EXTH-143. Preclinical Efficacy of Brain Penetrant, Single Agent Avapritinib in PDGFRA EcDNA-amplified Glioblastoma Article Swipe
Artem Berezovsky
,
Indrani Datta
,
Katherine Gurdziel
,
Andrea Transou
,
Susan M. Irtenkauf
,
Laura Hasselbach
,
Ruicong She
,
S. Rosenfeld
,
James M. Snyder
,
Laila Poisson
,
Ana C. deCarvalho
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noaf201.1474
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noaf201.1474
The high prevalence of platelet derived growth factor receptor alpha (PDGFRA) alterations and its mitogenic function in oligodendrocyte precursor cells (OPC) make PDGFRA a promising therapeutic target in adult glioblastoma (GBM). Towards validating PDGFRA as an essential driver of GBM tumor maintenance, we have isolated subpopulations from a patient-derived model (HF3253), harboring two alterations in PDGFRA: internal deletion leading to constitutive activation and extrachromosomal (ecDNA) amplification driving high copy number and heterogeneity. HF3253 symptom-free survival correlated with the initial frequency of PDGFRA ecDNA(+) population implanted; prolonged symptom-free survival was due to selection for initially low-frequency PDGFRA ecDNA(+) clones. Employing bulk and single-cell RNA sequencing, PDGFRA modulated a biphasic injury response/developmental transcriptional signature corresponding to hijacked functions of OPCs and CNS fibroblasts. Exploiting intra-tumoral heterogeneity, we have isolated single cell clones from bulk cells that exhibit diploid PDGFRA copy number, very low levels of PDGFRA mRNA and undetectable PDGFRA protein. Symptom-free survival was substantially increased in 4 ecDNA(-) clones compared to parental ecDNA(+) (Log rank p< 0.0001; n≥4/group). Rescue of wild-type PDGFRA by lentivirus in two ecDNA(-) populations decreased median survival by 50% in orthotopic xenograft relative to controls (log rank p = 0.3118, 0.0028; n=5/group). Avapritinib, a PDGFRA/KIT-selective kinase inhibitor, has shown promising efficacy in PDGFRA-mutated pediatric high-grade glioma. 5-week avapritinib (40 mg/kg) treatment abrogated HF3253 tumor growth by bioluminescent imaging. While treatment significantly improved survival compared to control in orthotopic male and female xenografts (log rank p=0.0047; n≥9/group), independent of sex (pairwise log rank p=0.232), PDGFRA+ tumors rapidly developed within two weeks of drug removal. Similar to 5-week treatment, continuous avapritinib therapy improved xenograft survival (log rank p > 0.0001; n≥8/group), increasing median survival by an additional 4 days in males. Our work validates PDGFRA ecDNA as a predictive biomarker for PDGFRA-targeted therapies and justifies the clinical implementation of avapritinib in the treatment of PDGFRA-altered brain tumors.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/neuonc/noaf201.1474
- https://academic.oup.com/neuro-oncology/article-pdf/27/Supplement_5/v372/65256222/noaf201.1474.pdf
- OA Status
- bronze
- OpenAlex ID
- https://openalex.org/W4416085436
All OpenAlex metadata
Raw OpenAlex JSON
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https://openalex.org/W4416085436Canonical identifier for this work in OpenAlex
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https://doi.org/10.1093/neuonc/noaf201.1474Digital Object Identifier
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EXTH-143. Preclinical Efficacy of Brain Penetrant, Single Agent Avapritinib in PDGFRA EcDNA-amplified GlioblastomaWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2025Year of publication
- Publication date
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2025-11-01Full publication date if available
- Authors
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Artem Berezovsky, Indrani Datta, Katherine Gurdziel, Andrea Transou, Susan M. Irtenkauf, Laura Hasselbach, Ruicong She, S. Rosenfeld, James M. Snyder, Laila Poisson, Ana C. deCarvalhoList of authors in order
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https://doi.org/10.1093/neuonc/noaf201.1474Publisher landing page
