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Angelo M. De Marzo

Researcher at Johns Hopkins University School of Medicine

Publications -  401
Citations -  39287

Angelo M. De Marzo is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Prostate cancer & Prostate. The author has an hindex of 98, co-authored 368 publications receiving 34888 citations. Previous affiliations of Angelo M. De Marzo include Johns Hopkins University & University of Amsterdam.

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Journal Article

Overexpression of Hypoxia-inducible Factor 1α in Common Human Cancers and Their Metastases

TL;DR: The first clinical data indicating that HIF-1alpha may play an important role in human cancer progression are provided, indicating adaptations to a hypoxic microenvironment that are correlated with tumor invasion, metastasis, and lethality.
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c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.

TL;DR: In this paper, the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells.
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Inflammation in prostate carcinogenesis

TL;DR: Whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease, is determined by developing new experimental animal models coupled with classical Epidemiological studies, genetic epidemiological studies and molecular pathological approaches.
Journal Article

Abstract #LB-186: c-Myc suppression of miR-23 enhances mitochondrial glutaminase and glutamine metabolism

TL;DR: The c-Myc oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miB-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells, which leads to upregulation of glutamine catabolism.