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Article ; Online: The emerging therapeutic landscape of relapsed/refractory multiple myeloma.

Tanenbaum, Benjamin / Miett, Timothy / Patel, Shyam A

2022 Volume 102, Issue 1, Page(s) 1–11

Abstract: From a historic lens, treatment for patients with relapsed/refractory multiple myeloma (R/R MM) has advanced significantly since the advent of immunomodulatory agents (IMiDs) in the 1990s, proteasome inhibitors in the 2000s, monoclonal antibodies in the ... ...

Abstract	From a historic lens, treatment for patients with relapsed/refractory multiple myeloma (R/R MM) has advanced significantly since the advent of immunomodulatory agents (IMiDs) in the 1990s, proteasome inhibitors in the 2000s, monoclonal antibodies in the 2010s, and CAR-T treatments in the 2020s. However, the availability of multiple new therapies has also created significant ambiguity regarding therapy selection and sequencing, as consensus guidelines are limited, and cross-trial comparisons of the novel agents are challenging. In this focused review, we discuss the novel Food & Drug Administration (FDA)-approved medications for R/R MM, including the recently approved first-in-class BCMA-directed bispecific antibody teclistamab. We highlight the seminal clinical trials data and discuss optimal sequencing considerations based on the goal of treatment, with an emphasis on the two novel CAR-T cell products. We consider the limited tolerability of certain agents, prospects for our aging population, and financial aspects of these therapies. Finally, we spotlight ongoing trials involving promising agents making their way through the pharmacologic pipeline including the BCMA-directed bispecific antibody elranatamab and the GPRC5D-directed bispecific antibody talquetamab. We summarize our recommendations based on the best available evidence as we enter 2023.
MeSH term(s)	Aged ; Humans ; Antibodies, Bispecific/therapeutic use ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Agents/therapeutic use ; B-Cell Maturation Antigen/therapeutic use ; Immunotherapy, Adoptive ; Multiple Myeloma/drug therapy ; Neoplasm Recurrence, Local/drug therapy ; Clinical Trials as Topic
Chemical Substances	Antibodies, Bispecific ; Antibodies, Monoclonal ; Antineoplastic Agents ; B-Cell Maturation Antigen
Language	English
Publishing date	2022-12-03
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1064950-5
ISSN	1432-0584 ; 0939-5555 ; 0945-8077
ISSN (online)	1432-0584
ISSN	0939-5555 ; 0945-8077
DOI	10.1007/s00277-022-05058-5
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Article ; Online: Protein interaction networks in the vasculature prioritize genes and pathways underlying coronary artery disease.

Zhu, Qiuyu Martin / Hsu, Yu-Han H / Lassen, Frederik H / MacDonald, Bryan T / Stead, Stephanie / Malolepsza, Edyta / Kim, April / Li, Taibo / Mizoguchi, Taiji / Schenone, Monica / Guzman, Gaelen / Tanenbaum, Benjamin / Fornelos, Nadine / Carr, Steven A / Gupta, Rajat M / Ellinor, Patrick T / Lage, Kasper

Communications biology

2024 Volume 7, Issue 1, Page(s) 87

Abstract: Population-based association studies have identified many genetic risk loci for coronary artery disease (CAD), but it is often unclear how genes within these loci are linked to CAD. Here, we perform interaction proteomics for 11 CAD-risk genes to map ... ...

Abstract	Population-based association studies have identified many genetic risk loci for coronary artery disease (CAD), but it is often unclear how genes within these loci are linked to CAD. Here, we perform interaction proteomics for 11 CAD-risk genes to map their protein-protein interactions (PPIs) in human vascular cells and elucidate their roles in CAD. The resulting PPI networks contain interactions that are outside of known biology in the vasculature and are enriched for genes involved in immunity-related and arterial-wall-specific mechanisms. Several PPI networks derived from smooth muscle cells are significantly enriched for genetic variants associated with CAD and related vascular phenotypes. Furthermore, the networks identify 61 genes that are found in genetic loci associated with risk of CAD, prioritizing them as the causal candidates within these loci. These findings indicate that the PPI networks we have generated are a rich resource for guiding future research into the molecular pathogenesis of CAD.
MeSH term(s)	Humans ; Coronary Artery Disease/genetics ; Protein Interaction Maps ; Gene Regulatory Networks ; Genetic Loci ; Proteomics
Language	English
Publishing date	2024-01-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-05705-1
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Article ; Online: Identification of a Novel Regulator of Clostridioides difficile Cortex Formation.

