EXTH-31. EXPLOITING THE GENETIC DEPENDENCY ON PI3K/MTOR SIGNALING FOR THE TREATMENT OF H3-ALTERED DIFFUSE MIDLINE GLIOMA Article Swipe
Ryan J. Duchatel
,
Evangeline R. Jackson
,
Sarah Parackal
,
Claire Sun
,
Paul Daniel
,
Abdul Mannan
,
Izac J. Findlay
,
Dilana E. Staudt
,
Zacary P. Germon
,
Sandra Laternser
,
Dylan J. Kiltschewskij
,
Padraic S. Kearney
,
M. Fairuz B. Jamaluddin
,
Alicia M. Douglas
,
Tyrone S. Beitaki
,
Mika Perrson
,
Bryce Thomas
,
Elizabeth E. Manning
,
Heather C. Murray
,
Nicole M. Verrills
,
Ricardo E. Vilain
,
David A. Skerrett‐Byrne
,
Brett Nixon
,
Susan Hua
,
Charles E. de Bock
,
Fátima Valdés‐Mora
,
Maria Tsoli
,
David S. Ziegler
,
Murray J. Cairns
,
Eric H. Raabe
,
Nicholas A. Vitanza
,
Timothy N. Phoenix
,
Carl Koschmann
,
Frank Alvaro
,
Christopher V. Dayas
,
Christopher L. Tinkle
,
David D. Eisenstat
,
Ron Firestein
,
Sabine Mueller
,
Javad Nazarian
,
Jason E. Cain
,
Matthew D. Dun
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noad179.0884
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/neuonc/noad179.0884
Recurring activating mutations, amplifications and allelic loss of the negative repressors of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) signaling genes are overarching contributors to the poor survival of patients with H3K27-altered diffuse midline gliomas (DMG) diagnosed in the pons (diffuse intrinsic pontine glioma – DIPG), highlighting the clinical potential of therapies that target this axis. Employing a loss-of-function CRISPR-Cas9 gene deletion screen, we identified PIK3CA and MTOR as survival dependences in DMG/DIPG patient derived cell line models (n=36), highlighting the clinical potential of targeting PI3K/Akt/mTOR. The brain-penetrant, PI3K/mTOR inhibitor paxalisib is currently under clinical investigation in DIPG (NCT03696355 and NCT05009992), but dosing limiting toxicities including hyperglycaemia, mucositis and skin irritation limit patient compliance. To exploit this therapeutic vulnerability, we optimized the preclinical use of paxalisib, identifying both precision medicine combination strategies and systemic interventions that reduced side effects and elicited profound tumor control in vivo. Mimicking the patient experience, paxalisib elevated blood glucose levels, promoting the phosphorylation of the insulin receptor (p-INSR) in patient derived DIPG xenograft models. Combining paxalisib with the anti-glycemic drug metformin, synergistically extended the survival of two DIPG xenograft models, decreasing p-Akt, p-mTOR and p-INSR in vivo. Phosphoproteomic profiling of DIPG cells identified paxalisib induced intracellular calcium-regulated PKC signaling. The brain penetrant PKC inhibitor enzastaurin extended the survival of DIPG xenograft models alone, and synergistically combined with paxalisib, enhanced using metformin in three DIPG xenograft models, as well as the immunocompetent H3f3aK27M, PdgfraD842Vmut, Trp53-/- murine brainstem glioma model. Mechanisms of adaptation/plasticity were assessed by ATAC-Seq and quantitative proteomic profiling xenograft tumors refractory to treatment. Here we address the intrinsic neoplastic sequela of DIPG, by combined targeting of PI3K/Akt/mTOR using paxalisib, compensatory PKC signaling using enzastaurin, coupled with strategies to manage treatment-related side-effects and reduced efficacy using metformin; providing the preclinical rationale for the addition of metformin to NCT05009992.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/neuonc/noad179.0884
- OA Status
- green
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4388588867
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4388588867Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1093/neuonc/noad179.0884Digital Object Identifier
- Title
-
