K
Kathleen G. Dickman
Researcher at Stony Brook University
Publications - 40
Citations - 2285
Kathleen G. Dickman is an academic researcher from Stony Brook University. The author has contributed to research in topics: Aristolochic acid & Kidney metabolism. The author has an hindex of 21, co-authored 39 publications receiving 1956 citations. Previous affiliations of Kathleen G. Dickman include University of Minnesota & State University of New York System.
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Journal ArticleDOI
Aristolochic acid-associated urothelial cancer in Taiwan
Chung-Hsin Chen,Kathleen G. Dickman,Masaaki Moriya,Jiri Zavadil,Viktoriya S. Sidorenko,Karen L. Edwards,Dmitri V. Gnatenko,Lin Wu,Robert J. Turesky,Xue-Ru Wu,Yeong-Shiau Pu,Arthur P. Grollman +11 more
TL;DR: It is concluded that exposure to aristolochic acid contributes significantly to the incidence of UUC in Taiwan, a finding with significant implications for global public health.
Journal ArticleDOI
Mutational Signature of Aristolochic Acid Exposure as Revealed by Whole-Exome Sequencing
Margaret L. Hoang,Chung-Hsin Chen,Viktoriya S. Sidorenko,Jian He,Kathleen G. Dickman,Byeong Hwa Yun,Masaaki Moriya,Noushin Niknafs,Christopher Douville,Rachel Karchin,Robert J. Turesky,Yeong-Shiau Pu,Bert Vogelstein,Nickolas Papadopoulos,Arthur P. Grollman,Kenneth W. Kinzler,Thomas A. Rosenquist +16 more
TL;DR: A “molecular signature” of AA-induced DNA damage is presented, which helps to explain the mutagenic effects of AA and may also be useful as a way to detect unsuspected AA exposure as a cause of cancer.
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Aristolactam-DNA adducts are a biomarker of environmental exposure to aristolochic acid
Bojan Jelaković,Sandra Karanović,Ivana Vuković-Lela,Frederick W. Miller,Karen L. Edwards,Jovan Nikolic,Karla Tomić,Neda Slade,Branko Brdar,Robert J. Turesky,Želimir Stipančić,Damir Dittrich,Arthur P. Grollman,Kathleen G. Dickman +13 more
TL;DR: Dietary exposure to aristolochic acid is causally related to endemic nephropathy and carcinomas of the upper urinary tract and TP53 mutations in tumor tissues are identified by chip sequencing.
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Moderate Pulmonary Arterial Hypertension in Male Mice Lacking the Vasoactive Intestinal Peptide Gene
Sami I. Said,Sayyed A. Hamidi,Kathleen G. Dickman,Anthony M. Szema,Sergey Lyubsky,Richard Z. Lin,Ya-Ping Jiang,John J. Chen,James A. Waschek,Smadar Kort +9 more
TL;DR: Deletion of the VIP gene leads to spontaneous expression of moderately severe PAH in mice during air breathing, and the VIP−/− mouse should be useful for studying molecular mechanisms of PAH and evaluating potential therapeutic agents.
Journal ArticleDOI
Akt and c-Myc differentially activate cellular metabolic programs and prime cells to bioenergetic inhibition.
TL;DR: Although both Akt and c-Myc promote aerobic glycolysis, they differentially affect mitochondrial functions and render cells susceptible to the perturbation of cellular metabolic programs, a dual-regulatable FL5.12 pre-B cell line is established and the effect of these oncoproteins on cell metabolism in an isogenic background is compared.