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1                                              DIPG cells compensate for ODC1 inhibition by upregulatio
2                                              DIPG is a lethal glioma, driven by a histone H3 lysine 2
3                                              DIPG models treated with paxalisib increased calcium-act
4 receiving IV GD2-CART on study (n = 3 DL1 (3 DIPG); n = 8 DL2 (6 DIPG, 2 sDMG)).
5 T on study (n = 3 DL1 (3 DIPG); n = 8 DL2 (6 DIPG, 2 sDMG)).
6                             More than 60-70% DIPG tumors harbor heterozygous mutations at genes encod
7 H3.3K27M+ status were enrolled in stratum A (DIPG) or stratum B (nonpontine DMG).
8  CAR T cell trafficking and efficacy against DIPG.
9 nt extension of survival in three aggressive DIPG orthotopic animal models.
10 S-mediated BBB opening, which may ameliorate DIPG chemotherapeutic approaches in children.
11 on factors which control differentiation and DIPG cell fitness.
12    Our data indicate that PFA ependymoma and DIPG are driven in part by the action of peptidyl PRC2 i
13 ALK2 mutant proteins associated with FOP and DIPG.
14 er promising approaches for treating GBM and DIPG, particularly by addressing the persistence of GSCs
15 GSCs holds potential for curing both GBM and DIPG.
16 methods synergizes with HDAC inhibition, and DIPG cells resistant to HDAC inhibitor therapy retain se
17  with recurrent or refractory CNS tumors and DIPG.
18 e discoveries coupled with the powerful anti-DIPG/DMG pharmacokinetic and pharmacodynamic properties
19 found truncated in pediatric gliomas such as DIPG, and uncover a synthetic lethal interaction between
20             A clinical diagnosis of atypical DIPG was associated with borderline significantly prolon
21 om Pediatric Brain Tumor Consortium clinical DIPG trials.
22    The possible roles of the two most common DIPG associated cytoplasmic ACVR1 receptor kinase domain
23                Suppression of ERK5 decreased DIPG cell proliferation and induced apoptosis in vitro a
24 helial cells, microglia, and patient-derived DIPG cell lines to self-assemble has been exploited to g
25 rformed a chemical screen in patient-derived DIPG cultures along with RNA-seq analyses and integrated
26 to overexpress H3.3K27M and patients-derived DIPG cell lines, we demonstrate that BMP2/7 synergizes w
27 -type and G328V mutant patient tumor derived DIPG cell lines at 20-50 uM doses.
28 trial at our institution for newly diagnosed DIPG (NCT03178032).
29 e in pediatric patients with newly diagnosed DIPG and evaluated the associations of (11)C-methionine
30 , 3 to 18 years of age, with newly diagnosed DIPG received 1x10(10) (the first 4 patients) or 5x10(10
31 ds: Twenty-two patients with newly diagnosed DIPG were prospectively enrolled on an institutional rev
32 umor cells, in patients with newly diagnosed DIPG.
33                          Methods: Forty-five DIPG patients who received 9.0-370.7 MBq of (124)I-ombur
34 tial drug targets and therapeutic agents for DIPG.
35 way activity has functional consequences for DIPG self-renewal capacity in neurosphere culture.
36 1/2, as a RAS pathway effector important for DIPG growth.
37 elf may provide alternative entry points for DIPG therapeutics.
38  advancing disease management strategies for DIPG in children.
39 suggest a promising therapeutic strategy for DIPG.
40  antigen receptor (CAR) T cell therapies for DIPG have demonstrated clinical tolerability and bioacti
41 ulatory proteins may be useful therapies for DIPG.
42 ved orthotopic xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout mice.