EXTH-31. EXPLOITING THE GENETIC DEPENDENCY ON PI3K/MTOR SIGNALING FOR THE TREATMENT OF H3-ALTERED DIFFUSE MIDLINE GLIOMAWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-11-01Full publication date if available
- Authors
-
Ryan J. Duchatel, Evangeline R. Jackson, Sarah Parackal, Claire Sun, Paul Daniel, Abdul Mannan, Izac J. Findlay, Dilana E. Staudt, Zacary P. Germon, Sandra Laternser, Dylan J. Kiltschewskij, Padraic S. Kearney, M. Fairuz B. Jamaluddin, Alicia M. Douglas, Tyrone S. Beitaki, Mika Perrson, Bryce Thomas, Elizabeth E. Manning, Heather C. Murray, Nicole M. Verrills, Ricardo E. Vilain, David A. Skerrett‐Byrne, Brett Nixon, Susan Hua, Charles E. de Bock, Fátima Valdés‐Mora, Maria Tsoli, David S. Ziegler, Murray J. Cairns, Eric H. Raabe, Nicholas A. Vitanza, Timothy N. Phoenix, Carl Koschmann, Frank Alvaro, Christopher V. Dayas, Christopher L. Tinkle, David D. Eisenstat, Ron Firestein, Sabine Mueller, Javad Nazarian, Jason E. Cain, Matthew D. DunList of authors in order
- Landing page
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https://doi.org/10.1093/neuonc/noad179.0884Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
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greenOpen access status per OpenAlex
- OA URL
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https://pmc.ncbi.nlm.nih.gov/articles/PMC10640372/pdf/noad179.0884.pdfDirect OA link when available
- Concepts
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PI3K/AKT/mTOR pathway, Protein kinase B, Kinome, Cancer research, Medicine, Metformin, Glioma, Pharmacology, Biology, Kinase, Insulin, Signal transduction, Internal medicine, Cell biologyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.diffuse | 30 |
| abstract_inverted_index.effects | 136 |
| abstract_inverted_index.exploit | 113 |
| abstract_inverted_index.gliomas | 32 |
| abstract_inverted_index.glucose | 151 |
| abstract_inverted_index.induced | 197 |
| abstract_inverted_index.insulin | 158 |
| abstract_inverted_index.levels, | 152 |
| abstract_inverted_index.midline | 31 |
| abstract_inverted_index.models, | 182, 228 |
| abstract_inverted_index.models. | 166 |
| abstract_inverted_index.patient | 71, 110, 146, 162 |
| abstract_inverted_index.pontine | 40 |
| abstract_inverted_index.reduced | 134, 286 |
| abstract_inverted_index.screen, | 60 |
| abstract_inverted_index.sequela | 263 |
| abstract_inverted_index.(diffuse | 38 |
| abstract_inverted_index.(p-INSR) | 160 |
| abstract_inverted_index.3-kinase | 15 |
| abstract_inverted_index.ATAC-Seq | 247 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.DMG/DIPG | 70 |
| abstract_inverted_index.Trp53-/- | 236 |
| abstract_inverted_index.addition | 296 |
| abstract_inverted_index.assessed | 245 |
| abstract_inverted_index.clinical | 46, 79, 92 |
| abstract_inverted_index.combined | 218, 267 |
| abstract_inverted_index.deletion | 59 |
| abstract_inverted_index.efficacy | 287 |
| abstract_inverted_index.elevated | 149 |
| abstract_inverted_index.elicited | 138 |
| abstract_inverted_index.enhanced | 221 |
| abstract_inverted_index.extended | 175, 208 |
| abstract_inverted_index.limiting | 101 |
| abstract_inverted_index.medicine | 127 |
| abstract_inverted_index.negative | 10 |
| abstract_inverted_index.patients | 27 |
| abstract_inverted_index.profound | 139 |
| abstract_inverted_index.receptor | 159 |
| abstract_inverted_index.survival | 25, 67, 177, 210 |
| abstract_inverted_index.systemic | 131 |
| abstract_inverted_index.Combining | 167 |
| abstract_inverted_index.Employing | 54 |
| abstract_inverted_index.Mimicking | 144 |
| abstract_inverted_index.PI3K/mTOR | 86 |
| abstract_inverted_index.Recurring | 1 |
| abstract_inverted_index.brainstem | 238 |
| abstract_inverted_index.currently | 90 |
| abstract_inverted_index.diagnosed | 34 |
| abstract_inverted_index.including | 103 |
| abstract_inverted_index.inhibitor | 87, 206 |
