about
Residual complexes containing SMARCA2 (BRM) underlie the oncogenic drive of SMARCA4 (BRG1) mutationTargeting EZH2 in cancerSWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2ARID1A mutations in cancer: another epigenetic tumor suppressor?Haploinsufficiency of Snf5 (integrase interactor 1) predisposes to malignant rhabdoid tumors in miceToward understanding and exploiting tumor heterogeneityIntegrated genetic and pharmacologic interrogation of rare cancersSMARCB1-mediated SWI/SNF complex function is essential for enhancer regulationARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice.The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancersEpigenetics and cancer without genomic instability.Inactivation of the Snf5 tumor suppressor stimulates cell cycle progression and cooperates with p53 loss in oncogenic transformation.Mechanisms by which SMARCB1 loss drives rhabdoid tumor growth.Exome sequencing of pleuropulmonary blastoma reveals frequent biallelic loss of TP53 and two hits in DICER1 resulting in retention of 5p-derived miRNA hairpin loop sequences.Fibroblast growth factor receptors as novel therapeutic targets in SNF5-deleted malignant rhabdoid tumorsFunctional epigenetics approach identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers.The SWI/SNF complex--chromatin and cancer.On the key role of secondary lymphoid organs in antiviral immune responses studied in alymphoplastic (aly/aly) and spleenless (Hox11(-)/-) mutant mice.Ezh2 regulates differentiation and function of natural killer cells through histone methyltransferase activityEpigenetics and cancer: altered chromatin remodeling via Snf5 loss leads to aberrant cell cycle regulation.Absence of oncogenic canonical pathway mutations in aggressive pediatric rhabdoid tumors.Establishment and characterization of MRT cell lines from genetically engineered mouse models and the influence of genetic background on their development.Oncogenesis caused by loss of the SNF5 tumor suppressor is dependent on activity of BRG1, the ATPase of the SWI/SNF chromatin remodeling complex.The role of SMARCB1/INI1 in development of rhabdoid tumor.CARMA: CARM1 methylation of SWI/SNF in breast cancer.SWI/SNF nucleosome remodellers and cancer.The SWI/SNF tumor suppressor complex: Regulation of promoter nucleosomes and beyond.Vulnerabilities of mutant SWI/SNF complexes in cancer.ARID1B is a specific vulnerability in ARID1A-mutant cancers.Loss of the tumor suppressor Snf5 leads to aberrant activation of the Hedgehog-Gli pathway.Multicenter Feasibility Study of Tumor Molecular Profiling to Inform Therapeutic Decisions in Advanced Pediatric Solid Tumors: The Individualized Cancer Therapy (iCat) Study.Functionally distinct patterns of nucleosome remodeling at enhancers in glucocorticoid-treated acute lymphoblastic leukemia.Renal Medullary Carcinoma: Establishing Standards in Practice.Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting.Loss of the epigenetic tumor suppressor SNF5 leads to cancer without genomic instability.Epigenetic inactivation of the tumor suppressor BIN1 drives proliferation of SNF5-deficient tumors.Activation of β-catenin/TCF targets following loss of the tumor suppressor SNF5.Molecular pathways: SWI/SNF (BAF) complexes are frequently mutated in cancer--mechanisms and potential therapeutic insights.CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2.Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer.
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description
researcher ORCID ID = 0000-0003-1135-1896
@en
wetenschapper
@nl
name
Charles W Roberts
@ast
Charles W Roberts
@en
Charles W Roberts
@es
Charles W Roberts
@nl
type
label
Charles W Roberts
@ast
Charles W Roberts
@en
Charles W Roberts
@es
Charles W Roberts
@nl
prefLabel
Charles W Roberts
@ast
Charles W Roberts
@en
Charles W Roberts
@es
Charles W Roberts
@nl
P108
P108
P31
P496
0000-0003-1135-1896