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003 OCoLC;

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007 cr bn|||||||||;

008 120529s2012 ncua ob 000 0 eng d;

035 a| (Sirsi) o794379237;

035 a| (OCoLC)794379237;

040 a| EREc| EREd| EREd| UtOrBLW;

049 a| EREE;

090 a| QH465;

100 1 a| Ferguson, Nicholas Foster.?| UNAUTHORIZED;

245 10 a| Analysis of complex DNA damage associated with tumor growth /c| by Nicholas Foster Ferguson.;

260 a| [Greenville, N.C.] :b| East Carolina University,c| 2012.;

300 a| 103 pages :b| illustrations (some color), digital, PDF file;

336 a| text2| rdacontent;

337 a| computer2| rdamedia;

338 a| online resource2| rdacarrier;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

502 b| M.S.c| East Carolina Universityd| 2012.;

500 a| Presented to the faculty of the Department of Biology.;

500 a| Advisor: Alexandros Georgakilas.;

500 a| Title from PDF t.p. (viewed July 16, 2012).;

520 3 a| The innate response of a fully functioning immune system's ability to recognize and react to the growth of a tumor by releasing reactive oxygen species (ROS) may lead to chronic inflammation in many cases. This chronic inflammation fueled by a healthy immune system will release enough ROS in unaffected areas that distant tissues begin to show signs of oxidatively induced stress. Focusing on this issue we analyzed tissues proximal and distal to tumor implantation sites of C57BL/6 mice. These mice were sacrificed two weeks into the developmental stages of the subcutaneous syngeneic grafts of either B16 melanoma or NSC-224131 Lewis lung carcinoma. A separate group had sterile phosphate buffer solution injected subcutaneously, to serve as the control in this experiment, and were sacrificed at the same time as their counterparts in the other two cohorts. This experiment focuses on the double strand breaks (DSB) and oxidatively induced non-DSB clustered lesions (OCDLs), analysis shows evidence of elevated levels of stated damage in tumor bearing mice when compared to age matched control cohort mice. Gel electrophoresis and number average length analysis (NALA) were able to determine the effect of tumor growth on tissues. The kidney was the most affected tissues due to the results that showed elevated susceptibility to ROS in the presence of either tumor. Epidemiological studies have established associations between oxidatively induced stress and the pathogenesis of diseases, specifically carcinogenesis in cases of chronic inflammation. Using OCDLs as biomarkers may prove to be essential to establishing a connection between oxidative stress mediating environments and tumor growth. This experiment will specifically focus on two prolific tumors and their initial interaction with a fully functioning immune system when compared to typical inflammatory responses, and the ability of a strong antioxidant to reduce the presence of ROS.;

504 a| Includes bibliographical references.;

650 0 a| DNA damage.=| ^A273441;

650 0 a| Inflammation.=| ^A79;

650 0 a| Tumors.=| ^A3233;

653 a| Biology;

700 1 a| Georgakilas, Alexandros G.=| ^A1114884;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/3830;

949 o| jgml;

994 a| C0b| ERE;

596 a| 1 4;

998 a| 3063772;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3063772-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 5/29/2012x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3063772-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 5/29/2012x| ETDz| HERESOURCE;

Analysis of complex DNA damage associated with tumor growth / by Nicholas Foster Ferguson.

Author/creator	Ferguson, Nicholas Foster
Other author	Georgakilas, Alexandros G.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Publication Info	[Greenville, N.C.] : East Carolina University, 2012.
Description	103 pages : illustrations (some color), digital, PDF file
Supplemental Content	Access via ScholarShip
Subjects	DNA damage. Inflammation. Tumors.

Summary	The innate response of a fully functioning immune system's ability to recognize and react to the growth of a tumor by releasing reactive oxygen species (ROS) may lead to chronic inflammation in many cases. This chronic inflammation fueled by a healthy immune system will release enough ROS in unaffected areas that distant tissues begin to show signs of oxidatively induced stress. Focusing on this issue we analyzed tissues proximal and distal to tumor implantation sites of C57BL/6 mice. These mice were sacrificed two weeks into the developmental stages of the subcutaneous syngeneic grafts of either B16 melanoma or NSC-224131 Lewis lung carcinoma. A separate group had sterile phosphate buffer solution injected subcutaneously, to serve as the control in this experiment, and were sacrificed at the same time as their counterparts in the other two cohorts. This experiment focuses on the double strand breaks (DSB) and oxidatively induced non-DSB clustered lesions (OCDLs), analysis shows evidence of elevated levels of stated damage in tumor bearing mice when compared to age matched control cohort mice. Gel electrophoresis and number average length analysis (NALA) were able to determine the effect of tumor growth on tissues. The kidney was the most affected tissues due to the results that showed elevated susceptibility to ROS in the presence of either tumor. Epidemiological studies have established associations between oxidatively induced stress and the pathogenesis of diseases, specifically carcinogenesis in cases of chronic inflammation. Using OCDLs as biomarkers may prove to be essential to establishing a connection between oxidative stress mediating environments and tumor growth. This experiment will specifically focus on two prolific tumors and their initial interaction with a fully functioning immune system when compared to typical inflammatory responses, and the ability of a strong antioxidant to reduce the presence of ROS.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Alexandros Georgakilas.
General note	Title from PDF t.p. (viewed July 16, 2012).
Dissertation note	M.S. East Carolina University 2012.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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