Chris Jones
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View article: Table 2 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Table 2 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Summary of toxicities graded as per Common Terminology Criteria for Adverse Events version 4.03 related to vandetanib and/or mTOR inhibitors in three children with newly diagnosed ACVR1-mutant DIPG for a total of 9 cycles of vandeta…
View article: Figure 7 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 7 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
Efficacy of combined dasatinib and trametinib on ex vivo brain slice preparations. A, Coronal slices of normal mouse brain, counterstained with Hoechst 33342 (aqua), are implanted in the pontine region with ICR-B169 parental …
View article: Figure 1 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 1 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
In vitro sensitivity to trametinib in patient-derived DIPG models. A, Oncoprint representation of an integrated annotation of single-nucleotide variants, DNA copy number changes, and structural variants for patient-derived mo…
View article: Figure 5 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 5 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
Reciprocity of drug sensitivities and gene expression signatures between trametinib and dasatinib in DIPG cells. A, Dose–response curves for ulixertinib tested against ICR-B169 parental cells (gray) and resistant clones T1 (MEK2<…
View article: Figure 2 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 2 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
PIK3R1 and NF1 mutations drive the sensitivity of DIPG cells to trametinib. A, Cartoon representing the protein domains of PIK3R1 showing the mutant residue for the observed hotspot N564D mutation observed in IC…
View article: Figure 3 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 3 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
MEK1/2 mutations drive resistance to trametinib in BRAFG469V-driven DIPG cells. A, Protein structure representation of BRAF showing the mutant residue (shaded orange) for the observed G469 missense mutation observed in IC…
View article: Figure 2 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Figure 2 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Validation of vandetanib as an ACVR1 inhibitor and everolimus as a P-gp inhibitor. A, Kinome selectivity map for vandetanib at 10 μmol/L, with red circles reflecting kinases inhibited by >65%. ACVR1 is labeled. The diameter of the c…
View article: Figure 3 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Figure 3 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Synergy of combined vandetanib and everolimus in vitro. A, Cell viability matrix for ACVR1R206H HSJD-DIPG-007 cells treated with distinct combinations of vandetanib (y-axis) and everolimus (x-a…
View article: Table 1 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Table 1 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Demographics of three children with newly diagnosed ACVR1-mutant DIPG treated with vandetanib and mTOR inhibitors upfront or at relapse
View article: Figure 6 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 6 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
Synergy of combined dasatinib and trametinib in BRAFG469V-driven DIPG cells. A, Cell viability matrices for ICR-B169 parental (gray) and trametinib-resistant clones T1 (MEK2I115N, pink), (T3 MEK1<…
View article: Figure 4 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Figure 4 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Efficacy of combined vandetanib and everolimus in vivo. A, Tolerability in NOD.SCID mice exposed to daily oral treatment with the combination of vandetanib and everolimus over 14 days, as assessed by body weight relative to d…
View article: Supplementary Figures S1-S3 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Supplementary Figures S1-S3 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Supplementary Figures S1-S3
View article: Figure 5 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Figure 5 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Clinical experience of combined vandetanib and everolimus in a 7-year-old girl with ACVR1-mutant DIPG (case 1). A, Timeline summarizing the clinical history of case 1, treated at the Royal Marsden Hospital, London, United Kingdom. *…
View article: Figure 4 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition
Figure 4 from DIPG Harbors Alterations Targetable by MEK Inhibitors, with Acquired Resistance Mechanisms Overcome by Combinatorial Inhibition Open
Integrated gene and protein expression profiling of trametinib-resistant DIPG cells. A, Coordinately downregulated genes (left), proteins (middle), and phospho-sites (right) in all three trametinib-resistant subclones of ICR-B169
View article: Figure 1 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma
Figure 1 from Repurposing Vandetanib plus Everolimus for the Treatment of <i>ACVR1</i>-Mutant Diffuse Intrinsic Pontine Glioma Open
