Results 61 to 70 of about 6,667 (221)

Senescence Induced by BMI1 Inhibition Is a Therapeutic Vulnerability in H3K27M-Mutant DIPG

open access: yesCell Reports, 2020
Summary: Diffuse intrinsic pontine glioma (DIPG) is an incurable brain tumor of childhood characterized by histone mutations at lysine 27, which results in epigenomic dysregulation.
Ilango Balakrishnan   +32 more
doaj   +1 more source

Reversal of cancer gene expression identifies repurposed drugs for diffuse intrinsic pontine glioma [PDF]

open access: yes, 2022
Diffuse intrinsic pontine glioma (DIPG) is an aggressive incurable brainstem tumor that targets young children. Complete resection is not possible, and chemotherapy and radiotherapy are currently only palliative.
Brat, Daniel J   +15 more
core   +1 more source

Addressing barriers in diffuse intrinsic pontine glioma: the transformative role of lipid nanoparticulate drug delivery

open access: yesADMET and DMPK
Background and purpose: The brainstem tumour known as diffuse intrinsic pontine glioma (DIPG), also known as pontine glioma, infiltrative brainstem glioma is uncommon and virtually always affects children.
Zenab Presswala   +2 more
doaj   +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

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

Epigenetic programming of pediatric high-grade glioma: Pushing beyond proof of concept to clinical benefit

open access: yesFrontiers in Cell and Developmental Biology, 2022
Pediatric high-grade gliomas (pHGG) are a molecularly diverse group of malignancies, each incredibly aggressive and in dire need of treatment advancements.
Andrew Groves, Tabitha M. Cooney
doaj   +1 more source

Pax3 expression enhances PDGF-B-induced brainstem gliomagenesis and characterizes a subset of brainstem glioma [PDF]

open access: yes, 2014
High-grade Brainstem Glioma (BSG), also known as Diffuse Intrinsic Pontine Glioma (DIPG), is an incurable pediatric brain cancer. Increasing evidence supports the existence of regional differences in gliomagenesis such that BSG is considered a distinct ...
Baker, Suzanne J.   +7 more
core   +3 more sources

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

Non-random aneuploidy specifies subgroups of pilocytic astrocytoma and correlates with older age [PDF]

open access: yes, 2015
Pilocytic astrocytoma (PA) is the most common brain tumor in children but is rare in adults, and hence poorly studied in this age group. We investigated 222 PA and report increased aneuploidy in older patients.
Amon   +55 more
core   +5 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

Home - About - Disclaimer - Privacy