Results 31 to 40 of about 8,953 (160)

Fragment-based discovery of a regulatory site in thioredoxin glutathione reductase acting as "doorstop" for NADPH entry [PDF]

open access: yes, 2018
Members of the FAD/NAD-linked reductase family are recognized as crucial targets in drug development for cancers, inflammatory disorders, and infectious diseases.
Angelucci, Francesco   +16 more
core   +4 more sources

A phase I/II study of gemcitabine during radiotherapy in children with newly diagnosed diffuse intrinsic pontine glioma [PDF]

open access: yes, 2017
The purpose of this phase I/II, open-label, single-arm trial is to investigate the safety, tolerability, maximum tolerated dose and preliminary efficacy of the potential radiosensitizer gemcitabine, administered concomitantly to radiotherapy, in children
Bakker, D.P. (Dewi P.)   +10 more
core   +1 more source

DIPG-32. AKT SIGNALING DRIVES RESISTANCE TO ONC201 IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG) [PDF]

open access: yesNeuro-Oncology, 2020
Abstract Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive, childhood brainstem cancer with a median overall survival of 10 months post diagnosis. Remarkably, 80–90% of patients harbor recurring point mutation in histone H3, which induces a lysine for methionine substitution at amino acid 27 (H3K27M) in either H3.1 (HIST1H3B
Jackson, Evangeline R   +8 more
openaire   +1 more source

Diffuse intrinsic pontine glioma: poised for progress [PDF]

open access: yes, 2012
Diffuse intrinsic pontine gliomas (DIPGs) are amongst the most challenging tumors to treat. Surgery is not an option, the effects of radiation therapy are temporary, and no chemotherapeutic agent has demonstrated significant efficacy.
Katherine E. Warren
core   +2 more sources

Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma. [PDF]

open access: yes, 2017
We collated data from 157 unpublished cases of pediatric high-grade glioma and diffuse intrinsic pontine glioma and 20 publicly available datasets in an integrated analysis of >1,000 cases.
Adam Resnick   +116 more
core   +8 more sources

Brainstem Glioma in Adults [PDF]

open access: yes, 2016
Brainstem gliomas are not nearly as common in adults as they are in children. They are likely the final common consequence not of a single disease process but of several. They can be difficult to diagnose, and are challenging to treat.
Jethro Hu   +2 more
core   +2 more sources

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

Strength through diversity: how cancers thrive when clones cooperate

open access: yesMolecular Oncology, EarlyView.
Intratumor heterogeneity can offer direct benefits to the tumor through cooperation between different clones. In this review, Kuiken et al. discuss existing evidence for clonal cooperativity to identify overarching principles, and highlight how novel technological developments could address remaining open questions.
Marije C. Kuiken   +3 more
wiley   +1 more source

Evaluation of a novel antibody to define histone 3.3 G34R mutant brain tumours [PDF]

open access: yes, 2017
Missense somatic mutations affecting histone H3.1 and H3.3 proteins are now accepted as the hallmark of paediatric diffuse intrinsic pontine gliomas (DIPG), non-brain stem paediatric high grade gliomas (pHGG) as well as a subset of adult glioblastoma ...
D Bechet   +12 more
core   +2 more sources

BMI‐1 modulation and trafficking during M phase in diffuse intrinsic pontine glioma

open access: yesFEBS Open Bio, EarlyView.
The schematic illustrates BMI‐1 phosphorylation during M phase, which triggers its translocation from the nucleus to the cytoplasm. In cycling cells, BMI‐1 functions within the PRC1 complex to mediate H2A K119 monoubiquitination. Following PTC596‐induced M phase arrest, phosphorylated BMI‐1 dissociates from PRC1 and is exported to the cytoplasm via its
Banlanjo Umaru   +6 more
wiley   +1 more source

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