Subventricular spread of diffuse intrinsic pontine glioma

Caretti, Viola; Bugiani, Marianna; Freret, Morgan E.; Schellen, Pepijn; Jansen, Marc; Vuurden, Dannis G. van; Kaspers, Gertjan J. L.; Fisher, Paul G.; Hulleman, Esther; Wesseling, Pieter; Vogel, Hannes; Monje, Michelle

doi:10.1007/s00401-014-1307-x

Cited by 82 publications

(79 citation statements)

References 9 publications

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“…EPH-ephrin signaling may represent an important pathogenic mechanism facilitating the diffuse and invasive spread of DIPG throughout the brainstem and, in most cases of DIPG, throughout much of the brain (Caretti et al 2014). …”

Section: Resultsmentioning

confidence: 99%

Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma

et al. 2017

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Summary Diffuse intrinsic pontine glioma (DIPG) is a fatal pediatric cancer with limited therapeutic options. The majority of cases of DIPG exhibit a mutation in histone-3 (H3K27M) that results in oncogenic transcriptional aberrancies. We show here that DIPG is vulnerable to transcriptional disruption using bromodomain inhibition or CDK7 blockade. Targeting oncogenic transcription through either of these methods synergizes with HDAC inhibition and DIPG cells resistant to HDAC inhibitor therapy retain sensitivity to CDK7 blockade. Identification of super-enhancers in DIPG provides insights toward the cell of origin, highlighting oligodendroglial lineage genes, and reveals unexpected mechanisms mediating tumor viability and invasion, including potassium channel function and EPH receptor signaling. The findings presented demonstrate transcriptional vulnerabilities and elucidate previously unknown mechanisms of DIPG pathobiology.

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Section: Resultsmentioning

confidence: 99%

Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma

et al. 2017

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“…[7, 8]. To our knowledge, our Trial 2 was the first to use multiple non-conventional agents concurrent with irradiation in the treatment of DIPG and in the setting of expanded CTV compared to conventional RT.…”

Section: Discussionmentioning

confidence: 99%

Treatment-Related Noncontiguous Radiologic Changes in Children With Diffuse Intrinsic Pontine Glioma Treated With Expanded Irradiation Fields and Antiangiogenic Therapy

Patay

Merchant

Nguyen

et al. 2017

International Journal of Radiation Oncology*Biology*Physics

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“…While DIPG histology can be heterogeneous, ranging from lower-grade astrocytoma to higher-grade astrocytoma,[5] H3.3 K27M mutations have been well described in over two-thirds of DIPGs[2] and may portend a worse overall survival. [5, 6] PDGFRA, MYC and PVT1 amplifications, ATRX, ACVR1 and TP53 mutations and alternative lengthening of telomeres have also been associated with DIPG.…”

Section: Discussionmentioning

confidence: 99%

“…[5, 7, 8] Also, a higher incidence of metastases in DIPG than previously appreciated has been described in recent publications, although our case is the first report of comprehensive phenotypic analysis comparing multiple sites in both primary and distant tumor. [2, 5]…”

Section: Discussionmentioning

confidence: 99%

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Histological and molecular analysis of a progressive diffuse intrinsic pontine glioma and synchronous metastatic lesions: a case report

Nazarian

Mason

et al. 2016

Oncotarget

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There is no curative treatment for patients with diffuse intrinsic pontine glioma (DIPG). However, with the recent availability of biopsy and autopsy tissue, new data regarding the biologic behavior of this tumor have emerged, allowing greater molecular characterization and leading to investigations which may result in improved therapeutic options. Treatment strategies must address both primary disease sites as well as any metastatic deposits, which may be variably sensitive to a particular approach.In this case report, we present a patient with DIPG treated with irradiation and serial investigational agents. The clinical, pathological and molecular phenotypes of both the progressive primary tumor as well as concomitant metastatic deposits obtained at autopsy are discussed. While some mRNA differences were demonstrated, all analyzed sites of disease shared similar mutational arrangements, suggesting that targeting the mutations of the primary tumor may be effective for all sites of disease.

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Subventricular spread of diffuse intrinsic pontine glioma

Cited by 82 publications

References 9 publications

Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma

Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma

Treatment-Related Noncontiguous Radiologic Changes in Children With Diffuse Intrinsic Pontine Glioma Treated With Expanded Irradiation Fields and Antiangiogenic Therapy

Histological and molecular analysis of a progressive diffuse intrinsic pontine glioma and synchronous metastatic lesions: a case report

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