Search Results - "Balboni Iniguez, Amanda"
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STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells
Published in eLife (08-01-2020)“…Alterations involving serine-threonine phosphatase PP2A subunits occur in a range of human cancers, and partial loss of PP2A function contributes to cell…”
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EWS–FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma
Published in Nature (London) (15-03-2018)“…The EWS–FLI1 fusion protein, expressed in Ewing sarcoma, increases global transcription, causes accumulation of R loops and replication stress, and impairs…”
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Genome-scale CRISPR-Cas9 screen identifies druggable dependencies in TP53 wild-type Ewing sarcoma
Published in The Journal of experimental medicine (06-08-2018)“…Ewing sarcoma is a pediatric cancer driven by EWS-ETS transcription factor fusion oncoproteins in an otherwise stable genomic background. The majority of…”
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The synergy of BET inhibitors with aurora A kinase inhibitors in MYCN-amplified neuroblastoma is heightened with functional TP53
Published in Neoplasia (New York, N.Y.) (01-06-2021)“…Amplification of MYCN is a poor prognostic feature in neuroblastoma (NBL) indicating aggressive disease. We and others have shown BET bromodomain inhibitors…”
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Selective gene dependencies in MYCN-amplified neuroblastoma include the core transcriptional regulatory circuitry
Published in Nature genetics (01-09-2018)“…Childhood high-risk neuroblastomas with MYCN gene amplification are difficult to treat effectively 1 . This has focused attention on tumor-specific gene…”
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EWS/FLI Confers Tumor Cell Synthetic Lethality to CDK12 Inhibition in Ewing Sarcoma
Published in Cancer cell (12-02-2018)“…Many cancer types are driven by oncogenic transcription factors that have been difficult to drug. Transcriptional inhibitors, however, may offer inroads into…”
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Resistance to Epigenetic-Targeted Therapy Engenders Tumor Cell Vulnerabilities Associated with Enhancer Remodeling
Published in Cancer cell (10-12-2018)“…Drug resistance represents a major challenge to achieving durable responses to cancer therapeutics. Resistance mechanisms to epigenetically targeted drugs…”
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CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2
Published in The Journal of clinical investigation (02-01-2018)“…Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma,…”
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Structure-activity relationship study of THZ531 derivatives enables the discovery of BSJ-01-175 as a dual CDK12/13 covalent inhibitor with efficacy in Ewing sarcoma
Published in European journal of medicinal chemistry (05-10-2021)“…Development of inhibitors targeting CDK12/13 is of increasing interest as a potential therapy for cancers as these compounds inhibit transcription of DNA…”
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STAG2 loss rewires oncogenic and developmental programs to promote metastasis in Ewing sarcoma
Published in Cancer cell (14-06-2021)“…The core cohesin subunit STAG2 is recurrently mutated in Ewing sarcoma but its biological role is less clear. Here, we demonstrate that cohesin complexes…”
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Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma
Published in Nature communications (03-06-2019)“…BET-bromodomain inhibition (BETi) has shown pre-clinical promise for MYC-amplified medulloblastoma. However, the mechanisms for its action, and ultimately for…”
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EWSFLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma
Published in Nature (London) (15-03-2018)Get full text
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MEDU-36. BCL2 FAMILY MEMBERS ATTENUATE RESPONSE OF MYC-DRIVEN MEDULLOBLASTOMAS TO BET-BROMODOMAIN INHIBITION
Published in Neuro-oncology (Charlottesville, Va.) (23-04-2019)“…Abstract BACKGROUND: BET-bromodomain proteins bind to H3K27ac enhancers and recruit transcriptional proteins to facilitate the expression of genes. Inhibition…”
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Author Correction: EWS–FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma
Published in Nature (London) (01-07-2018)“…In this Letter, the sentence beginning “This work was funded….” in the Acknowledgements should have read “CPRIT (RP140105) to J.C.R.” rather than “CPRIT…”
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Abstract 2062: Selective gene dependencies in MYCN -amplified neuroblastoma include the core transcriptional regulatory circuitry
Published in Cancer research (Chicago, Ill.) (01-07-2018)“…Abstract Childhood neuroblastomas with MYCN gene amplification form a particularly high-risk subset of this disease and are difficult to treat effectively…”
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Abstract 2352: Defining a pediatric cancer dependency map
Published in Cancer research (Chicago, Ill.) (01-07-2018)“…Abstract Many children with metastatic or recurrent pediatric solid tumors continue to have poor survival, and there is an immense need to identify novel…”
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MEDU-37. NEURONAL DIFFERENTIATION AND CELL-CYCLE PROGRAMS MEDIATE RESPONSE AND RESISTANCE TO BET-BROMODOMAIN INHIBITION IN MYC-DRIVEN MEDULLOBLASTOMA
Published in Neuro-oncology (Charlottesville, Va.) (23-04-2019)“…Abstract BET-bromodomain inhibition (BETi) has shown pre-clinical promise for MYC-amplified medulloblastoma. However, the mechanisms for its action, and…”
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CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2
Published in The Journal of clinical investigation (01-01-2018)“…Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma,…”
Get full text
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