Skip to main content
U.S. flag

An official website of the United States government

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites.

Search Publications by:

Search Title, Abstract, Conference, Citation, Keyword or Author
Displaying 26 - 50 of 123

Oxidatively-induced DNA damage and base excision repair in euthymic patients with bipolar disorder

May 1, 2018
Author(s)
Deniz Ceylan, Gamze Tuna, Guldal Kirkali, Zeliha Tunca, Gunes Can, Hidayet E. Arat, Melis Kant, Miral M. Dizdar, Aysegul Ozerdem
Oxidatively-induced DNA damage has previously been associated with bipolar disorder. More recently, impairments in DNA repair mechanisms have also been reported. We aimed to investigate oxidatively-induced DNA lesions and expression of DNA glycosylases

Small molecule inhibitors of DNA glycosylases as potential drugs in cancer therapy

August 31, 2017
Author(s)
M Miral Dizdar, Aaron C. Jacobs, Nathan Donley, Marcus J. Calkins, Ajit Jadhav, Dorjbal Dorjsuren, David Maloney, Anton Simeonov, Pawel Jaruga, Erdem Coskun, Amanda K. McCullough, R. S. Lloyd
Statement of the Problem: Most chemotherapeutic agents kill cancer cells by damaging DNA. Cancer cells overexpress DNA repair proteins and thus increase DNA repair capacity that can cause resistance to therapy by removing DNA lesions before they become

Enhancing the Efficacy of Cancer Therapy: Use of Small Molecule Inhibitors of DNA Glycosylases as Potential Drugs

March 12, 2017
Author(s)
Erdem Coskun, Aaron C. Jacobs, Nathan Donley, Marcus J. Calkins, Dorjbal Dorjsuren, David Maloney, Anton Simeonov, Pawel Jaruga, Amanda K. McCullough, M Miral Dizdar, R. S. Lloyd
Chemotherapy aims to destroy cancer cells by damaging their DNA. However, the overexpression of DNA repair proteins in cancer cells causes the removal of DNA lesions before they become toxic and thus leads to an increased DNA repair capacity resulting in

Repair of Oxidatively Induced DNA Damage by DNA Glycosylases

February 16, 2017
Author(s)
M Miral Dizdar, Erdem Coskun, Pawel Jaruga
Endogenous and exogenous reactive species cause oxidatively induced DNA damage in living organisms by a variety of mechanisms. As a result, a plethora of mutagenic and/or cytotoxic products are formed in cellular DNA. This type of DNA damage is repaired by

Oxidatively Induced DNA Damage and Its Repair

December 30, 2016
Author(s)
M Miral Dizdar
Endogenous and exogenous reactive species react with DNA in living organisms by numerous mechanisms and cause oxidatively induced DNA damage with multiple lesions. If not repaired, DNA lesions can cause genetic instability, leading to mutagenesis and cell

Enhanced Sensitivity of Neil1-/- Mice to Chronic UVB Exposure

December 1, 2016
Author(s)
M Miral Dizdar, Marcus J. Calkins, Vladimir Vartanian, Guldal Kirkali, Amanda K. McCullough, R. S. Lloyd, Pawel Jaruga
DNA base damage induced by oxidative stress and reactive oxygen species (ROS) are thought to be central mediators of ultraviolet light (UV)-induced carcinogenesis and skin aging. However, increased steady-state levels of ROS-induced DNA base damage have

Enhanced Sensitivity of Neil1-/- Mice to Chronic UVB Exposure

October 28, 2016
Author(s)
Pawel Jaruga, M Miral Dizdar, Marcus J. Calkins, Vladimir Vartanian, Amanda McCullough, R. S. Lloyd, Guldal Kirkali
Oxidative stress and oxidatively induced DNA base damage are central mediators of UV-induced carcinogenesis and skin aging. However, increased steady-state levels of oxidatively induced DNA base damage have not been reported after chronic UV exposure

Elevated urinary levels of 8-hydroxy-2-deoxyguanosine, (5R)- and (5S)-8,5-cyclo-2- deoxyadenosines, and 8-iso-prostaglandin F2? as potential biomarkers of oxidative stress in patients with prediabetes

September 26, 2016
Author(s)
M Miral Dizdar, Melis Kant, Merve Akis, Mehmet Calan, Tugba Arkan, Firat Bayraktar, Huray Islekel
Prediabetes is the preclinical stage of type 2 diabetes mellitus with intermediate state of hyperglycemia. Hyperglycemia results in a state of oxidative stress and that reactive oxygen species contribute to the production of insulin resistance, β-cell

Inhibition of DNA glycosylases in development of cancer therapeutics

September 4, 2016
Author(s)
M Miral Dizdar, Pawel Jaruga, Erdem Coskun, Marcus J. Calkins, Nathan Donley, Dorjbal Dorjsuren, Anton Simeonov, Amanda K. McCullough, R S. Lloyd, Ajit Jadhav
In cancer therapy, the efficacy of therapeutic agents may be influenced by increased DNA repair capacity. This may be due to overexpression of DNA repair proteins that repair therapy-induced DNA lesions in tumors before they become toxic. Inhibition of DNA

Measurement of DNA repair protein apurinic/apyrimidinic endonuclease 1 (APE1) in human tissues by liquid chromatography/tandem mass spectrometry with isotope dilution

June 5, 2016
Author(s)
Pawel Jaruga, Guldal Kirkali, Prasad T. Reddy, Alessandro Tona, Bryant C. Nelson, Li Mengxia, David M. Wilson III, Erdem Coskun, M Miral Dizdar
Introduction DNA repair proteins may be used as biomarkers in disease etiology and therapy. Thus, the accurate determination of DNA repair protein expression and genotype in human tissues is of fundamental importance. Apurinic/apyrimidinic endonuclease 1