Touchette, Megan H / Benito de la Puebla, Hector / Alves Feliciano, Carolina / Tanenbaum, Benjamin / Schenone, Monica / Carr, Steven A / Shen, Aimee

mSphere

2021 Volume 6, Issue 3, Page(s) e0021121

Abstract: Clostridioides difficile is a leading cause of health care-associated infections worldwide. These infections are transmitted by C. difficile's metabolically dormant, aerotolerant spore form. Functional spore formation depends on the assembly of two ... ...

Abstract	Clostridioides difficile is a leading cause of health care-associated infections worldwide. These infections are transmitted by C. difficile's metabolically dormant, aerotolerant spore form. Functional spore formation depends on the assembly of two protective layers, a thick layer of modified peptidoglycan known as the cortex layer and a multilayered proteinaceous meshwork known as the coat. We previously identified two spore morphogenetic proteins, SpoIVA and SipL, that are essential for recruiting coat proteins to the developing forespore and making functional spores. While SpoIVA and SipL directly interact, the identities of the proteins they recruit to the forespore remained unknown. Here, we used mass spectrometry-based affinity proteomics to identify proteins that interact with the SpoIVA-SipL complex. These analyses identified the
MeSH term(s)	Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Cell Wall/chemistry ; Cell Wall/genetics ; Cell Wall/physiology ; Clostridioides difficile/genetics ; Clostridioides difficile/physiology ; Gene Expression Regulation, Bacterial/genetics ; Gene Expression Regulation, Bacterial/physiology ; Mass Spectrometry/methods ; Peptidoglycan/genetics ; Peptidoglycan/metabolism ; Proteomics ; Spores, Bacterial/genetics ; Spores, Bacterial/growth & development
Chemical Substances	Bacterial Proteins ; Peptidoglycan
Language	English
Publishing date	2021-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-5042
ISSN (online)	2379-5042
DOI	10.1128/mSphere.00211-21
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Article ; Online: Prognostic heterogeneity and clonal dynamics within distinct subgroups of myelodysplastic syndrome and acute myeloid leukemia with

Patel, Shyam A / Cerny, Jan / Gerber, William K / Ramanathan, Muthalagu / Ediriwickrema, Asiri / Tanenbaum, Benjamin / Hutchinson, Lloyd / Meng, Xiuling / Flahive, Julie / Barton, Bruce / Gillis-Smith, Andrew J / Suzuki, Sakiko / Khedr, Salwa / Selove, William / Higgins, Anne W / Miron, Patricia M / Simin, Karl / Woda, Bruce / Gerber, Jonathan M

EJHaem

2023 Volume 4, Issue 4, Page(s) 1059–1070

Abstract: ... ...

Abstract	TP53
Language	English
Publishing date	2023-09-11
Publishing country	United States
Document type	Journal Article
ISSN	2688-6146
ISSN (online)	2688-6146
DOI	10.1002/jha2.791
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Article ; Online: Using brain cell-type-specific protein interactomes to interpret neurodevelopmental genetic signals in schizophrenia.

Hsu, Yu-Han H / Pintacuda, Greta / Liu, Ruize / Nacu, Eugeniu / Kim, April / Tsafou, Kalliopi / Petrossian, Natalie / Crotty, William / Suh, Jung Min / Riseman, Jackson / Martin, Jacqueline M / Biagini, Julia C / Mena, Daya / Ching, Joshua K T / Malolepsza, Edyta / Li, Taibo / Singh, Tarjinder / Ge, Tian / Egri, Shawn B /

Tanenbaum, Benjamin / Stanclift, Caroline R / Apffel, Annie M / Carr, Steven A / Schenone, Monica / Jaffe, Jake / Fornelos, Nadine / Huang, Hailiang / Eggan, Kevin C / Lage, Kasper

iScience

2023 Volume 26, Issue 5, Page(s) 106701

Abstract: Genetics have nominated many schizophrenia risk genes and identified convergent signals between schizophrenia and neurodevelopmental disorders. However, functional interpretation of the nominated genes in the relevant brain cell types is often lacking. ... ...

Abstract	Genetics have nominated many schizophrenia risk genes and identified convergent signals between schizophrenia and neurodevelopmental disorders. However, functional interpretation of the nominated genes in the relevant brain cell types is often lacking. We executed interaction proteomics for six schizophrenia risk genes that have also been implicated in neurodevelopment in human induced cortical neurons. The resulting protein network is enriched for common variant risk of schizophrenia in Europeans and East Asians, is down-regulated in layer 5/6 cortical neurons of individuals affected by schizophrenia, and can complement fine-mapping and eQTL data to prioritize additional genes in GWAS loci. A sub-network centered on HCN1 is enriched for common variant risk and contains proteins (HCN4 and AKAP11) enriched for rare protein-truncating mutations in individuals with schizophrenia and bipolar disorder. Our findings showcase brain cell-type-specific interactomes as an organizing framework to facilitate interpretation of genetic and transcriptomic data in schizophrenia and its related disorders.
Language	English
Publishing date	2023-04-18
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106701
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Article ; Online: STAG2 loss rewires oncogenic and developmental programs to promote metastasis in Ewing sarcoma.

