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Nucleotide excision repair deficiency in melanoma in response to UVA

Overview of attention for article published in Experimental Hematology & Oncology, February 2016
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Citations

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16 Dimensions

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39 Mendeley
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1 CiteULike
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Title
Nucleotide excision repair deficiency in melanoma in response to UVA
Published in
Experimental Hematology & Oncology, February 2016
DOI 10.1186/s40164-016-0035-4
Pubmed ID
Authors

Heather C. Murray, Vicki E. Maltby, Doug W. Smith, Nikola A. Bowden

Abstract

The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely characterised. UVA and UVB components of sunlight are implicated in melanomagenesis; however the majority of studies have focused on the effects of UVB and UVC light. Interestingly, melanoma tumour sequencing has revealed an overrepresentation of mutations signature of unrepaired UV-induced DNA damage. Repair of UVA-induced DNA damage is thought to occur primarily through the Nucleotide Excision Repair (NER) pathway, which recognises and repairs damage either coupled to transcription (Transcription Coupled Repair; TCR), or through global genome scanning (Global Genome Repair; GGR). Current literature suggests NER is deficient in melanoma, however the cause of this remains unknown; and whether reduced NER activity in response to UVA may be involved in melanoma development remains uncharacterised. In this study we aimed to determine if melanoma cells exhibit reduced levels of NER activity in response to UVA. Melanocyte and melanoma cell lines were UVA-irradiated, and DNA damage levels assessed by immunodetection of Cyclobutane Pyrimidine Dimer (CPD) and (6-4) Photoproduct [(6-4)PP] lesions. Expression of NER pathway components and p53 following UVA treatment was quantified by qPCR and western blot. UVA did not induce detectable induction of (6-4)PP lesions, consistent with previous studies. Repair of CPDs induced by UVA was initiated at 4 h and complete within 48 h in normal melanocytes, whereas repair initiation was delayed to 24 h and >40 % of lesions remained in melanoma cell lines at 48 h. This was coupled with a delayed and reduced induction of GGR component XPC in melanoma cells, independent of p53. These findings support that NER activity is reduced in melanoma cells due to deficient GGR. Further investigation into the role of NER in UVA-induced melanomagenesis is warranted and may have implications for melanoma treatment.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 39 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Poland 1 3%
Brazil 1 3%
Unknown 37 95%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 23%
Student > Bachelor 6 15%
Student > Doctoral Student 4 10%
Researcher 4 10%
Student > Master 3 8%
Other 8 21%
Unknown 5 13%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 16 41%
Agricultural and Biological Sciences 8 21%
Medicine and Dentistry 4 10%
Unspecified 2 5%
Neuroscience 2 5%
Other 2 5%
Unknown 5 13%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 April 2016.
All research outputs
#3,890,955
of 7,534,762 outputs
Outputs from Experimental Hematology & Oncology
#27
of 55 outputs
Outputs of similar age
#153,993
of 284,261 outputs
Outputs of similar age from Experimental Hematology & Oncology
#2
of 4 outputs
Altmetric has tracked 7,534,762 research outputs across all sources so far. This one is in the 27th percentile – i.e., 27% of other outputs scored the same or lower than it.
So far Altmetric has tracked 55 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.7. This one is in the 32nd percentile – i.e., 32% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 284,261 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 35th percentile – i.e., 35% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 4 others from the same source and published within six weeks on either side of this one. This one has scored higher than 2 of them.