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Displaying 51 - 75 of 239

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, (5’R)- and (5’S)-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