Adane, Biniam / Alexe, Gabriela / Seong, Bo Kyung A / Lu, Diana / Hwang, Elizabeth E / Hnisz, Denes / Lareau, Caleb A / Ross, Linda / Lin, Shan / Dela Cruz, Filemon S / Richardson, Melissa / Weintraub, Abraham S / Wang, Sarah / Iniguez, Amanda Balboni / Dharia, Neekesh V / Conway, Amy Saur / Robichaud, Amanda L / Tanenbaum, Benjamin / Krill-Burger, John M /

Vazquez, Francisca / Schenone, Monica / Berman, Jason N / Kung, Andrew L / Carr, Steven A / Aryee, Martin J / Young, Richard A / Crompton, Brian D / Stegmaier, Kimberly

Cancer cell

2021 Volume 39, Issue 6, Page(s) 827–844.e10

Abstract: The core cohesin subunit STAG2 is recurrently mutated in Ewing sarcoma but its biological role is less clear. Here, we demonstrate that cohesin complexes containing STAG2 occupy enhancer and polycomb repressive complex (PRC2)-marked regulatory regions. ... ...

Abstract	The core cohesin subunit STAG2 is recurrently mutated in Ewing sarcoma but its biological role is less clear. Here, we demonstrate that cohesin complexes containing STAG2 occupy enhancer and polycomb repressive complex (PRC2)-marked regulatory regions. Genetic suppression of STAG2 leads to a compensatory increase in cohesin-STAG1 complexes, but not in enhancer-rich regions, and results in reprogramming of cis-chromatin interactions. Strikingly, in STAG2 knockout cells the oncogenic genetic program driven by the fusion transcription factor EWS/FLI1 was highly perturbed, in part due to altered enhancer-promoter contacts. Moreover, loss of STAG2 also disrupted PRC2-mediated regulation of gene expression. Combined, these transcriptional changes converged to modulate EWS/FLI1, migratory, and neurodevelopmental programs. Finally, consistent with clinical observations, functional studies revealed that loss of STAG2 enhances the metastatic potential of Ewing sarcoma xenografts. Our findings demonstrate that STAG2 mutations can alter chromatin architecture and transcriptional programs to promote an aggressive cancer phenotype.
MeSH term(s)	Animals ; Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Movement/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Enhancer Elements, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Mice, Inbred NOD ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oncogene Proteins, Fusion/genetics ; POU Domain Factors/genetics ; POU Domain Factors/metabolism ; Polycomb Repressive Complex 2/genetics ; Polycomb Repressive Complex 2/metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Protein c-fli-1/genetics ; RNA-Binding Protein EWS/genetics ; Sarcoma, Ewing/genetics ; Sarcoma, Ewing/pathology ; Xenograft Model Antitumor Assays ; Zebrafish/genetics ; Cohesins ; Mice
Chemical Substances	Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; EWS-FLI fusion protein ; Homeodomain Proteins ; Nuclear Proteins ; Oncogene Proteins, Fusion ; POU Domain Factors ; Proto-Oncogene Protein c-fli-1 ; RNA-Binding Protein EWS ; STAG1 protein, human ; STAG2 protein, human ; transcription factor Brn-2 ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2021-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2021.05.007
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article ; Online: SOX9 drives WNT pathway activation in prostate cancer.

Ma, Fen / Ye, Huihui / He, Housheng Hansen / Gerrin, Sean J / Chen, Sen / Tanenbaum, Benjamin A / Cai, Changmeng / Sowalsky, Adam G / He, Lingfeng / Wang, Hongyun / Balk, Steven P / Yuan, Xin

The Journal of clinical investigation

2016 Volume 126, Issue 5, Page(s) 1745–1758

Abstract: The transcription factor SOX9 is critical for prostate development, and dysregulation of SOX9 is implicated in prostate cancer (PCa). However, the SOX9-dependent genes and pathways involved in both normal and neoplastic prostate epithelium are largely ... ...

Abstract	The transcription factor SOX9 is critical for prostate development, and dysregulation of SOX9 is implicated in prostate cancer (PCa). However, the SOX9-dependent genes and pathways involved in both normal and neoplastic prostate epithelium are largely unknown. Here, we performed SOX9 ChIP sequencing analysis and transcriptome profiling of PCa cells and determined that SOX9 positively regulates multiple WNT pathway genes, including those encoding WNT receptors (frizzled [FZD] and lipoprotein receptor-related protein [LRP] family members) and the downstream β-catenin effector TCF4. Analyses of PCa xenografts and clinical samples both revealed an association between the expression of SOX9 and WNT pathway components in PCa. Finally, treatment of SOX9-expressing PCa cells with a WNT synthesis inhibitor (LGK974) reduced WNT pathway signaling in vitro and tumor growth in murine xenograft models. Together, our data indicate that SOX9 expression drives PCa by reactivating the WNT/β-catenin signaling that mediates ductal morphogenesis in fetal prostate and define a subgroup of patients who would benefit from WNT-targeted therapy.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Mice ; Mice, Nude ; Mice, SCID ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Pyrazines/pharmacology ; Pyridines/pharmacology ; SOX9 Transcription Factor/biosynthesis ; SOX9 Transcription Factor/genetics ; Transcription Factor 4 ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Wnt Signaling Pathway ; Xenograft Model Antitumor Assays
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; LGK974 ; Neoplasm Proteins ; Pyrazines ; Pyridines ; SOX9 Transcription Factor ; SOX9 protein, human ; TCF4 protein, human ; Transcription Factor 4 ; Transcription Factors
Language	English
Publishing date	2016-05-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI78815
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Article ; Online: Genome-scale analysis identifies paralog lethality as a vulnerability of chromosome 1p loss in cancer.

Viswanathan, Srinivas R / Nogueira, Marina F / Buss, Colin G / Krill-Burger, John M / Wawer, Mathias J / Malolepsza, Edyta / Berger, Ashton C / Choi, Peter S / Shih, Juliann / Taylor, Alison M / Tanenbaum, Benjamin / Pedamallu, Chandra Sekhar / Cherniack, Andrew D / Tamayo, Pablo / Strathdee, Craig A / Lage, Kasper / Carr, Steven A / Schenone, Monica / Bhatia, Sangeeta N /

Vazquez, Francisca / Tsherniak, Aviad / Hahn, William C / Meyerson, Matthew

Nature genetics

2018 Volume 50, Issue 7, Page(s) 937–943

Abstract: Functional redundancy shared by paralog genes may afford protection against genetic perturbations, but it can also result in genetic vulnerabilities due to mutual ... ...

Abstract	Functional redundancy shared by paralog genes may afford protection against genetic perturbations, but it can also result in genetic vulnerabilities due to mutual interdependency
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Nucleus/genetics ; Chromosomes, Human, Pair 1 ; Exons/genetics ; Female ; Gene Deletion ; HEK293 Cells ; Humans ; Karyopherins/genetics ; Mice ; Mice, Nude ; Neoplasms/genetics ; Nuclear Proteins/genetics ; RNA Splicing/genetics ; RNA, Small Interfering/genetics
Chemical Substances	Karyopherins ; Nuclear Proteins ; RNA, Small Interfering
Language	English
Publishing date	2018-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-018-0155-3
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Zs.A 3613: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: ZBTB33

Beauchamp, Ellen M / Leventhal, Matthew / Bernard, Elsa / Hoppe, Emma R / Todisco, Gabriele / Creignou, Maria / Gallì, Anna / Castellano, Cecilia A / McConkey, Marie / Tarun, Akansha / Wong, Waihay / Schenone, Monica / Stanclift, Caroline / Tanenbaum, Benjamin / Malolepsza, Edyta / Nilsson, Björn / Bick, Alexander G / Weinstock, Joshua S / Miller, Mendy /

Blood cancer discovery

2021 Volume 2, Issue 5, Page(s) 500–517

Abstract: Clonal hematopoiesis results from somatic mutations in cancer driver genes in hematopoietic stem cells. We sought to identify novel drivers of clonal expansion using an unbiased analysis of sequencing data from 84,683 persons and identified common ... ...

Abstract	Clonal hematopoiesis results from somatic mutations in cancer driver genes in hematopoietic stem cells. We sought to identify novel drivers of clonal expansion using an unbiased analysis of sequencing data from 84,683 persons and identified common mutations in the 5-methylcytosine reader,
MeSH term(s)	Animals ; Clonal Hematopoiesis ; Hematopoiesis/genetics ; Hematopoietic Stem Cells ; Humans ; Mice ; Myelodysplastic Syndromes/genetics ; RNA Splicing/genetics ; Transcription Factors/genetics
Chemical Substances	Transcription Factors ; Zbtb33 protein, mouse
Language	English
Publishing date	2021-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3028898-8
ISSN	2643-3249 ; 2643-3230
ISSN (online)	2643-3249
ISSN	2643-3230
DOI	10.1158/2643-3230.BCD-20-0224
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Article ; Online: Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma.

