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Javad Golji

Researcher at Novartis

Publications -  15
Citations -  3388

Javad Golji is an academic researcher from Novartis. The author has contributed to research in topics: Cancer & Epigenomics. The author has an hindex of 7, co-authored 13 publications receiving 1896 citations.

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Next-generation characterization of the Cancer Cell Line Encyclopedia

Mahmoud Ghandi, +79 more
- 08 May 2019 - 
TL;DR: The original Cancer Cell Line Encyclopedia is expanded with deeper characterization of over 1,000 cell lines, including genomic, transcriptomic, and proteomic data, and integration with drug-sensitivity and gene-dependency data, which reveals potential targets for cancer drugs and associated biomarkers.
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Quantitative Proteomics of the Cancer Cell Line Encyclopedia

TL;DR: An analysis of microsatellite instable (MSI) cell lines reveals the dysregulation of specific protein complexes associated with surveillance of mutation and translation and these and other protein complexes were associated with sensitivity to knockdown of several different genes.
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Project DRIVE: A Compendium of Cancer Dependencies and Synthetic Lethal Relationships Uncovered by Large-Scale, Deep RNAi Screening

E. Robert McDonald, +99 more
- 27 Jul 2017 - 
TL;DR: A large-scale RNAi screen is conducted in which viability effects of mRNA knockdown were assessed for 7,837 genes using an average of 20 shRNAs per gene in 398 cancer cell lines, outlining the classes of cancer dependency genes and their relationships to genetic, expression, and lineage features.
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CRISPR screens provide a comprehensive assessment of cancer vulnerabilities but generate false-positive hits for highly amplified genomic regions

TL;DR: It is shown that CRISPR-based screens have a significantly lower false-negative rate compared with RNAi- based screens, but have specific liabilities particularly in the interrogation of regions of genome amplification, therefore, this study provides critical insights for applying CRISpr-based screening toward the systematic identification of new cancer targets.
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Tumor-derived IFN triggers chronic pathway agonism and sensitivity to ADAR loss.

TL;DR: The output of IFN signaling, specifically IFN-stimulated gene (ISG) signatures, in primary tumors from The Cancer Genome Atlas is characterized and it is shown that ISG transcriptional state creates a novel genetic vulnerability.