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Mathew C. Casimiro

Researcher at Thomas Jefferson University

Publications -  72
Citations -  6038

Mathew C. Casimiro is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Cyclin D1 & Cyclin D. The author has an hindex of 38, co-authored 69 publications receiving 5447 citations. Previous affiliations of Mathew C. Casimiro include Georgetown University & Georgetown University Medical Center.

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The reverse Warburg effect: Aerobic glycolysis in cancer associated fibroblasts and the tumor stroma

TL;DR: In this alternative model of tumorigenesis, the epithelial cancer cells instruct the normal stroma to transform into a wound-healing stroma, providing the necessary energy-rich micro-environment for facilitating tumor growth and angiogenesis, explaining its powerful predictive value.
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A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation

TL;DR: These studies identify a novel cyclin D1/miR-17/20 regulatory feedback loop through which cyclinD1 induces miR- 17-5p/mi R-20a and limits the proliferative function of cyclIn D1, thus linking expression of a specific miRNA cluster to the regulation of oncogenesis.
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The autophagic tumor stroma model of cancer: Role of oxidative stress and ketone production in fueling tumor cell metabolism

TL;DR: Transcriptional profiling of Cav-1 (-/-) stromal cells and human tumor stroma from breast cancer patients directly supported an association with oxidative stress, mitochondrial dysfunction, and autophagy/mitophagy, as well as ADMA and ketone production.
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Targeted disruption of the Kcnq1 gene produces a mouse model of Jervell and Lange– Nielsen Syndrome

TL;DR: In this paper, a line of transgenic mice that have a targeted disruption in the Kcnq1 gene was generated to generate a mouse model for JLNS, and behavioral analysis revealed that the mice are deaf and exhibit a shaker/waltzer phenotype.

Targeted disruption of the Kcnq1 gene produces a mouse model of Jervell and Lange

TL;DR: Data suggest that Kcnq1−/− mice are a potentially valuable animal model of JLNS, a disorder characterized by profound bilateral deafness and a cardiac phenotype caused by loss-of-function mutations in the human KCNQ1 gene.