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DNA repair and arsenical skin cancer...
~
Wu, Meei-Maan.
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DNA repair and arsenical skin cancer: A case-control study in a blackfoot disease endemic area in Taiwan.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
DNA repair and arsenical skin cancer: A case-control study in a blackfoot disease endemic area in Taiwan./
作者:
Wu, Meei-Maan.
面頁冊數:
252 p.
附註:
Source: Dissertation Abstracts International, Volume: 58-04, Section: B, page: 1839.
Contained By:
Dissertation Abstracts International58-04B.
標題:
Public health. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9730811
ISBN:
9780591401288
DNA repair and arsenical skin cancer: A case-control study in a blackfoot disease endemic area in Taiwan.
Wu, Meei-Maan.
DNA repair and arsenical skin cancer: A case-control study in a blackfoot disease endemic area in Taiwan.
- 252 p.
Source: Dissertation Abstracts International, Volume: 58-04, Section: B, page: 1839.
Thesis (Ph.D.)--The Johns Hopkins University, 1997.
DNA repair deficiency has recently been suggested as a host susceptibility factor predisposing Caucasians to basal cell carcinoma of the skin when exposed to sunlight. In view of this finding, we are interested whether DNA repair deficiency can explain the differences in susceptibility to the risk of developing skin cancer associated with arsenic exposure. Arsenic has recently been shown to interfere with DNA repair activities in cell-culture studies, which supports the possible involvement of DNA repair in the etiology of arsenical skin carcinogenesis. This finding also suggests that DNA repair may be modulated by environmental exposures. The objectives of this study, therefore, were twofold. First, we want to determine if DNA repair capacity plays a role in the development of arsenical skin cancer. Second, we sought to determine the factors which are associated with DNA repair capacity.
ISBN: 9780591401288Subjects--Topical Terms:
534748
Public health.
DNA repair and arsenical skin cancer: A case-control study in a blackfoot disease endemic area in Taiwan.
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Source: Dissertation Abstracts International, Volume: 58-04, Section: B, page: 1839.
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Thesis (Ph.D.)--The Johns Hopkins University, 1997.
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DNA repair deficiency has recently been suggested as a host susceptibility factor predisposing Caucasians to basal cell carcinoma of the skin when exposed to sunlight. In view of this finding, we are interested whether DNA repair deficiency can explain the differences in susceptibility to the risk of developing skin cancer associated with arsenic exposure. Arsenic has recently been shown to interfere with DNA repair activities in cell-culture studies, which supports the possible involvement of DNA repair in the etiology of arsenical skin carcinogenesis. This finding also suggests that DNA repair may be modulated by environmental exposures. The objectives of this study, therefore, were twofold. First, we want to determine if DNA repair capacity plays a role in the development of arsenical skin cancer. Second, we sought to determine the factors which are associated with DNA repair capacity.
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To address the objectives of this study, a community-based case-control study was conducted. The study area centered on three villages located in a blackfoot disease (BFD) endemic area on the island of Taiwan, where skin cancer has been prevalent since the late 1950s. Cases were patients with clinically diagnosed skin cancer and controls were subjects without any cancers. Data collection, which included a questionnaire interview, a skin lesions examination, and the drawing of blood from each study subject, was performed at a screening clinic located in the study area. The blood sample was processed for lymphocytes isolation and were frozen in Taiwan. The collective frozen lymphocytes were then delivered to the United States, where tests of DNA repair capacity were carried out. A total of 304 study subjects, including 57 arsenical skin cancer patients and 247 noncancerous controls, were included in our study to analyze the risk factors associated with the development of arsenical skin cancer as well as their interactions with DNA repair capacity. In the analysis for the factors associated with DNA repair capacity, 53 arsenical skin cancer patients and 227 noncancerous controls were included and analyzed separately.
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It was found that low education level, cumulative arsenic exposure, and family history of any cancer in siblings were significant risk factors for the high risk of arsenical skin cancer. Aside from arsenic exposure, the associations of the risk factors with developing skin cancer were modified by the level of DNA repair capacity suggesting a synergistic or antagonistic interaction. Our data also show that residential village, cumulative arsenic exposure, particularly in the first ten years of life, and family history of any cancer in siblings were associated with low DNA repair level in the control group, but not in the cases. On the other hand, low education level, and tobacco use were found to be associated with low DNA repair level in the cases, but not in the controls. The mechanisms of interactions between low DNA repair capacity and the three risk factors and their implications in the development of arsenical skin cancer were discussed. (Abstract shortened by UMI.).
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