43            Diffuse intrinsic pontine glioma (DIPG) and other H3K27M-mutated diffuse midline gliomas (
44  pediatric diffuse intrinsic pontine glioma (DIPG) and to correlate these metrics with baseline MRI a
45 ldren with diffuse intrinsic pontine glioma (DIPG) by measuring the tumor uptake of (89)Zr-labeled be
46 reduced in diffuse intrinsic pontine glioma (DIPG) cells that carry a lysine-to-methionine substituti
47            Diffuse intrinsic pontine glioma (DIPG) comprise a subset of HGG that arise in the brainst
48 ients with diffuse intrinsic pontine glioma (DIPG) have a poor prognosis, with a median survival of l
49 adults and diffuse intrinsic pontine glioma (DIPG) in children, are among the most aggressive and dea
50            Diffuse intrinsic pontine glioma (DIPG) is a childhood brainstem tumor with a universally
51            Diffuse intrinsic pontine glioma (DIPG) is a devastating brain tumor with a need for novel
52            Diffuse intrinsic pontine glioma (DIPG) is a fatal brain cancer that arises in the brainst
53            Diffuse intrinsic pontine glioma (DIPG) is a fatal brainstem tumor desperately in need of
54            Diffuse intrinsic pontine glioma (DIPG) is a fatal central nervous system (CNS) tumor that
55            Diffuse intrinsic pontine glioma (DIPG) is a fatal childhood cancer.
56            Diffuse intrinsic pontine glioma (DIPG) is a fatal malignancy of the childhood pons charac
57            Diffuse intrinsic pontine glioma (DIPG) is a fatal pediatric cancer with limited therapeut
58            Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive pediatric brainstem tumor c
59            Diffuse intrinsic pontine glioma (DIPG) is a lethal pediatric brain cancer whose median su
60            Diffuse intrinsic pontine glioma (DIPG) is a lethal pediatric tumor with no currently avai
61            Diffuse intrinsic pontine glioma (DIPG) is a rare childhood malignancy with poor prognosis
62            Diffuse intrinsic pontine glioma (DIPG) is a surgically unresectable and devasting tumour
63            Diffuse intrinsic pontine glioma (DIPG) is an aggressive brain stem tumor and the leading
64            Diffuse intrinsic pontine glioma (DIPG) is an aggressive childhood tumor of the brainstem
65            Diffuse intrinsic pontine glioma (DIPG) is an incurable malignant childhood brain tumor, w
66            Diffuse intrinsic pontine glioma (DIPG) is an incurable pediatric brain tumor, with approx
67 ldren with diffuse intrinsic pontine glioma (DIPG) is less than 10%, and new therapeutic targets are
68 ldren with diffuse intrinsic pontine glioma (DIPG) is less than one year.
69 essment of diffuse intrinsic pontine glioma (DIPG) is poorly defined.
70            Diffuse intrinsic pontine glioma (DIPG) kills more children than any other type of brain t
71 rch on new diffuse intrinsic pontine glioma (DIPG) treatments, little or no progress has been made on
72 ntified in diffuse intrinsic pontine glioma (DIPG) tumors.
73 utation in diffuse intrinsic pontine glioma (DIPG), a deadly pediatric brain tumor.
74 eatment of diffuse intrinsic pontine glioma (DIPG), an aggressive pediatric cancer resident in the po
75 as such as diffuse intrinsic pontine glioma (DIPG), and pediatric low-grade optic gliomas.
76  (GBM) and diffuse intrinsic pontine glioma (DIPG), are morbid brain tumors.
77  Pediatric diffuse intrinsic pontine glioma (DIPG), classified under diffuse midline glioma, is a dea
78  including diffuse intrinsic pontine glioma (DIPG), have dismal outcomes.
79 tely fatal diffuse intrinsic pontine glioma (DIPG), now categorized as a diffuse midline glioma.
80  pediatric diffuse intrinsic pontine glioma (DIPG), we performed whole-genome sequencing of DNA from
81  lines of diffused intrinsic pontine glioma (DIPG).
82 -type (WT) diffuse intrinsic pontine glioma (DIPG).
83 ain tumor, diffuse intrinsic pontine glioma (DIPG).
84 lioma, and diffuse intrinsic pontine glioma (DIPG).
85 brainstem (diffuse intrinsic pontine glioma; DIPG), are uniformly fatal brain tumors that lack effect
86           Diffuse intrinsic pontine gliomas (DIPG) are incurable brain tumors with an aggressive onse
87 including diffuse intrinsic pontine gliomas (DIPG), are the most lethal of childhood cancers.
88 including diffuse intrinsic pontine gliomas (DIPG), exhibit cellular heterogeneity comprising less-di
89 re termed diffuse intrinsic pontine gliomas (DIPG).
90 e investigate the role of H3K36me2 in H3K27M-DIPG by tackling its upstream catalyzing enzymes (writer
91                     Loss of NSD1/2 in H3K27M-DIPG impedes cellular proliferation and tumorigenesis by
92 GF/HDGF2 as an acquired dependency in H3K27M-DIPG.
93 fically inhibits the proliferation of H3K27M-DIPG.
