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Paul B. Fisher

Researcher at Virginia Commonwealth University

Publications -  486
Citations -  35304

Paul B. Fisher is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Cancer & Cancer cell. The author has an hindex of 80, co-authored 449 publications receiving 31149 citations. Previous affiliations of Paul B. Fisher include Discovery Institute & Columbia University Medical Center.

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Book ChapterDOI

Molecular-Genetic Imaging of Cancer

TL;DR: This chapter will provide an introduction to the components of molecular-genetic imaging and recent advances on each component leading to safe, efficient clinical applications for detecting cancer.
Journal ArticleDOI

MDA-9/Syntenin/SDCBP: new insights into a unique multifunctional scaffold protein

TL;DR: Melanoma differentiation associated gene-9 ( mda-9) (also known as Syntenin-1 and SDCBP (Syndecan binding protein)) was identified by subtraction hybridization as a novel gene displaying differential temporal expression during differentiation of melanoma.
Journal Article

Transfer of a dominant-acting tumor-inducing oncogene from human prostatic carcinoma cells to cloned rat embryo fibroblast cells by DNA-transfection.

TL;DR: The present study indicates that the human prostatic carcinoma cell line, LNCaP, contains a dominant-acting tumor-inducing oncogene which does not induce morphological transformation of CREF-Trans 6 or NIH-3T3 cells in monolayer culture.
Journal ArticleDOI

Adenovirus-mediated hPNPase(old-35) gene transfer as a therapeutic strategy for neuroblastoma.

TL;DR: The data demonstrate that efficient adenoviral transduction of neuroblastoma cells and robust transgene expression are feasible objectives, and suggest that combination with the PEG‐3 promoter holds promise for creating a potent and selective Neuroblastoma therapeutic.
Book ChapterDOI

New Insights Into Beclin-1: Evolution and Pan-Malignancy Inhibitor Activity.

TL;DR: Experimental evidence suggests that Beclin-1 inhibits tumor formation, angiogenesis, and metastasis alone and in cooperation with the tumor suppressive molecules UVRAG, Bif-1, Ambra1, and MDA-7/IL-24 via diverse mechanisms of action.