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https://academic.oup.com/neuro-oncology/article-pdf/27/Supplement_5/v372/65256222/noaf201.1474.pdfDirect link to full text PDF
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YesWhether a free full text is available
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bronzeOpen access status per OpenAlex
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https://academic.oup.com/neuro-oncology/article-pdf/27/Supplement_5/v372/65256222/noaf201.1474.pdfDirect OA link when available
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| abstract_inverted_index.rank | 164, 190, 237, 245, 268 |
| abstract_inverted_index.that | 134 |
| abstract_inverted_index.very | 140 |
| abstract_inverted_index.with | 77 |
| abstract_inverted_index.work | 284 |
| abstract_inverted_index.(OPC) | 21 |
| abstract_inverted_index.While | 222 |
| abstract_inverted_index.adult | 29 |
| abstract_inverted_index.alpha | 10 |
| abstract_inverted_index.brain | 307 |
| abstract_inverted_index.cells | 20, 133 |
| abstract_inverted_index.ecDNA | 287 |
| abstract_inverted_index.model | 50 |
| abstract_inverted_index.shown | 202 |
| abstract_inverted_index.tumor | 41, 217 |
| abstract_inverted_index.weeks | 253 |
| abstract_inverted_index.(GBM). | 31 |
| abstract_inverted_index.5-week | 210, 259 |
| abstract_inverted_index.HF3253 | 73, 216 |
| abstract_inverted_index.PDGFRA | 23, 34, 82, 96, 105, 137, 144, 148, 171, 286 |
| abstract_inverted_index.Rescue | 168 |
| abstract_inverted_index.clones | 130, 158 |
| abstract_inverted_index.driver | 38 |
| abstract_inverted_index.factor | 8 |
| abstract_inverted_index.female | 234 |
| abstract_inverted_index.growth | 7, 218 |
| abstract_inverted_index.injury | 109 |
| abstract_inverted_index.kinase | 199 |
| abstract_inverted_index.levels | 142 |
| abstract_inverted_index.males. | 282 |
| abstract_inverted_index.median | 179, 274 |
| abstract_inverted_index.mg/kg) | 213 |
| abstract_inverted_index.number | 70 |
| abstract_inverted_index.single | 128 |
| abstract_inverted_index.target | 27 |
| abstract_inverted_index.tumors | 248 |
| abstract_inverted_index.within | 251 |
| abstract_inverted_index.(ecDNA) | 65 |
| abstract_inverted_index.0.0001; | 166, 271 |
| abstract_inverted_index.0.0028; | 194 |
| abstract_inverted_index.0.3118, | 193 |
| abstract_inverted_index.PDGFRA+ | 247 |
| abstract_inverted_index.PDGFRA: | 56 |
| abstract_inverted_index.Similar | 257 |
| abstract_inverted_index.Towards | 32 |
| abstract_inverted_index.clones. | 98 |
| abstract_inverted_index.control | 229 |
| abstract_inverted_index.derived | 6 |
| abstract_inverted_index.diploid | 136 |
| abstract_inverted_index.driving | 67 |
| abstract_inverted_index.exhibit | 135 |
| abstract_inverted_index.glioma. | 209 |
| abstract_inverted_index.initial | 79 |
| abstract_inverted_index.leading | 59 |
| abstract_inverted_index.number, | 139 |
| abstract_inverted_index.rapidly | 249 |
| abstract_inverted_index.therapy | 263 |
| abstract_inverted_index.tumors. | 308 |
| abstract_inverted_index.&gt; | 270 |
| abstract_inverted_index.(PDGFRA) | 11 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.biphasic | 108 |
| abstract_inverted_index.clinical | 298 |
| abstract_inverted_index.compared | 159, 227 |
| abstract_inverted_index.controls | 188 |
| abstract_inverted_index.deletion | 58 |
| abstract_inverted_index.ecDNA(+) | 83, 97, 162 |
| abstract_inverted_index.ecDNA(-) | 157, 176 |
| abstract_inverted_index.efficacy | 204 |
| abstract_inverted_index.function | 16 |
| abstract_inverted_index.hijacked | 115 |
| abstract_inverted_index.imaging. | 221 |
| abstract_inverted_index.improved | 225, 264 |
| abstract_inverted_index.internal | 57 |
| abstract_inverted_index.isolated | 45, 127 |
| abstract_inverted_index.parental | 161 |
| abstract_inverted_index.platelet | 5 |
| abstract_inverted_index.protein. | 149 |
| abstract_inverted_index.receptor | 9 |
| abstract_inverted_index.relative | 186 |
| abstract_inverted_index.removal. | 256 |
| abstract_inverted_index.survival | 75, 88, 151, 180, 226, 266, 275 |
