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  • 2016SteelPhd

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Characterising the biological response to ultraviolet radiation

Research output: ThesisDoctoral Thesis

Unpublished

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Characterising the biological response to ultraviolet radiation. / Steel, Harriet.

Lancaster University, 2016. 320 p.

Research output: ThesisDoctoral Thesis

Harvard

Steel, H 2016, 'Characterising the biological response to ultraviolet radiation', PhD, Lancaster University.

APA

Vancouver

Steel H. Characterising the biological response to ultraviolet radiation. Lancaster University, 2016. 320 p.

Author

Steel, Harriet. / Characterising the biological response to ultraviolet radiation. Lancaster University, 2016. 320 p.

Bibtex

@phdthesis{c52af201cb364539b9f79fbc77ce9507,
title = "Characterising the biological response to ultraviolet radiation",
abstract = "Once considered fairly harmless due to its low energy UVA is now considered a class one carcinogen, the ability of UVA alone to induce Non-melanoma skin cancer is well accepted and although more controversial there is now significant evidence from epidemiological studies and animal models to suggest a role for UVA in the development of melanoma. Furthermore due to its high penetrance UVA is thought to play a larger role in photoaging than UVB.Despite this current sum protection methods assess UVA protection only as a ratio of UVA: UVB that is blocked by the sun cream. Therefore it is desirable to have a more biologically relevant method to assess UVA protection offered by a sun cream. The work in this thesis focuses on the identification of a robust biomarker of UVA exposure, with the aim to identify biomarkers of UVA that could be used to assess the protection offered by different sun creams in order to develop a method in assessing protection similar to SPF that is currently used for UVB.The primary focus was on looking at the DNA damage response following UVA irradiation, and the data presented here shows distinct differences in the mechanism underpinning the DNA damage response in directly irradiated cells and in the UVA bystander cells. The response following UVA has also been shown to be distinct to that following UVB irradiation, both in terms of the DDR and apoptosis induction.",
keywords = "Ultraviolet irradiation, DNA damage, Double-strand break, REPLICATION FORK PROGRESSION, ROS",
author = "Harriet Steel",
year = "2016",
language = "English",
publisher = "Lancaster University",
school = "Lancaster University",

}

RIS

TY - THES

T1 - Characterising the biological response to ultraviolet radiation

AU - Steel, Harriet

PY - 2016

Y1 - 2016

N2 - Once considered fairly harmless due to its low energy UVA is now considered a class one carcinogen, the ability of UVA alone to induce Non-melanoma skin cancer is well accepted and although more controversial there is now significant evidence from epidemiological studies and animal models to suggest a role for UVA in the development of melanoma. Furthermore due to its high penetrance UVA is thought to play a larger role in photoaging than UVB.Despite this current sum protection methods assess UVA protection only as a ratio of UVA: UVB that is blocked by the sun cream. Therefore it is desirable to have a more biologically relevant method to assess UVA protection offered by a sun cream. The work in this thesis focuses on the identification of a robust biomarker of UVA exposure, with the aim to identify biomarkers of UVA that could be used to assess the protection offered by different sun creams in order to develop a method in assessing protection similar to SPF that is currently used for UVB.The primary focus was on looking at the DNA damage response following UVA irradiation, and the data presented here shows distinct differences in the mechanism underpinning the DNA damage response in directly irradiated cells and in the UVA bystander cells. The response following UVA has also been shown to be distinct to that following UVB irradiation, both in terms of the DDR and apoptosis induction.

AB - Once considered fairly harmless due to its low energy UVA is now considered a class one carcinogen, the ability of UVA alone to induce Non-melanoma skin cancer is well accepted and although more controversial there is now significant evidence from epidemiological studies and animal models to suggest a role for UVA in the development of melanoma. Furthermore due to its high penetrance UVA is thought to play a larger role in photoaging than UVB.Despite this current sum protection methods assess UVA protection only as a ratio of UVA: UVB that is blocked by the sun cream. Therefore it is desirable to have a more biologically relevant method to assess UVA protection offered by a sun cream. The work in this thesis focuses on the identification of a robust biomarker of UVA exposure, with the aim to identify biomarkers of UVA that could be used to assess the protection offered by different sun creams in order to develop a method in assessing protection similar to SPF that is currently used for UVB.The primary focus was on looking at the DNA damage response following UVA irradiation, and the data presented here shows distinct differences in the mechanism underpinning the DNA damage response in directly irradiated cells and in the UVA bystander cells. The response following UVA has also been shown to be distinct to that following UVB irradiation, both in terms of the DDR and apoptosis induction.

KW - Ultraviolet irradiation

KW - DNA damage

KW - Double-strand break

KW - REPLICATION FORK PROGRESSION

KW - ROS

M3 - Doctoral Thesis

PB - Lancaster University

ER -