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DNA damage accumulation in aging and...

Cabelof, Diane Cress.

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DNA damage accumulation in aging and cancer: A role for modulation of DNA repair capacity by caloric restriction.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	DNA damage accumulation in aging and cancer: A role for modulation of DNA repair capacity by caloric restriction./
作者:	Cabelof, Diane Cress.
面頁冊數:	215 p.
附註:	Adviser: Ahmad R. Heydari.
Contained By:	Dissertation Abstracts International63-03B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3047541
ISBN:	0493620311

DNA damage accumulation in aging and cancer: A role for modulation of DNA repair capacity by caloric restriction.
Cabelof, Diane Cress.

DNA damage accumulation in aging and cancer: A role for modulation of DNA repair capacity by caloric restriction. - 215 p.

Adviser: Ahmad R. Heydari.

Thesis (Ph.D.)--Wayne State University, 2002.

The data presented in this work are important in establishing a plausible biological explanation for the role of base excision repair (BER) in carcinogenesis. It is understood that genetic predisposition to disease is an important variable in determining susceptibility to disease. The particular problem with firmly establishing a role for BER in carcinogenesis is that this pathway repairs endogenous damage, and lesions that mimic such damages. In this research, I have shown that the β-pol heterozygous knockout mice express less β-pol mRNA and protein, and exhibit a 50% decline in BER activity as measured by an <italic>in vitro</italic> system. In addition this BER-deficient animal model shows more susceptibility to the effects of a usually well-tolerated carcinogen and demonstrates an accumulation of higher levels of spontaneous DNA damage. These findings are an important first step in delineating a role for the BER pathway in cancer development. Future investigation into the possibility that an inefficient BER system may become readily saturated may provide further insight into the molecular mechanisms of carcinogenesis.

ISBN: 0493620311Subjects--Topical Terms:

1017719
Biology, Molecular.

DNA damage accumulation in aging and cancer: A role for modulation of DNA repair capacity by caloric restriction.
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245 1 0 $a DNA damage accumulation in aging and cancer: A role for modulation of DNA repair capacity by caloric restriction.
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520 $a The data presented in this work are important in establishing a plausible biological explanation for the role of base excision repair (BER) in carcinogenesis. It is understood that genetic predisposition to disease is an important variable in determining susceptibility to disease. The particular problem with firmly establishing a role for BER in carcinogenesis is that this pathway repairs endogenous damage, and lesions that mimic such damages. In this research, I have shown that the β-pol heterozygous knockout mice express less β-pol mRNA and protein, and exhibit a 50% decline in BER activity as measured by an <italic>in vitro</italic> system. In addition this BER-deficient animal model shows more susceptibility to the effects of a usually well-tolerated carcinogen and demonstrates an accumulation of higher levels of spontaneous DNA damage. These findings are an important first step in delineating a role for the BER pathway in cancer development. Future investigation into the possibility that an inefficient BER system may become readily saturated may provide further insight into the molecular mechanisms of carcinogenesis.
520 $a Additionally, the role of caloric restriction (CR) in preventing cancer and delaying the onset of aging may be achieved through modulation of BER capacity. Data presented in this work demonstrate a reversal in the age-related decline of BER, and define a role for caloric restriction in the up-regulation of BER. It is exciting to consider that the CR reversal of the age-related BER decline may provide the beginnings of a mechanistic explanation for the life-extending effects of CR and the CR-induced up-regulation of BER in young animals may provide a mechanistic explanation for the anti-tumor effects of CR. While the life-extending and tumor-preventing effects of CR are often considered together, it is intriguing to consider that they may, in some ways, be distinct. In addition, the data presented in this work support a role for an improved ability of CR animals to tolerate exogenous stressors (i.e., carcinogens) which is likely important in both the aging and carcinogenesis processes.
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