| abstract_inverted_index.(HF3253), | 51 |
| abstract_inverted_index.(pairwise | 243 |
| abstract_inverted_index.Employing | 99 |
| abstract_inverted_index.abrogated | 215 |
| abstract_inverted_index.biomarker | 291 |
| abstract_inverted_index.decreased | 178 |
| abstract_inverted_index.developed | 250 |
| abstract_inverted_index.essential | 37 |
| abstract_inverted_index.frequency | 80 |
| abstract_inverted_index.functions | 116 |
| abstract_inverted_index.harboring | 52 |
| abstract_inverted_index.increased | 154 |
| abstract_inverted_index.initially | 94 |
| abstract_inverted_index.justifies | 296 |
| abstract_inverted_index.mitogenic | 15 |
| abstract_inverted_index.modulated | 106 |
| abstract_inverted_index.p&lt; | 165 |
| abstract_inverted_index.p=0.0047; | 238 |
| abstract_inverted_index.p=0.232), | 246 |
| abstract_inverted_index.pediatric | 207 |
| abstract_inverted_index.precursor | 19 |
| abstract_inverted_index.prolonged | 86 |
| abstract_inverted_index.promising | 25, 203 |
| abstract_inverted_index.selection | 92 |
| abstract_inverted_index.signature | 112 |
| abstract_inverted_index.therapies | 294 |
| abstract_inverted_index.treatment | 214, 223, 304 |
| abstract_inverted_index.validates | 285 |
| abstract_inverted_index.wild-type | 170 |
| abstract_inverted_index.xenograft | 185, 265 |
| abstract_inverted_index.Exploiting | 122 |
| abstract_inverted_index.activation | 62 |
| abstract_inverted_index.additional | 278 |
| abstract_inverted_index.continuous | 261 |
| abstract_inverted_index.correlated | 76 |
| abstract_inverted_index.high-grade | 208 |
| abstract_inverted_index.implanted; | 85 |
| abstract_inverted_index.increasing | 273 |
| abstract_inverted_index.inhibitor, | 200 |
| abstract_inverted_index.lentivirus | 173 |
| abstract_inverted_index.orthotopic | 184, 231 |
| abstract_inverted_index.population | 84 |
| abstract_inverted_index.predictive | 290 |
| abstract_inverted_index.prevalence | 3 |
| abstract_inverted_index.treatment, | 260 |
| abstract_inverted_index.validating | 33 |
| abstract_inverted_index.xenografts | 235 |
| abstract_inverted_index.alterations | 12, 54 |
| abstract_inverted_index.avapritinib | 211, 262, 301 |
| abstract_inverted_index.independent | 240 |
| abstract_inverted_index.n=5/group). | 195 |
| abstract_inverted_index.populations | 177 |
| abstract_inverted_index.sequencing, | 104 |
| abstract_inverted_index.single-cell | 102 |
| abstract_inverted_index.therapeutic | 26 |
| abstract_inverted_index.Avapritinib, | 196 |
| abstract_inverted_index.Symptom-free | 150 |
| abstract_inverted_index.constitutive | 61 |
| abstract_inverted_index.fibroblasts. | 121 |
| abstract_inverted_index.glioblastoma | 30 |
| abstract_inverted_index.maintenance, | 42 |
| abstract_inverted_index.symptom-free | 74, 87 |
| abstract_inverted_index.undetectable | 147 |
| abstract_inverted_index.amplification | 66 |
| abstract_inverted_index.corresponding | 113 |
| abstract_inverted_index.intra-tumoral | 123 |
| abstract_inverted_index.low-frequency | 95 |
| abstract_inverted_index.n≥4/group). | 167 |
| abstract_inverted_index.n≥8/group), | 272 |
| abstract_inverted_index.n≥9/group), | 239 |
| abstract_inverted_index.significantly | 224 |
| abstract_inverted_index.substantially | 153 |
| abstract_inverted_index.PDGFRA-altered | 306 |
| abstract_inverted_index.PDGFRA-mutated | 206 |
| abstract_inverted_index.bioluminescent | 220 |
| abstract_inverted_index.heterogeneity, | 124 |
| abstract_inverted_index.heterogeneity. | 72 |
| abstract_inverted_index.implementation | 299 |
| abstract_inverted_index.subpopulations | 46 |
| abstract_inverted_index.PDGFRA-targeted | 293 |
| abstract_inverted_index.oligodendrocyte | 18 |
| abstract_inverted_index.patient-derived | 49 |
| abstract_inverted_index.transcriptional | 111 |
| abstract_inverted_index.extrachromosomal | 64 |
| abstract_inverted_index.PDGFRA/KIT-selective | 198 |
| abstract_inverted_index.response/developmental | 110 |
| cited_by_percentile_year | |
| countries_distinct_count | 1 |
| institutions_distinct_count | 11 |
| citation_normalized_percentile |