DNA Damage and Repair in Cancer

May 26, 2016
Author(s)
M Miral Dizdar
Oxygen- and nitrogen-derived reactive species are constantly generated in living organisms by endogenous and exogenous sources. Reactions of reactive species such as free radicals with DNA cause the formation of multiple mutagenic and cytotoxic lesions

Combined Effects of High-Dose Bisphenol A and Oxidizing Agent (KBrO3) on Cellular Microenvironment, Gene Expression, and Chromatin Structure of Ku70-deficient Mouse Embryonic Fibroblasts

April 15, 2016
Author(s)
Erdem Coskun, Pawel Jaruga, Miral M. Dizdar, Natalie Gassman, Samuel Wilson
Background: Exposure to the environmental endocrine disrupting chemical bisphenol A (BPA) has been reported to alter global gene expression, induce epigenetic modifications, and interfere with the complex regulatory networks of cells. In addition to these

Inhibitors of DNA glycosylases as potential therapeutic drugs in cancer

April 4, 2016
Author(s)
M Miral Dizdar, Aaron C. Jacobs, Nathan Donley, Ajit Jadhav, Dorjbal Dorjsuren, David Maloney, Anton Simeonov, Pawel Jaruga, Erdem Coskun, Amanda K. McCullough, R. S. Lloyd
Ionizing radiation and most chemotherapeutic agents kill tumor cells by damaging DNA. The efficacy of DNA-damaging agents may be influenced by increased DNA repair capacity in tumors that results from overexpression of DNA repair proteins. Inhibition of

SMALL MOLECULE INHIBITORS OF DNA GLYCOSYLASES AS POTENTIAL DRUGS IN CHEMO- AND RADIOTHERAPIES

March 19, 2016
Author(s)
M Miral Dizdar, Aaron C. Jacobs, Nathan Donley, Marcus J. Calkins, Ajit Jadhav, Dorjbal Dorjsuren, David Maloney, Anton Simeonov, Amanda K. McCullough, R S. Lloyd, Erdem Coskun, Pawel Jaruga
Introduction: Ionizing radiation and most chemotherapeutic agents kill tumor cells by damag-ing DNA. The efficacy of DNA-damaging agents may be influenced by increased DNA repair capacity in tumors that results from overexpression of DNA repair proteins

GC-MS/MS Measurement of Nanomaterial Induced Genotoxicity in Isolated DNA

November 24, 2015
Author(s)
Bryant C. Nelson, Elijah J. Petersen, Pawel Jaruga, M Miral Dizdar
Making accurate measurements of the environmental fate and environmental and biological effects of engineered nanomaterials (ENMs) is critical for reliable risk assessment of these materials. ENM induced oxidative stress and/or direct binding of ENMs to

GC/MS Measurement of Nanomaterial Induced Genotoxicity in Isolated DNA

November 24, 2015
Author(s)
Bryant C. Nelson, Elijah J. Petersen, Pawel Jaruga, M Miral Dizdar
Making accurate measurements of the environmental fate and environmental and biological effects of engineered nanomaterials (ENMs) is critical for reliable risk assessment of these materials. ENM induced oxidative stress and/or direct binding of ENMs to

LC-MS/MS Measurement of Nanomaterial Induced Genotoxicity in Isolated DNA

November 24, 2015
Author(s)
Bryant C. Nelson, Elijah J. Petersen, Pawel Jaruga, M Miral Dizdar
Making accurate measurements of the environmental fate and environmental and biological effects of engineered nanomaterials (ENMs) is critical for reliable risk assessment of these materials. However, the unique behaviors of ENMs may cause artifacts in

MEASUREMENT OF DNA REPAIR PROTEINS IN RELATION TO DISEASE BIOMARKERS AND DRUG DEVELOPMENT

November 7, 2015
Author(s)
Erdem Coskun, Pawel Jaruga, Leona D. Scanlan, Alessandro Tona, Mark S. Lowenthal, Prasad T. Reddy, M Miral Dizdar, Ann-Sofie Jemth, Olga Loseva, Thomas Helleday
Introduction: In aerobic organisms, intracellular metabolism and exogenous sources such as ionizing radiation and carcinogenic compounds generate reactive species including free radicals derived from either oxygen or nitrogen. Oxidative stress thereby

DNA Extraction and DNA Damage Measurement in the Nematode Caenorhabditis elegans

November 1, 2015
Author(s)
Leona D. Scanlan, Pawel Jaruga, Sanem Hosbas Coskun, Jamie L. Almeida, David N. Catoe, Jennifer McDaniel, Miral M. Dizdar
Little is known about endogenous DNA damage in the nematode. In this work, we standardized the growth of the nematode in two different growth media (axenic CeHR supplemented with 20% milk and S-basal with E. coli), and developed a novel high-salt, phenol

Extreme expression of DNA repair protein apurinic/apyrimi-dinic endonuclease I (APE1) in human breast cancer as measured by liquid-chromatography isotope-dilution tandem mass spectrometry

September 15, 2015
Author(s)
Erdem Coskun, Pawel Jaruga, Prasad T. Reddy, Miral M. Dizdar
Apurinic/apyrimidinic endonuclease 1 (APE1) is a DNA re-pair protein and plays other important roles. Increased lev-els of APE1 in cancer have been reported. However, avail-able methods to measure APE1 levels are indirect and not quantitative. We
Was this page helpful?