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David G. Ginzinger

Researcher at University of California, San Francisco

Publications -  60
Citations -  7747

David G. Ginzinger is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Cancer & Comparative genomic hybridization. The author has an hindex of 38, co-authored 59 publications receiving 7473 citations. Previous affiliations of David G. Ginzinger include University of British Columbia & Thermo Fisher Scientific.

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Gene quantification using real-time quantitative PCR: an emerging technology hits the mainstream.

TL;DR: The recent flood of reports using real-time Q-PCR testifies to the transformation of this technology from an experimental tool into the scientific mainstream and this review will help guide the reader through the variables that can limit the usefulness of thistechnology.
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miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells.

TL;DR: Investigation of the role of microRNAs in regulating the differentiation and proliferation of neural stem cells and glioblastoma-multiforme tumor cells suggests that targeted delivery of microRNA-124 and/or micro RNA-137 to gliobeasts tumor cells may be therapeutically efficacious for the treatment of this disease.
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Optimized high-throughput microRNA expression profiling provides novel biomarker assessment of clinical prostate and breast cancer biopsies

TL;DR: Findings demonstrate that optimized high-throughput microRNA expression profiling offers novel biomarker identification from typically small clinical samples such as breast and prostate cancer biopsies.
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Silk Properties Determined by Gland-Specific Expression of a Spider Fibroin Gene Family

TL;DR: A gene family from the spider Araneus diadematus was found to encode silk-forming proteins (fibroins) with different proportions of amorphous glycine-rich domains and crystal domains built from poly(alanine) and poly(glycine-alanine), which allows for a range of mechanical properties according to the crystal-forming potential of the constituent fibroins.
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Amplification of PVT1 Contributes to the Pathophysiology of Ovarian and Breast Cancer

TL;DR: The results suggest that MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities, and suggest that PVT 1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms.