Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.657283
Title: The genetics of cutaneous sensitivity to UVR
Author: Manson, C.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2005
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Abstract:
UVR is present in the sunlight that reaches the Earth, and can also be artificially produced. Artificial sources of UVR are used therapeutically, for the treatment of skin disease such as psoriasis. UVR is a source of DNA damage, and the major causative agent for the development of skin cancers. UV-induced DNA damage can be repaired by a number of DNA repair pathways, principally the nucleotide excision repair (NER) pathway and the base excision repair pathway (BER), preventing DNA lesions from becoming incorporated into the genome. Defects in the genes involved wit NER lead to three, rare, recessive syndromes: Xeroderma pigmentosum (XP), Cockayne’s Syndrome (CS) and Trichothiodystrophy (TTD). Individuals affected with any of these syndromes have varying degrees of photosensitivity, with XP patients also having a greater than 1000 fold increased risk of skin cancer. As UVR is one of the most frequently exposed to sources of DNA damage, and also used as a therapeutic reagent, it would be useful to have a genetic marker which might predict an individual’s response to UVR. Polymorphisms in the genes involved with the NER, BER and other repair pathways will be examined in this thesis, to determine if any are associated with sensitivity to UVR. Sensitivity to UVR will be determined as the level of erythema induced by an incremental range of UV doses in two independent study groups, of 74 and 31 individuals. Erythema will be measured using reflectance spectrophotometry, which is an analytical measure, rather than the widely used minimal erythemal dose (MED).
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.657283  DOI: Not available
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