Data from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition Article Swipe
Alexandre Puissant
,
Stacey M. Frumm
,
Gabriela Alexe
,
Christopher F. Bassil
,
Jun Qi
,
Yvan H. Chanthery
,
Erin A. Nekritz
,
Rhamy Zeid
,
W. Clay Gustafson
,
Patricia Greninger
,
Matthew J. Garnett
,
Ultan McDermott
,
Cyril H. Benes
,
Andrew L. Kung
,
William A. Weiss
,
James E. Bradner
,
Kimberly Stegmaier
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.c.6546123.v1
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.c.6546123.v1
Bromodomain inhibition comprises a promising therapeutic strategy in cancer, particularly for hematologic malignancies. To date, however, genomic biomarkers to direct clinical translation have been lacking. We conducted a cell-based screen of genetically defined cancer cell lines using a prototypical inhibitor of BET bromodomains. Integration of genetic features with chemosensitivity data revealed a robust correlation between MYCN amplification and sensitivity to bromodomain inhibition. We characterized the mechanistic and translational significance of this finding in neuroblastoma, a childhood cancer with frequent amplification of MYCN. Genome-wide expression analysis showed downregulation of the MYCN transcriptional program accompanied by suppression of MYCN transcription. Functionally, bromodomain-mediated inhibition of MYCN impaired growth and induced apoptosis in neuroblastoma. BRD4 knockdown phenocopied these effects, establishing BET bromodomains as transcriptional regulators of MYCN. BET inhibition conferred a significant survival advantage in 3 in vivo neuroblastoma models, providing a compelling rationale for developing BET bromodomain inhibitors in patients with neuroblastoma.Significance: Biomarkers of response to small-molecule inhibitors of BET bromodomains, a new compound class with promising anticancer activity, have been lacking. Here, we reveal MYCN amplification as a strong genetic predictor of sensitivity to BET bromodomain inhibitors, show a mechanistic rationale for this finding, and provide a translational framework for clinical trial development of BET bromodomain inhibitors for pediatric patients with MYCN-amplified neuroblastoma. Cancer Discov; 3(3); 308–23. ©2012 AACR.See related commentary by Schnepp and Maris, p. 255This article is highlighted in the In This Issue feature, p. 239
Related Topics
Concepts
Bromodomain
Neuroblastoma
BRD4
Gene knockdown
Cancer research
BET inhibitor
Epigenetics
Biology
Downregulation and upregulation
Molecular biology
Genetics
Apoptosis
Cell culture
Gene
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/2159-8290.c.6546123.v1
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4362482598
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4362482598Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/2159-8290.c.6546123.v1Digital Object Identifier
- Title
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Data from Targeting MYCN in Neuroblastoma by BET Bromodomain InhibitionWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-04-03Full publication date if available
- Authors
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Alexandre Puissant, Stacey M. Frumm, Gabriela Alexe, Christopher F. Bassil, Jun Qi, Yvan H. Chanthery, Erin A. Nekritz, Rhamy Zeid, W. Clay Gustafson, Patricia Greninger, Matthew J. Garnett, Ultan McDermott, Cyril H. Benes, Andrew L. Kung, William A. Weiss, James E. Bradner, Kimberly StegmaierList of authors in order
- Landing page
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https://doi.org/10.1158/2159-8290.c.6546123.v1Publisher landing page
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://doi.org/10.1158/2159-8290.c.6546123.v1Direct OA link when available
- Concepts
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Bromodomain, Neuroblastoma, BRD4, Gene knockdown, Cancer research, BET inhibitor, Epigenetics, Biology, Downregulation and upregulation, Molecular biology, Genetics, Apoptosis, Cell culture, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.screen | 29 |
| abstract_inverted_index.showed | 85 |
| abstract_inverted_index.strong | 176 |
| abstract_inverted_index.©2012 | 215 |
| abstract_inverted_index.Discov; | 212 |
| abstract_inverted_index.Schnepp | 220 |
| abstract_inverted_index.article | 225 |
| abstract_inverted_index.between | 54 |
| abstract_inverted_index.cancer, | 8 |
| abstract_inverted_index.defined | 32 |
| abstract_inverted_index.finding | 71 |
| abstract_inverted_index.genetic | 45, 177 |
| abstract_inverted_index.genomic | 16 |
| abstract_inverted_index.induced | 106 |
| abstract_inverted_index.models, | 135 |
