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Results: 51

Targeting DIPG through pharmacological activation of mitochondrial biogenesis: as in ...

Diffuse intrinsic pontine gliomas (DIPG) are infiltrative, highly aggressive pediatric brainstem tumors with limited therapeutic options. Despite international efforts to improve outcome, DIPG show poor response to conventional radiation and chemotherapeutic strategies. Only within the last decade have studies really begun to decipher the molecular mechanisms behind DIPG tumorigenesis, with ...

Targeting EZH2 as a theraputic strategy in DIPG

Malignant brain tumors are the leading cause of cancer-related mortality in children (1), and diffuse intrinsic pontine glioma (DIPG) is one of the most devastating, with a median survival of <1 year following treatment with radiation therapy (2). Despite more than 250 clinical trials over the past 30 years (3), not a single chemotherapeutic agent ...

Elucidating the underlying mechanisms of radio resistance at diagnosis and ...

Backgound. Radiotherapy is still the mainstay of the treatment for DIPG. If the majority of children experience an improvement of their neurological condition following irradiation, this effect is not observed in all patients and is universally only transient. Determinants of the response to radiotherapy have yet to be defined. We ...

Targeting DIPG through combining a super-activator (MCB-613) of steroid receptor ...

The objective of this application is to demonstrate that combining MCB-613, a small molecule stimulator of the oncogenic steroid receptor co-activator (SRC), with ionizing radiation would synergistically kill tumor cells of diffuse intrinsic pontine glioma (DIPG) in vivo and significantly prolong survival times in patient tumor-derived orthotopic (intra-brain stem) xenograft (...

Defining the molecular mechanisms of DIPG development and progression to ...

  Diffuse Intrinsic Pontine Gliomas (DIPGs) are devastating pediatric brainstem tumors that lack effective treatment and are uniformly fatal. Patient studies have identified recurrent genetic lesions that drive the development of these tumors. Almost all DIPGs carry mutations in genes encoding either replication-dependent histone-H3 proteins (mostly HIST1H3B) or ...