94 xenografts were more representative of human DIPG with an intact BBB.
95 e brainstem gliomas that recapitulated human DIPG gene expression signatures and showed global change
96 ative tumour growth pattern similar to human DIPG.
97  emission tomography (PET) probe for imaging DIPG in vivo In human histological tissues, the probes t
98 mutation as an enhancer of RAS activation in DIPG and ERK5 as a novel, immediately actionable molecul
99 pmental and oncogenic processes is active in DIPG tumor cells.
100 THX6) accomplishes its antitumor activity in DIPG cell lines.
101 ed therapeutic efficacy both in vitro and in DIPG orthotopic xenograft models.
102 insights for future clinical applications in DIPG.
103 burtamab is a novel theranostics approach in DIPG.
104 H3K27me3, PRC2 activity is still detected in DIPG cells positive for H3K27M.
105         Identification of super-enhancers in DIPG provides insights toward the cell of origin, highli
106 robes target, PARP1, was highly expressed in DIPG compared to normal brain.
107  cells, mainly microglia and macrophages, in DIPG.
108 oral homogeneity of main driver mutations in DIPG implies they will be captured by limited biopsies a
109 s by heterotypic H3K27M-K27ac nucleosomes in DIPG cells, we performed treatments in vivo with BET bro
110 on of hidden oncogenic signaling pathways in DIPG such as TbetaRI that are not limited to ACVR1 itsel
111 or AMXT 1501 reduces uptake of polyamines in DIPG cells, and co-administration of AMXT 1501 and DFMO
112 e the functional roles of H3K27M and PRC2 in DIPG pathogenesis, we profiled the epigenome of H3K27M-m
113 wo epigenetically distinct subpopulations in DIPG, reflecting inherent heterogeneity in expression of
114 work uncovers TIM-3 as a bona fide target in DIPG and supports its clinical translation.
115 ss of compounds as potential therapeutics in DIPG.
116  correlating with increased survival time in DIPG patients.
117 onal distinctions previously unidentified in DIPG.
118 w that polyamine synthesis is upregulated in DIPG, leading to sensitivity to DFMO.
119 take as a therapeutic strategy for incurable DIPG.
120 hibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.
121 s (TTA), designed to replicate the intricate DIPG microenvironment.
122 sidual PRC2 activity is required to maintain DIPG proliferative potential, by repressing neuronal dif
123                                         Most DIPG cells harbor mutations in genes encoding histone H3
124 noncanonical histone H3.3 is present in most DIPG tumors.
125 y prolongs survival, with human ACVR1 mutant DIPG cell lines also being sensitive to LDN212854 treatm
126 , we profiled the epigenome of H3K27M-mutant DIPG cells and found that H3K27M associates with increas
127  the first four patients with H3K27M-mutated DIPG or spinal cord DMG treated with GD2-CAR T cells at
128 ic approach for patients with H3K27M-mutated DIPG or spinal cord DMG.
129 structures of whole autopsy brains from nine DIPG patients.
130  receptor serine/threonine kinase, in 21% of DIPG samples.
131                     The majority of cases of DIPG exhibit a mutation in histone-3 (H3K27M) that resul
132 aging allowed for the sensitive detection of DIPG in a genetically engineered mouse model, and probe
133 his is hypothesized to be a driving event of DIPG oncogenesis.
134 elative studies of the molecular features of DIPG and antitumor immune responses.
135 equently demonstrated that serial imaging of DIPG in mouse models enables monitoring of tumor growth,
136 ions correlate closely with the incidence of DIPG and highlight a candidate cell of origin.
137 ese tumors limits the clinical management of DIPG, resulting in poor outcomes for patients.
138 d elucidate previously unknown mechanisms of DIPG pathobiology.
139 to enhance drug delivery in a mouse model of DIPG.
140 sia mutated (Atm) in primary mouse models of DIPG can enhance tumor radiosensitivity.
141 t inhibition of TIM-3 in syngeneic models of DIPG prolongs survival and produces long-term survivors
142 ependencies across patient derived models of DIPG, highlighting the therapeutic potential of the bloo
143  when paired with MRgFUS in murine models of DIPG.
