ArticleThe Journal of investigative dermatology2008
Defective cell cycle checkpoint functions in melanoma are associated with altered patterns of gene expression.
Article in The Journal of investigative dermatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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
35 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Downregulation of Cyclin Kinase Inhibitors p16INK4a and p27 in Conjunctival Melanomas.Investigative ophthalmology & visual science · 2026Article
- A Novel Role for RNF126 in the Promotion of G2 Arrest via Interaction With 14-3-3σ.International journal of radiation oncology, biology, physics · 2022Article
- The Power of Fish Models to Elucidate Skin Cancer Pathogenesis and Impact the Discovery of New Therapeutic Opportunities.International journal of molecular sciences · 2018Review
- Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.Environmental and molecular mutagenesis · 2018Review
- The Adhesion G-Protein-Coupled Receptor, GPR56/ADGRG1, Inhibits Cell-Extracellular Matrix Signaling to Prevent Metastatic Melanoma Growth.Frontiers in oncology · 2018Article
- Mechanisms and prevention of UV-induced melanoma.Photodermatology, photoimmunology & photomedicine · 2018Review
- Synthetic lethality: emerging targets and opportunities in melanoma.Pigment cell & melanoma research · 2017Review
- Targeted deactivation of cancer-associated fibroblasts by β-catenin ablation suppresses melanoma growth.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Article
- Effective intra-S checkpoint responses to UVC in primary human melanocytes and melanoma cell lines.Pigment cell & melanoma research · 2016Article
- Article
- PLX4032 Mediated Melanoma Associated Antigen Potentiation in Patient Derived Primary Melanoma Cells.Journal of Cancer · 2015Article
- Nestin depletion induces melanoma matrix metalloproteinases and invasion.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- ERBB3 is required for metastasis formation of melanoma cells.Oncogenesis · 2014Article
- Mechanisms of chromosomal instability in melanoma.Environmental and molecular mutagenesis · 2014Article
- Development of DNA damage response signaling biomarkers using automated, quantitative image analysis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014Article
- Dominant effects of Δ40p53 on p53 function and melanoma cell fate.The Journal of investigative dermatology · 2014Article
- Article
- Is activation of the intra-S checkpoint in human fibroblasts an important factor in protection against UV-induced mutagenesis?Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
Defects in DNA damage responses may underlie genetic instability and malignant progression in melanoma. Cultures of normal human melanocytes (NHMs) and melanoma lines were analyzed to determine whether global patterns of gene expression could predict the efficacy of DNA damage cell cycle checkpoints that arrest growth and suppress genetic instability. NHMs displayed effective G1 and G2 checkpoint responses to ionizing radiation-induced DNA damage. A majority of melanoma cell lines (11/16) displayed significant quantitative defects in one or both checkpoints. Melanomas with B-RAF mutations as a class displayed a significant defect in DNA damage G2 checkpoint function. In contrast the epithelial-like subtype of melanomas with wild-type N-RAS and B-RAF alleles displayed an effective G2 checkpoint but a significant defect in G1 checkpoint function. RNA expression profiling revealed that melanoma lines with defects in the DNA damage G1 checkpoint displayed reduced expression of p53 transcriptional targets, such as CDKN1A and DDB2, and enhanced expression of proliferation-associated genes, such as CDC7 and GEMININ. A Bayesian analysis tool was more accurate than significance analysis of microarrays for predicting checkpoint function using a leave-one-out method. The results suggest that defects in DNA damage checkpoints may be recognized in melanomas through analysis of gene expression.
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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.