| abstract_inverted_index.intrinsic | 39, 261 |
| abstract_inverted_index.metformin | 223, 298 |
| abstract_inverted_index.mucositis | 105 |
| abstract_inverted_index.optimized | 118 |
| abstract_inverted_index.paxalisib | 88, 148, 168, 196 |
| abstract_inverted_index.penetrant | 204 |
| abstract_inverted_index.potential | 47, 80 |
| abstract_inverted_index.precision | 126 |
| abstract_inverted_index.profiling | 191, 251 |
| abstract_inverted_index.promoting | 153 |
| abstract_inverted_index.proteomic | 250 |
| abstract_inverted_index.providing | 290 |
| abstract_inverted_index.rationale | 293 |
| abstract_inverted_index.signaling | 17, 275 |
| abstract_inverted_index.targeting | 82, 268 |
| abstract_inverted_index.therapies | 49 |
| abstract_inverted_index.xenograft | 165, 181, 213, 227, 252 |
| abstract_inverted_index.H3f3aK27M, | 234 |
| abstract_inverted_index.Mechanisms | 241 |
| abstract_inverted_index.activating | 2 |
| abstract_inverted_index.decreasing | 183 |
| abstract_inverted_index.identified | 62, 195 |
| abstract_inverted_index.irritation | 108 |
| abstract_inverted_index.metformin, | 173 |
| abstract_inverted_index.metformin; | 289 |
| abstract_inverted_index.mutations, | 3 |
| abstract_inverted_index.neoplastic | 262 |
| abstract_inverted_index.paxalisib, | 123, 220, 272 |
| abstract_inverted_index.refractory | 254 |
| abstract_inverted_index.repressors | 11 |
| abstract_inverted_index.signaling. | 201 |
| abstract_inverted_index.strategies | 129, 280 |
| abstract_inverted_index.toxicities | 102 |
| abstract_inverted_index.treatment. | 256 |
| abstract_inverted_index.CRISPR-Cas9 | 57 |
| abstract_inverted_index.combination | 128 |
| abstract_inverted_index.compliance. | 111 |
| abstract_inverted_index.dependences | 68 |
| abstract_inverted_index.enzastaurin | 207 |
| abstract_inverted_index.experience, | 147 |
| abstract_inverted_index.identifying | 124 |
| abstract_inverted_index.overarching | 20 |
| abstract_inverted_index.preclinical | 120, 292 |
| abstract_inverted_index.therapeutic | 115 |
| abstract_inverted_index.(NCT03696355 | 96 |
| abstract_inverted_index.NCT05009992. | 300 |
| abstract_inverted_index.compensatory | 273 |
| abstract_inverted_index.contributors | 21 |
| abstract_inverted_index.enzastaurin, | 277 |
| abstract_inverted_index.highlighting | 44, 77 |
| abstract_inverted_index.quantitative | 249 |
| abstract_inverted_index.side-effects | 284 |
| abstract_inverted_index.H3K27-altered | 29 |
| abstract_inverted_index.NCT05009992), | 98 |
| abstract_inverted_index.PI3K/Akt/mTOR | 270 |
| abstract_inverted_index.anti-glycemic | 171 |
| abstract_inverted_index.interventions | 132 |
| abstract_inverted_index.intracellular | 198 |
| abstract_inverted_index.investigation | 93 |
| abstract_inverted_index.PI3K/Akt/mTOR. | 83 |
| abstract_inverted_index.amplifications | 4 |
| abstract_inverted_index.vulnerability, | 116 |
| abstract_inverted_index.PdgfraD842Vmut, | 235 |
| abstract_inverted_index.hyperglycaemia, | 104 |
| abstract_inverted_index.immunocompetent | 233 |
| abstract_inverted_index.phosphorylation | 155 |
| abstract_inverted_index.synergistically | 174, 217 |
| abstract_inverted_index.Phosphoproteomic | 190 |
| abstract_inverted_index.brain-penetrant, | 85 |
| abstract_inverted_index.loss-of-function | 56 |
| abstract_inverted_index.calcium-regulated | 199 |
| abstract_inverted_index.treatment-related | 283 |
| abstract_inverted_index.adaptation/plasticity | 243 |
| abstract_inverted_index.phosphatidylinositol-4,5-bisphosphate | 14 |
| cited_by_percentile_year | |
| countries_distinct_count | 3 |
| institutions_distinct_count | 42 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.4699999988079071 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.45302542 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |