ライフサイエンスコーパス: DIPG

1 ALK2 mutant proteins associated with FOP and DIPG.

2 methods synergizes with HDAC inhibition, and DIPG cells resistant to HDAC inhibitor therapy retain se

3 om Pediatric Brain Tumor Consortium clinical DIPG trials.

4 rformed a chemical screen in patient-derived DIPG cultures along with RNA-seq analyses and integrated

5 way activity has functional consequences for DIPG self-renewal capacity in neurosphere culture.

6 suggest a promising therapeutic strategy for DIPG.

7 ulatory proteins may be useful therapies for DIPG.

8 ved orthotopic xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout mice.

9 pediatric diffuse intrinsic pontine glioma (DIPG) and to correlate these metrics with baseline MRI a

10 ldren with diffuse intrinsic pontine glioma (DIPG) by measuring the tumor uptake of (89)Zr-labeled be

11 Diffuse intrinsic pontine glioma (DIPG) comprise a subset of HGG that arise in the brainst

12 Diffuse intrinsic pontine glioma (DIPG) is a childhood brainstem tumor with a universally

13 Diffuse intrinsic pontine glioma (DIPG) is a fatal brain cancer that arises in the brainst

14 Diffuse intrinsic pontine glioma (DIPG) is a fatal childhood cancer.

15 Diffuse intrinsic pontine glioma (DIPG) is a fatal pediatric cancer with limited therapeut

16 Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive pediatric brainstem tumor c

17 ldren with diffuse intrinsic pontine glioma (DIPG) is less than 10%, and new therapeutic targets are

18 ldren with diffuse intrinsic pontine glioma (DIPG) is less than one year.

19 ntified in diffuse intrinsic pontine glioma (DIPG) tumors.

20 pediatric diffuse intrinsic pontine glioma (DIPG), we performed whole-genome sequencing of DNA from

21 lioma, and diffuse intrinsic pontine glioma (DIPG).

22 ain tumor, diffuse intrinsic pontine glioma (DIPG).

23 emission tomography (PET) probe for imaging DIPG in vivo In human histological tissues, the probes t

24 pmental and oncogenic processes is active in DIPG tumor cells.

25 ed therapeutic efficacy both in vitro and in DIPG orthotopic xenograft models.

26 H3K27me3, PRC2 activity is still detected in DIPG cells positive for H3K27M.

27 Identification of super-enhancers in DIPG provides insights toward the cell of origin, highli

28 robes target, PARP1, was highly expressed in DIPG compared to normal brain.

29 oral homogeneity of main driver mutations in DIPG implies they will be captured by limited biopsies a

30 s by heterotypic H3K27M-K27ac nucleosomes in DIPG cells, we performed treatments in vivo with BET bro

31 e the functional roles of H3K27M and PRC2 in DIPG pathogenesis, we profiled the epigenome of H3K27M-m

32 ss of compounds as potential therapeutics in DIPG.

33 sidual PRC2 activity is required to maintain DIPG proliferative potential, by repressing neuronal dif

34 , we profiled the epigenome of H3K27M-mutant DIPG cells and found that H3K27M associates with increas

35 structures of whole autopsy brains from nine DIPG patients.

36 receptor serine/threonine kinase, in 21% of DIPG samples.

37 The majority of cases of DIPG exhibit a mutation in histone-3 (H3K27M) that resul

38 aging allowed for the sensitive detection of DIPG in a genetically engineered mouse model, and probe

39 his is hypothesized to be a driving event of DIPG oncogenesis.

40 equently demonstrated that serial imaging of DIPG in mouse models enables monitoring of tumor growth,

41 ions correlate closely with the incidence of DIPG and highlight a candidate cell of origin.

42 d elucidate previously unknown mechanisms of DIPG pathobiology.

43 anding the cellular and molecular origins of DIPG, and suggest that the Hh pathway represents a poten

44 ET and MR ADC histogram metrics in pediatric DIPG demonstrate different characteristics with often a

45 Using early postmortem DIPG tumor tissue, we have established in vitro and xeno

46 erall, this validated method for quantifying DIPG burden would serve useful in monitoring treatment r

47 Seven DIPG patients (4 boys; 6-17 y old) were scanned without

48 Results: Seven DIPG patients (4 boys; 6-17 y old) were scanned without

49 We show here that DIPG is vulnerable to transcriptional disruption using b

50 es and gene expression signatures underlying DIPG.

51 ab PET studies are feasible in children with DIPG.

52 y in drug delivery among patients and within DIPG tumors and a positive, but not 1:1, correlation bet