Endogenous retroelements and the viral mimicry response in cancer therapy and cellular homeostasis

R Chen, CA Ishak, DD De Carvalho - Cancer discovery, 2021 - AACR
Features of the cancer epigenome distinguish cancers from their respective cell of origin and
establish therapeutic vulnerabilities that can be exploited through pharmacologic inhibition …

Epigenomic reprogramming as a driver of malignant glioma

RE Phillips, AA Soshnev, CD Allis - Cancer cell, 2020 - cell.com
Malignant gliomas are central nervous system tumors and remain among the most treatment-
resistant cancers. Exome sequencing has revealed significant heterogeneity and important …

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, SR Sweha… - Cancer discovery, 2023 - AACR
Abstract Patients with H3K27M-mutant diffuse midline glioma (DMG) have no proven
effective therapies. ONC201 has recently demonstrated efficacy in these patients, but the …

K27M in canonical and noncanonical H3 variants occurs in distinct oligodendroglial cell lineages in brain midline gliomas

S Jessa, A Mohammadnia, AS Harutyunyan… - Nature …, 2022 - nature.com
Abstract Canonical (H3. 1/H3. 2) and noncanonical (H3. 3) histone 3 K27M-mutant gliomas
have unique spatiotemporal distributions, partner alterations and molecular profiles. The …

Epigenetic therapy induces transcription of inverted SINEs and ADAR1 dependency

P Mehdipour, SA Marhon, I Ettayebi, A Chakravarthy… - Nature, 2020 - nature.com
Cancer therapies that target epigenetic repressors can mediate their effects by activating
retroelements within the human genome. Retroelement transcripts can form double …

[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 …

[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 …

Stalled developmental programs at the root of pediatric brain tumors

S Jessa, A Blanchet-Cohen, B Krug, M Vladoiu… - Nature …, 2019 - nature.com
Childhood brain tumors have suspected prenatal origins. To identify vulnerable
developmental states, we generated a single-cell transcriptome atlas of> 65,000 cells from …

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 …