144 nd future evaluation in orthotopic models of DIPG.
145 pment and evaluation in orthotopic models of DIPG.
146 n tested the lead ASO in two mouse models of DIPG: an immunocompetent mouse model using transduced mu
147 ment of H3K27me2/3, promoting oncogenesis of DIPG.
148 anding the cellular and molecular origins of DIPG, and suggest that the Hh pathway represents a poten
149 TTA model recapitulates clinical patterns of DIPG growth, evidenced by resistance to chemotherapy, HD
150 significant longer overall survival times of DIPG patients harboring ACVR1 G328V tumors.
151 chanisms on cell membranes, the treatment of DIPG cells with 36 (THX6) causes a change in levels of f
152  have provided the rationale for the ongoing DIPG/DMG phase II combination clinical trial NCT05009992
153 ered intracerebroventricularly in orthotopic DIPG mouse models, CXCR3-A-modified CAR T cells show enh
154 ET and MR ADC histogram metrics in pediatric DIPG demonstrate different characteristics with often a
155 CART to patients with H3K27M-mutant pontine (DIPG) or spinal DMG (sDMG) at two dose levels (DL1, 1 x
156                       Using early postmortem DIPG tumor tissue, we have established in vitro and xeno
157  mitochondrial protease hClpP is a potential DIPG therapeutic target, and this study describes the sy
158 ul resource of epigenomic data in 25 primary DIPG samples and 5 rare normal pediatric pontine tissue
159 eted therapeutically in isogenic and primary DIPG cell lines with H3.3K27M mutations, providing an ex
160                              Through primary DIPG tumor characterization and isogenic oncohistone exp
161 erall, this validated method for quantifying DIPG burden would serve useful in monitoring treatment r
162  what we believe to be a clinically relevant DIPG therapeutic combinational strategy.
163 ine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors.
164                                        Seven DIPG patients (4 boys; 6-17 y old) were scanned without
165                               Results: Seven DIPG patients (4 boys; 6-17 y old) were scanned without
166                                           SU-DIPG-IV cells harboring the histone H3.1K27M and activat
167 sed orthotopically injected SU-DIPG-6 and SU-DIPG-17 xenografts which demonstrated a diffusely infilt
168      We also used orthotopically injected SU-DIPG-6 and SU-DIPG-17 xenografts which demonstrated a di
169                             In our study, SU-DIPG-17 xenografts were more representative of human DIP
170 d higher concentration of drug within the SU-DIPG-17 brainstem tumours compared to controls.
171 nalysis of the genomic landscape surrounding DIPG has revealed that activin receptor-like kinase-2 (A
172                            We show here that DIPG is vulnerable to transcriptional disruption using b
173  for delivery of high radiation doses to the DIPG lesions, with high lesion activities and low system
174 ated improved mOS from onset compared to the DIPG patients in our center's retrospective study (mOS,
175 y LDN212854 as a promising compound to treat DIPG.
176 as a therapeutic vulnerability, they treated DIPG-bearing mice with paxalisib and saw responses but a
177   These data suggest a strategy for treating DIPG by simultaneously inhibiting LSD1 and HDACs.
178 eveal novel therapeutic targets for treating DIPG tumors.
179 es and gene expression signatures underlying DIPG.
180 ate with treatment outcomes in children with DIPG in this study.
181 ab PET studies are feasible in children with DIPG.
182 rvival of mice intracranially engrafted with DIPG cells.
183  way for improved outcomes for patients with DIPG and other brain tumors.
184 d neurological improvements in patients with DIPG and those with sDMG.
185 ing oncolytic viral therapy in patients with DIPG are lacking.
186                  A total of 23 patients with DIPG enrolled, and 21 were treated with repeated doses o
187 s in pediatric and young adult patients with DIPG is tolerable, including multiyear repeated dosing,
188 d by radiotherapy in pediatric patients with DIPG resulted in changes in T-cell activity and a reduct
189                                Patients with DIPG with below-median baseline levels of myeloid-derive
190                     Similar to patients with DIPG, mice with p53 wild-type tumors had improved surviv
191 ective therapies available for patients with DIPG, who have a median survival time of less than one y
192 ults from Arm C, restricted to patients with DIPG.
193 y in drug delivery among patients and within DIPG tumors and a positive, but not 1:1, correlation bet

 
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