Bandopadhayay, Pratiti / Piccioni, Federica / O'Rourke, Ryan / Ho, Patricia / Gonzalez, Elizabeth M / Buchan, Graham / Qian, Kenin / Gionet, Gabrielle / Girard, Emily / Coxon, Margo / Rees, Matthew G / Brenan, Lisa / Dubois, Frank / Shapira, Ofer / Greenwald, Noah F / Pages, Melanie / Balboni Iniguez, Amanda / Paolella, Brenton R / Meng, Alice /

Sinai, Claire / Roti, Giovanni / Dharia, Neekesh V / Creech, Amanda / Tanenbaum, Benjamin / Khadka, Prasidda / Tracy, Adam / Tiv, Hong L / Hong, Andrew L / Coy, Shannon / Rashid, Rumana / Lin, Jia-Ren / Cowley, Glenn S / Lam, Fred C / Goodale, Amy / Lee, Yenarae / Schoolcraft, Kathleen / Vazquez, Francisca / Hahn, William C / Tsherniak, Aviad / Bradner, James E / Yaffe, Michael B / Milde, Till / Pfister, Stefan M / Qi, Jun / Schenone, Monica / Carr, Steven A / Ligon, Keith L / Kieran, Mark W / Santagata, Sandro / Olson, James M / Gokhale, Prafulla C / Jaffe, Jacob D / Root, David E / Stegmaier, Kimberly / Johannessen, Cory M / Beroukhim, Rameen

Nature communications

2019 Volume 10, Issue 1, Page(s) 2400

Abstract: BET-bromodomain inhibition (BETi) has shown pre-clinical promise for MYC-amplified medulloblastoma. However, the mechanisms for its action, and ultimately for resistance, have not been fully defined. Here, using a combination of expression profiling, ... ...

Abstract	BET-bromodomain inhibition (BETi) has shown pre-clinical promise for MYC-amplified medulloblastoma. However, the mechanisms for its action, and ultimately for resistance, have not been fully defined. Here, using a combination of expression profiling, genome-scale CRISPR/Cas9-mediated loss of function and ORF/cDNA driven rescue screens, and cell-based models of spontaneous resistance, we identify bHLH/homeobox transcription factors and cell-cycle regulators as key genes mediating BETi's response and resistance. Cells that acquire drug tolerance exhibit a more neuronally differentiated cell-state and expression of lineage-specific bHLH/homeobox transcription factors. However, they do not terminally differentiate, maintain expression of CCND2, and continue to cycle through S-phase. Moreover, CDK4/CDK6 inhibition delays acquisition of resistance. Therefore, our data provide insights about the mechanisms underlying BETi effects and the appearance of resistance and support the therapeutic use of combined cell-cycle inhibitors with BETi in MYC-amplified medulloblastoma.
MeSH term(s)	Animals ; Azepines/pharmacology ; Basic Helix-Loop-Helix Transcription Factors/drug effects ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; CRISPR-Cas Systems ; Cell Cycle/drug effects ; Cell Cycle Proteins/drug effects ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Lineage ; Cerebellar Neoplasms/drug therapy ; Cerebellar Neoplasms/genetics ; Cyclin D2/drug effects ; Cyclin D2/metabolism ; Cyclin-Dependent Kinase 4/antagonists & inhibitors ; Cyclin-Dependent Kinase 6/antagonists & inhibitors ; Drug Resistance, Neoplasm ; Gene Expression Profiling ; Humans ; Medulloblastoma/drug therapy ; Medulloblastoma/genetics ; Mice ; Neural Stem Cells/drug effects ; Neural Stem Cells/metabolism ; Neurogenesis/drug effects ; Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins c-myc/genetics ; S Phase/drug effects ; Triazoles/pharmacology
Chemical Substances	(+)-JQ1 compound ; Azepines ; Basic Helix-Loop-Helix Transcription Factors ; Cell Cycle Proteins ; Cyclin D2 ; MYC protein, human ; Proteins ; Proto-Oncogene Proteins c-myc ; Triazoles ; bromodomain and extra-terminal domain protein, human ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22)
Language	English
Publishing date	2019-06-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-10307-9
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