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Reuven Agami

Researcher at Netherlands Cancer Institute

Publications -  143
Citations -  25050

Reuven Agami is an academic researcher from Netherlands Cancer Institute. The author has contributed to research in topics: Gene & microRNA. The author has an hindex of 60, co-authored 129 publications receiving 23388 citations. Previous affiliations of Reuven Agami include Leiden University Medical Center & Rotterdam University of Applied Sciences.

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A System for Stable Expression of Short Interfering RNAs in Mammalian Cells

TL;DR: It is shown that siRNA expression mediated by this vector causes efficient and specific down-regulation of gene expression, resulting in functional inactivation of the targeted genes.
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A Genetic Screen Implicates miRNA-372 and miRNA-373 As Oncogenes in Testicular Germ Cell Tumors

TL;DR: It is provided evidence that these miRNAs are potential novel oncogenes participating in the development of human testicular germ cell tumors by numbing the p53 pathway, thus allowing tumorigenic growth in the presence of wild-type p53.
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Stable suppression of tumorigenicity by virus-mediated RNA interference.

TL;DR: Viral delivery of small interfering RNAs can be used for tumor-specific gene therapy to reverse the oncogenic phenotype of cancer cells, and this work uses a retroviral version of this vector to specifically and stably inhibit expression of only the onCogenic K-RAS(V12) allele in human tumor cells.
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A large-scale RNAi screen in human cells identifies new components of the p53 pathway

TL;DR: The construction of a set of retroviral vectors encoding 23,742 distinct shRNAs, which target 7,914 different human genes for suppression, is reported, which confers resistance to both p53-dependent and p19ARF-dependent proliferation arrest, and abolishes a DNA-damage-induced G1 cell-cycle arrest.
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The microRNAs miR-373 and miR-520c promote tumour invasion and metastasis

TL;DR: It is found that humanmiR-373 and miR-520c stimulated cancer cell migration and invasion in vitro and in vivo, and that certain cancer cell lines depend on endogenous miD-373 activity to migrate efficiently.