M
Matthew R. Young
Researcher at National Institutes of Health
Publications - 62
Citations - 4781
Matthew R. Young is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Carcinogenesis & Tumor promotion. The author has an hindex of 35, co-authored 59 publications receiving 4321 citations. Previous affiliations of Matthew R. Young include Science Applications International Corporation.
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Journal ArticleDOI
Association of Arsenic-Induced Malignant Transformation with DNA Hypomethylation and Aberrant Gene Expression
Christopher Q. Zhao,Matthew R. Young,Bhalchandra A. Diwan,Timothy P. Coogan,Michael P. Waalkes +4 more
TL;DR: Results indicate arsenic can act as a carcinogen by inducing DNA hypomethylation, which in turn facilitates aberrant gene expression, and they constitute a tenable theory of mechanism in arsenic carcinogenesis.
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Transgenic mice demonstrate AP-1 (activator protein-1) transactivation is required for tumor promotion.
Matthew R. Young,Jian Jian Li,Jian Jian Li,Mercedes Rincon,Richard A. Flavell,B. K. Sathyanarayana,Rosemarie Hunziker,Rosemarie Hunziker,Nancy H. Colburn +8 more
TL;DR: It is concluded that transactivation of a subset of AP-1-dependent genes is required for tumor promotion and may be targeted for cancer prevention.
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Rapid Cancer Detection by Topically Spraying a γ-Glutamyltranspeptidase–Activated Fluorescent Probe
Yasuteru Urano,Masayo Sakabe,Nobuyuki Kosaka,Mikako Ogawa,Makoto Mitsunaga,Daisuke Asanuma,Mako Kamiya,Matthew R. Young,Tetsuo Nagano,Peter L. Choyke,Hisataka Kobayashi +10 more
TL;DR: A rapidly activatable, cancer-selective fluorescence imaging probe that fluoresces upon cleavage by a cancer-specific enzyme and can be used during surgical or endoscopic tumor removal procedures, and several other aminopeptidase–based reagents identified by the authors could help surgeons to track down tiny tumors dispersed throughout body cavities.
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Targeting AMPK for cancer prevention and treatment
TL;DR: The role of AMPK in regulating inflammation, metabolism, and other regulatory processes with an emphasis on cancer is reviewed and the potential for targeting AMPK to treat various types of cancer is discussed.
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Activator protein 1 (AP-1)– and nuclear factor κB (NF-κB)–dependent transcriptional events in carcinogenesis
TL;DR: It is demonstrated that AP-1 and NF-κB are both required for maintaining the transformed phenotypes where inhibition of either activity suppresses transformation response in JB6 cells as well as human keratinocytes and transgenic mouse.