Schema for AI-based identification of a repurposed drug combination strategy for ACVR1-mutant DIPG. The BenevolentAI knowledge graph was employed to identify approved drugs with potential potency against ACVR1 and sufficient CNS pen…
View article: A Systematic Study of Molecular Diagnosis, Treatment and Prognosis in Infant-Type Hemispheric Glioma): An Individual Patient Data Meta-analysis of 164 patients
A Systematic Study of Molecular Diagnosis, Treatment and Prognosis in Infant-Type Hemispheric Glioma): An Individual Patient Data Meta-analysis of 164 patients Open
Background Due to the novelty and rarity of infant-type hemispheric glioma (IHG), optimal treatment and factors determining clinical outcomes are yet to be established. Methods We curated a series of 164 patients with IHG; 155 identified b…
View article: EXTH-93. Combination of ALK2 and cholesterol targeting agents exploits linked genetic and metabolic dependencies in diffuse midline glioma
EXTH-93. Combination of ALK2 and cholesterol targeting agents exploits linked genetic and metabolic dependencies in diffuse midline glioma Open
The discovery that ACVR1-mutations arise in ~25% of DMG H3K27-altered patients has led assessment of both the dependency of ACVR1-mutant cells on ALK2 and the effectiveness of ALK2 inhibitors (ALK2i), however as single-agents these are yet…
View article: DDDR-39. Untangling MEK inhibitor resistance in DMG-MAPK using coupled lineage tracing and single cell RNA sequencing
DDDR-39. Untangling MEK inhibitor resistance in DMG-MAPK using coupled lineage tracing and single cell RNA sequencing Open
MAPK pathway alterations occur in 10-20% of diffuse midline glioma, H3K27-altered (DMG-H3K27), resulting in a proposed novel subtype of the disease with distinct clinical features. In a previous co-clinical trial platform, we showed an inc…
View article: A PROGNOSTIC HUMAN BRAIN NETWORK FOR DIFFUSE MIDLINE GLIOMA
A PROGNOSTIC HUMAN BRAIN NETWORK FOR DIFFUSE MIDLINE GLIOMA Open
AIMS Diffuse midline glioma (DMG) are near-universally lethal tumours of the paediatric central nervous system. In animal models, DMG form brain-wide, integrated networks through neuron-to-glioma synapses and glioma- to-glioma gap junction…
View article: Supplementary Figure S5 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Figure S5 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary figure 5 Features of the GBM_CBM and GBM_MES_ATYP subgroups
View article: Supplementary Figure S6 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Figure S6 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary figure 6 Multivariate analyses within the TYA cohort.
View article: Supplementary Table S2 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Table S2 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary Table 2 Copy number analysis. Gene amplifications derived from methylation array analysis for the TYA cohort with associated frequencies.
View article: Supplementary Table S4 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Table S4 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary Table 4 Sequencing data analysis. Mutations in Cancer Census Genes identified in TYA HGG cases from available whole exome sequencing data (n=107).
View article: Supplementary Figure S4 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Figure S4 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary figure 4 Mutations in TYA gliomas
View article: Supplementary Figure S2 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Figure S2 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary figure 2 DNA Methylation profiling of the TYA HGG cohort.
View article: Supplementary Table S3 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Table S3 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary Table 3 Copy number analysis. Gene deletions derived from methylation array analysis for the TYA cohort with associated frequencies.
View article: Supplementary Figure S1 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Figure S1 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary figure 1 A, Bar plot showing the frequency of age distribution across the TYA cohort, and the gender proportions. Blue representing male, pink representing female. B, Pie chart representing the original diagnoses of the TYA c…
View article: Supplementary Figure S3 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Figure S3 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary figure 3 DNA copy number profiling of the TYA cohort.
View article: Supplementary Table S1 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Supplementary Table S1 from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Supplementary Table 1 Sample cohort. Clinicopathological and molecular profiling data of the TYA HGG cohort (n=207).
View article: Data from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations
Data from The Spectrum of IDH- and H3-Wildtype High-Grade Glioma Subgroups Occurring across Teenage and Young Adult Patient Populations Open
Purpose:High-grade gliomas (HGG) occur in any central nervous system location and at any age. HGGs in teenagers/young adults (TYA) are understudied. This project aimed to characterize these tumors to support accurate stratification of pati…