31 Result(s)
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Charles W. M. Roberts
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Author Correction: Developmental origins shape the paediatric cancer genome
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Developmental origins shape the paediatric cancer genome
In the past two decades, technological advances have brought unprecedented insights into the paediatric cancer genome revealing characteristics distinct from those of adult cancer. Originating from develo** ...
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Author Correction: Targeting DCAF5 suppresses SMARCB1-mutant cancer by stabilizing SWI/SNF
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Targeting DCAF5 suppresses SMARCB1-mutant cancer by stabilizing SWI/SNF
Whereas oncogenes can potentially be inhibited with small molecules, the loss of tumour suppressors is more common and is problematic because the tumour-suppressor proteins are no longer present to be targeted...
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Mitotic bookmarking by SWI/SNF subunits
For cells to initiate and sustain a differentiated state, it is necessary that a ‘memory’ of this state is transmitted through mitosis to the daughter cells1–3. Mammalian switch/sucrose non-fermentable (SWI/SNF) ...
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cBAF complex components and MYC cooperate early in CD8+ T cell fate
The identification of mechanisms to promote memory T (Tmem) cells has important implications for vaccination and anti-cancer immunotherapy1–4. Using a CRISPR-based screen for negative regulators of Tmem cell gene...
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A first-generation pediatric cancer dependency map
Exciting therapeutic targets are emerging from CRISPR-based screens of high mutational-burden adult cancers. A key question, however, is whether functional genomic approaches will yield new targets in pediatri...
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Author Correction: PGBD5 promotes site-specific oncogenic mutations in human tumors
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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The SWI/SNF complex in cancer — biology, biomarkers and therapy
Cancer genome-sequencing studies have revealed a remarkably high prevalence of mutations in genes encoding subunits of the SWI/SNF chromatin-remodelling complexes, with nearly 25% of all cancers harbouring abe...
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Open AccessAuthor Correction: BRD9 defines a SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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Open AccessBRD9 defines a SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors
Bromodomain-containing protein 9 (BRD9) is a recently identified subunit of SWI/SNF(BAF) chromatin remodeling complexes, yet its function is poorly understood. Here, using a genome-wide CRISPR-Cas9 screen, we ...
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Mutational processes shape the landscape of TP53 mutations in human cancer
Unlike most tumor suppressor genes, the most common genetic alterations in tumor protein p53 (TP53) are missense mutations1,2. Mutant p53 protein is often abundantly expressed in cancers and specific allelic vari...
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Erratum: PGBD5 promotes site-specific oncogenic mutations in human tumors
Nat. Genet.; doi:10.1038/ng.3866; corrected online 24 May 2017 In the version of this article initially published online, the affiliations for Jiali Zhuang listed an incorrect present address instead of an equ...
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PGBD5 promotes site-specific oncogenic mutations in human tumors
Alex Kentsis and colleagues identify somatic genomic rearrangements in primary human rhabdoid tumors characterized by deletions and inversions involving PGBD5-specific signal sequences at their breakpoints. Th...
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Open AccessThe SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers
Genes encoding subunits of SWI/SNF (BAF) chromatin remodelling complexes are collectively altered in over 20% of human malignancies, but the mechanisms by which these complexes alter chromatin to modulate tran...
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ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice
Charles Roberts and colleagues show that deletion of Arid1a from mouse intestinal epithelium results in invasive adenocarcinomas resembling human colorectal cancer. They further show that ARID1A loss impairs SWI/...
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SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation
Charles Roberts, Peter Park, Bradley Bernstein and colleagues examine the consequences of SMARCB1 loss on enhancer landscapes in human rhabdoid tumors. They show that SMARCB1 is essential for the integrity and...
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Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer
Depletion of Smarcb1 activates the Myc network of signalling cascades, increasing protein metabolism and activation of survival pathways allowing highly aggressive Kras-independent pancreatic cancer cells to deve...
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Open AccessIntegrated genetic and pharmacologic interrogation of rare cancers
Identifying therapeutic targets in rare cancers remains challenging due to the paucity of established models to perform preclinical studies. As a proof-of-concept, we developed a patient-derived cancer cell li...
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Targeting EZH2 in cancer
Roberts and Kim discuss the mechanistic roles played by EZH2 in cancer as well as efforts to therapeutically target this epigenetic modifier.
