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Mandy Madiredjo

Researcher at Netherlands Cancer Institute

Publications -  8
Citations -  3808

Mandy Madiredjo is an academic researcher from Netherlands Cancer Institute. The author has contributed to research in topics: RNA interference & Small hairpin RNA. The author has an hindex of 8, co-authored 8 publications receiving 3602 citations.

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A functional genetic approach identifies the PI3K pathway as a major determinant of trastuzumab resistance in breast cancer.

TL;DR: Assessment of PI3K pathway activation may provide a biomarker to identify patients unlikely to respond to trastuzumab-based therapy, and the combined analysis of PTEN and PIK3CA identified twice as many patients at increased risk for progression compared to PTEN alone.
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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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Human Immunodeficiency Virus Type 1 Escapes from RNA Interference-Mediated Inhibition

TL;DR: It is reported here that an siRNA directed against the viral Nef gene (siRNA-Nef) confers resistance to HIV-1 replication, and RNAi could become a realistic gene therapy approach with which to overcome the devastating effect of HIV- 1 on the immune system.
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The ubiquitin-specific protease USP28 is required for MYC stability

TL;DR: The MYC proto-oncogene encodes a transcription factor that has been implicated in the genesis of many human tumours and one of these genes encodes USP28, an ubiquitin-specific protease required for MYC stability in human tumour cells.
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An shRNA barcode screen provides insight into cancer cell vulnerability to MDM2 inhibitors

TL;DR: The results suggest that nutlin-3's tumor specificity may result from its ability to turn a cancer cell–specific property (activated DNA damage signaling3) into a weakness that can be exploited therapeutically.