.
Indexed as
Identifiers
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.