| abstract_inverted_index.program | 91 |
| abstract_inverted_index.provide | 193 |
| abstract_inverted_index.related | 217 |
| abstract_inverted_index.analysis | 84 |
| abstract_inverted_index.clinical | 20, 198 |
| abstract_inverted_index.compound | 160 |
| abstract_inverted_index.effects, | 114 |
| abstract_inverted_index.feature, | 233 |
| abstract_inverted_index.features | 46 |
| abstract_inverted_index.finding, | 191 |
| abstract_inverted_index.frequent | 78 |
| abstract_inverted_index.however, | 15 |
| abstract_inverted_index.impaired | 103 |
| abstract_inverted_index.lacking. | 24, 168 |
| abstract_inverted_index.patients | 146, 207 |
| abstract_inverted_index.response | 151 |
| abstract_inverted_index.revealed | 50 |
| abstract_inverted_index.strategy | 6 |
| abstract_inverted_index.survival | 128 |
| abstract_inverted_index.308–23. | 214 |
| abstract_inverted_index.activity, | 165 |
| abstract_inverted_index.advantage | 129 |
| abstract_inverted_index.apoptosis | 107 |
| abstract_inverted_index.childhood | 75 |
| abstract_inverted_index.comprises | 2 |
| abstract_inverted_index.conducted | 26 |
| abstract_inverted_index.conferred | 125 |
| abstract_inverted_index.framework | 196 |
| abstract_inverted_index.inhibitor | 39 |
| abstract_inverted_index.knockdown | 111 |
| abstract_inverted_index.pediatric | 206 |
| abstract_inverted_index.predictor | 178 |
| abstract_inverted_index.promising | 4, 163 |
| abstract_inverted_index.providing | 136 |
| abstract_inverted_index.rationale | 139, 188 |
| abstract_inverted_index.Biomarkers | 149 |
| abstract_inverted_index.anticancer | 164 |
| abstract_inverted_index.biomarkers | 17 |
| abstract_inverted_index.cell-based | 28 |
| abstract_inverted_index.commentary | 218 |
| abstract_inverted_index.compelling | 138 |
| abstract_inverted_index.developing | 141 |
| abstract_inverted_index.expression | 83 |
| abstract_inverted_index.inhibition | 1, 100, 124 |
| abstract_inverted_index.inhibitors | 144, 154, 204 |
| abstract_inverted_index.regulators | 120 |
| abstract_inverted_index.<i>in | 132 |
| abstract_inverted_index.Genome-wide | 82 |
| abstract_inverted_index.Integration | 43 |
| abstract_inverted_index.accompanied | 92 |
| abstract_inverted_index.bromodomain | 60, 143, 183, 203 |
| abstract_inverted_index.correlation | 53 |
| abstract_inverted_index.development | 200 |
| abstract_inverted_index.genetically | 31 |
| abstract_inverted_index.hematologic | 11 |
| abstract_inverted_index.highlighted | 227 |
| abstract_inverted_index.inhibition. | 61 |
| abstract_inverted_index.inhibitors, | 184 |
| abstract_inverted_index.mechanistic | 65, 187 |
| abstract_inverted_index.phenocopied | 112 |
| abstract_inverted_index.sensitivity | 58, 180 |
| abstract_inverted_index.significant | 127 |
| abstract_inverted_index.suppression | 94 |
| abstract_inverted_index.therapeutic | 5 |
| abstract_inverted_index.translation | 21 |
| abstract_inverted_index.bromodomains | 117 |
| abstract_inverted_index.establishing | 115 |
| abstract_inverted_index.particularly | 9 |
| abstract_inverted_index.prototypical | 38 |
| abstract_inverted_index.significance | 68 |
| abstract_inverted_index.Functionally, | 98 |
| abstract_inverted_index.amplification | 56, 79, 173 |
| abstract_inverted_index.bromodomains, | 157 |
| abstract_inverted_index.bromodomains. | 42 |
| abstract_inverted_index.characterized | 63 |
| abstract_inverted_index.malignancies. | 12 |
| abstract_inverted_index.neuroblastoma | 134 |
| abstract_inverted_index.translational | 67, 195 |
| abstract_inverted_index.downregulation | 86 |
| abstract_inverted_index.neuroblastoma, | 73 |
| abstract_inverted_index.neuroblastoma. | 109, 210 |
| abstract_inverted_index.small-molecule | 153 |
| abstract_inverted_index.transcription. | 97 |
| abstract_inverted_index.vivo</i> | 133 |
| abstract_inverted_index.<i>Cancer | 211 |
| abstract_inverted_index.transcriptional | 90, 119 |
| abstract_inverted_index.chemosensitivity | 48 |
| abstract_inverted_index.bromodomain-mediated | 99 |
| abstract_inverted_index.<i>MYCN</i> | 55, 96, 172 |
| abstract_inverted_index.<i>MYCN</i>. | 81, 122 |
| abstract_inverted_index.239</p></div> | 235 |
| abstract_inverted_index.255</p><p>This | 224 |
| abstract_inverted_index.<i>MYCN</i>-amplified | 209 |
| abstract_inverted_index.AACR.</i></p><p>See | 216 |
| abstract_inverted_index.<div>Abstract<p>Bromodomain | 0 |
| abstract_inverted_index.neuroblastoma.</p><p><b>Significance:</b> | 148 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 17 |
| citation_normalized_percentile.value | 0.1645348 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |