ArticleNature genetics2005
Use of human tissue to assess the oncogenic activity of melanoma-associated mutations.
Article in Nature genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.
- TERT-CLPTM1L polymorphism rs401681 contributes to cancers risk: evidence from a meta-analysis based on 29 publications.PloS one · 2012Pooled it
- Leveraging genome-wide association studies to better understand the etiology of cancers.Cancer science · 2025Review
- Progress in construction of mouse models to investigate the pathogenesis and immune therapy of human hematological malignancy.Frontiers in immunology · 2023Review
- Conserved features of TERT promoter duplications reveal an activation mechanism that mimics hotspot mutations in cancer.Nature communications · 2022Article
- Endogenous DOPA inhibits melanoma through suppression of CHRM1 signaling.Science advances · 2022Article
- Nanotechnology Addressing Cutaneous Melanoma: The Italian Landscape.Pharmaceutics · 2021Review
- Comparative intravital imaging of human and rodent malaria sporozoites reveals the skin is not a species-specific barrier.EMBO molecular medicine · 2021Article
- Humanized Rodent Models for Cancer Research.Frontiers in oncology · 2020Review
- Human Immune System Mice With Autologous Tumor for Modeling Cancer Immunotherapies.Frontiers in immunology · 2020Review
- Lysosomes Support the Degradation, Signaling, and Mitochondrial Metabolism Necessary for Human Epidermal Differentiation.The Journal of investigative dermatology · 2018Article
- Article
- Pathology and genomics of pediatric melanoma: A critical reexamination and new insights.Pediatric blood & cancer · 2018Review
- Article
- Systematic Epigenomic Analysis Reveals Chromatin States Associated with Melanoma Progression.Cell reports · 2017Article
- Article
- Cross-species models of human melanoma.The Journal of pathology · 2016Review
- MEK plus PI3K/mTORC1/2 Therapeutic Efficacy Is Impacted by TP53 Mutation in Preclinical Models of Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- CDKN2B Loss Promotes Progression from Benign Melanocytic Nevus to Melanoma.Cancer discovery · 2015Article
- IQGAP1 and IQGAP3 Serve Individually Essential Roles in Normal Epidermal Homeostasis and Tumor Progression.The Journal of investigative dermatology · 2015Article
- Comparing in vivo pump-probe and multiphoton fluorescence microscopy of melanoma and pigmented lesions.Journal of biomedical optics · 2015Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple genetic alterations occur in melanoma, a lethal skin malignancy of increasing incidence. These include mutations that activate Ras and two of its effector cascades, Raf and phosphoinositide 3-kinase (PI3K). Induction of Ras and Raf can be caused by active N-Ras and B-Raf mutants as well as by gene amplification. Activation of PI3K pathway components occurs by PTEN loss and by AKT3 amplification. Melanomas also commonly show impairment of the p16(INK4A)-CDK4-Rb and ARF-HDM2-p53 tumor suppressor pathways. CDKN2A mutations can produce p16(INK4A) and ARF protein loss. Rb bypass can also occur through activating CDK4 mutations as well as by CDK4 amplification. In addition to ARF deletion, p53 pathway disruption can result from dominant negative TP53 mutations. TERT amplification also occurs in melanoma. The extent to which these mutations can induce human melanocytic neoplasia is unknown. Here we characterize pathways sufficient to generate human melanocytic neoplasia and show that genetically altered human tissue facilitates functional analysis of mutations observed in human tumors.
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.