A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene.

By Ji Luo, Michael J. Emanuele, Danan Li, Chad Creighton, M. Schlabach, Thomas F. Westbrook, Kwok-kin Wong, Stephen J. Elledge. Cell, 2009

1,047 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a48d30b029e2799746a34ecde31cff054e58d9dd

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Citations in the corpus

Targeting the cancer kinome through polypharmacology (2010, neutral): “Three recent papers illustrate the power of large-scale RNAi screens to address this problem by looking for genes that are selectively required for the growth of tumour cells expressing an activated KRAS mutant 72–74 .”
Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of TNF-induced necrosis (2012, methodology): “protein ubiquination, and genes implicated in cancer as described (24).”
Prioritizing candidate disease genes by network-based boosting of genome-wide association data. (2011, background): “The second found genes acting as synthetic lethal interaction partners with oncogenic KRAS mutants expressed in a colorectal cancer cell line, screening for genes whose knockdown in the activated KRAS background resulted in cellular lethality (Luo et al. 2009).”
An interactive resource to identify cancer genetic and lineage dependencies targeted by small molecules (2013, methodology): “Exploiting oncogene-induced dependencies contrasts to a related approach based on targeting cellbiological ‘hallmarks’ common to cancers (Hanahan and Weinberg, 2011) without linking these ‘non-oncogene addictions’ to specific genomic alterations (Luo et al., 2009).”
HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers. (2012, neutral): “The Elledge lab recently conducted a whole-genome siRNA screen to identify genes that are required to maintain growth when cells are transformed with a malignantly activated Ras gene (Luo et al., 2009).”
The microcosmos of cancer (2012, background): “Such approaches have identified potential targets for KRAS -expressing tumour”
Multifaceted polo-like kinases: drug targets and antitargets for cancer therapy (2010, background): “A recent study used 74,905 retroviral short hairpin RNAs (shRNAs), targeting 32,293 transcripts, to identify the vulnerabilities of cancers that have oncogenic mutations in the small GTPase Ra”
A CRISPR Dropout Screen Identifies Genetic Vulnerabilities and Therapeutic Targets in Acute Myeloid Leukemia (2016, background): “Previously, this was typically conducted using RNA interference (RNAi) in the form of short interfering RNA (siRNA) or short hairpin RNA (shRNA) libraries (Boutros and Ahringer, 2008; Luo et al., 2009; Schlabach et al., 2008; Silva et al., 2008; Zuber et al., 2011).”
The pINDUCER lentiviral toolkit for inducible RNA interference in vitro and in vivo (2011, background): “To date, most studies have relied upon clonally derived isolates (9).”
RAS isoforms and mutations in cancer at a glance (2016, background): “…and glutamine metabolism), (v) unbiased genetic or chemical screens for synthetic lethal interactors (Barbie et al., 2009; Kumar et al., 2012; Luo et al., 2009; Sarthy et al., 2007; Scholl et al., 2009) and (vi) RNA interference (RNAi) of KRAS expression (Pecot et al., 2014; Xue et al.,…”
Shared and separate functions of polo-like kinases and aurora kinases in cancer (2010, background): “Most recently, tumour cell lines carrying a KRAS-G13D mutation were shown to be hypersensitive to inhibition of PLK1 (Ref”