Signaling pathways in brain tumors and therapeutic interventions

S Li, C Wang, J Chen, Y Lan, W Zhang… - … and Targeted Therapy, 2023 - nature.com
Brain tumors, although rare, contribute to distinct mortality and morbidity at all ages.
Although there are few therapeutic options for brain tumors, enhanced biological …

Biomolecular condensates and cancer

A Boija, IA Klein, RA Young - Cancer cell, 2021 - cell.com
Malignant transformation is characterized by dysregulation of diverse cellular processes that
have been the subject of detailed genetic, biochemical, and structural studies, but only …

[HTML][HTML] Clinical efficacy of ONC201 in H3K27M-mutant diffuse midline gliomas is driven by disruption of integrated metabolic and epigenetic pathways

S Venneti, AR Kawakibi, S Ji, SM Waszak… - Cancer …, 2023 - aacrjournals.org
Patients with H3K27M-mutant diffuse midline glioma (DMG) have no proven effective
therapies. ONC201 has recently demonstrated efficacy in these patients, but the mechanism …

Multimodal analysis of cell-free DNA whole-genome sequencing for pediatric cancers with low mutational burden

P Peneder, AM Stütz, D Surdez, M Krumbholz… - Nature …, 2021 - nature.com
Sequencing of cell-free DNA in the blood of cancer patients (liquid biopsy) provides
attractive opportunities for early diagnosis, assessment of treatment response, and minimally …

Developmental origins and emerging therapeutic opportunities for childhood cancer

M Filbin, M Monje - Nature medicine, 2019 - nature.com
Cancer is the leading disease-related cause of death in children in developed countries.
Arising in the context of actively growing tissues, childhood cancers are fundamentally …

[HTML][HTML] Histone H3. 3G34-mutant interneuron progenitors co-opt PDGFRA for gliomagenesis

CCL Chen, S Deshmukh, S Jessa, D Hadjadj, V Lisi… - Cell, 2020 - cell.com
Summary Histone H3. 3 glycine 34 to arginine/valine (G34R/V) mutations drive deadly
gliomas and show exquisite regional and temporal specificity, suggesting a developmental …

PFA ependymoma-associated protein EZHIP inhibits PRC2 activity through a H3 K27M-like mechanism

SU Jain, TJ Do, PJ Lund, AQ Rashoff, KL Diehl… - Nature …, 2019 - nature.com
Posterior fossa type A (PFA) ependymomas exhibit very low H3K27 methylation and express
high levels of EZHIP (Enhancer of Zeste Homologs Inhibitory Protein, also termed …

[HTML][HTML] Integrated metabolic and epigenomic reprograming by H3K27M mutations in diffuse intrinsic pontine gliomas

C Chung, SR Sweha, D Pratt, B Tamrazi, P Panwalkar… - Cancer cell, 2020 - cell.com
Summary H3K27M diffuse intrinsic pontine gliomas (DIPGs) are fatal and lack treatments.
They mainly harbor H3. 3K27M mutations resulting in H3K27me3 reduction. Integrated …

H3 K27M and EZHIP impede H3K27-methylation spreading by inhibiting allosterically stimulated PRC2

SU Jain, AQ Rashoff, SD Krabbenhoft, D Hoelper… - Molecular Cell, 2020 - cell.com
Diffuse midline gliomas and posterior fossa type A ependymomas contain the recurrent
histone H3 lysine 27 (H3 K27M) mutation and express the H3 K27M-mimic EZHIP (CXorf67) …

Histone variant and cell context determine H3K27M reprogramming of the enhancer landscape and oncogenic state

S Nagaraja, MA Quezada, SM Gillespie, M Arzt… - Molecular cell, 2019 - cell.com
Development of effective targeted cancer therapies is fundamentally limited by our
molecular understanding of disease pathogenesis. Diffuse intrinsic pontine glioma (DIPG) is …