ArticleCancer research2010
Similar nucleotide excision repair capacity in melanocytes and melanoma cells.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 57 citations in OpenAlex.
- TREX1 degrades the 3' end of the small DNA oligonucleotide products of nucleotide excision repair in human cells.Nucleic acids research · 2022Article
- UVB mutagenesis differs inLife science alliance · 2021Article
- Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events.BMC genomics · 2021Article
- A Nobel-Winning Scientist: Aziz Sancar and the Impact of his Work on the Molecular Pathology of Neoplastic Diseases.Turk patoloji dergisi · 2021Review
- Solar ultraviolet-induced DNA damage response: Melanocytes story in transformation to environmental melanomagenesis.Environmental and molecular mutagenesis · 2020Review
- Multiple interaction nodes define the postreplication repair response to UV-induced DNA damage that is defective in melanomas and correlated with UV signature mutation load.Molecular oncology · 2020Article
- Mechanistic Study of TTF-1 Modulation of Cellular Sensitivity to Cisplatin.Scientific reports · 2019Article
- Chemoprotective Effects of Dietary Grape Powder on UVB Radiation-Mediated Skin Carcinogenesis in SKH-1 Hairless Mice.The Journal of investigative dermatology · 2019Article
- Spironolactone Depletes the XPB Protein and Inhibits DNA Damage Responses in UVB-Irradiated Human Skin.The Journal of investigative dermatology · 2019Article
- Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.Environmental and molecular mutagenesis · 2018Review
- The circadian clock regulates cisplatin-induced toxicity and tumor regression in melanoma mouse and human models.Oncotarget · 2018Article
- Simultaneous detection of nucleotide excision repair events and apoptosis-induced DNA fragmentation in genotoxin-treated cells.Scientific reports · 2018Article
- Mechanisms and prevention of UV-induced melanoma.Photodermatology, photoimmunology & photomedicine · 2018Review
- Dynamic maps of UV damage formation and repair for the human genome.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Targeting melanoma with front-line therapy does not abrogate Nodal-expressing tumor cells.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Impact of the Circadian Clock on UV-Induced DNA Damage Response and Photocarcinogenesis.Photochemistry and photobiology · 2017Review
- Repair of UVB-induced DNA damage is reduced in melanoma due to low XPC and global genome repair.Oncotarget · 2016Article
- Nucleotide excision repair by dual incisions in plants.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- ATR Kinase Inhibition Protects Non-cycling Cells from the Lethal Effects of DNA Damage and Transcription Stress.The Journal of biological chemistry · 2016Article
- Genome-wide kinetics of DNA excision repair in relation to chromatin state and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Sunlight UV exposure produces DNA photoproducts in skin that are repaired solely by nucleotide excision repair in humans. A significant fraction of melanomas are thought to result from UV-induced DNA damage that escapes repair; however, little evidence is available about the functional capacity of normal human melanocytes, malignant melanoma cells, and metastatic melanoma cells to repair UV-induced photoproducts in DNA. In this study, we measured nucleotide excision repair in both normal melanocytes and a panel of melanoma cell lines. Our results show that in 11 of 12 melanoma cell lines tested, UV photoproduct repair occurred as efficiently as in primary melanocytes. Importantly, repair capacity was not affected by mutation in the N-RAS or B-RAF oncogenes, nor was a difference observed between a highly metastatic melanoma cell line (A375SM) or its parental line (A375P). Lastly, we found that although p53 status contributed to photoproduct removal efficiency, its role did not seem to be mediated by enhanced expression or activity of DNA binding protein DDB2. We concluded that melanoma cells retain capacity for nucleotide excision repair, the loss of which probably does not commonly contribute to melanoma progression.
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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.