Results 31 to 40 of about 43,675 (258)

Targeting the EZH2–EED Interaction Inhibits EZH2 Activity [PDF]

open access: yesCancer Discovery, 2013
Abstract A peptide that prevents EZH2 from binding EED inhibits growth of EZH2-dependent cancer cells.
openaire   +1 more source

Review: Targeting EZH2 in neuroblastoma

open access: yesCancer Treatment Reviews, 2023
Neuroblastoma is one of the commonest extra-cranial pediatric tumors, and accounts for over 15% of all childhood cancer mortality. Risk stratification for children with neuroblastoma is based on age, stage, histology, and tumor cytogenetics. The majority of patients are considered to have high-risk neuroblastoma, for which the long-term survival is ...
Jinhui Gao   +5 more
openaire   +2 more sources

EZH2 does it [PDF]

open access: yesScience-Business eXchange, 2010
Epizyme researchers have clarified how mutations in the histone methyltransferase EZH2 lead to increased enzyme activity. With small molecule inhibitors in hand, the biotech now will put EZH2-targeted therapy to the test in mouse models of lymphomas and other EZH2-associated cancers.
openaire   +1 more source

Easy Stress Relief by EZH2 [PDF]

open access: yesCell, 2016
While we are beginning to appreciate the cellular roles played by long noncoding RNAs, the function of transcripts emerging from repetitive genomic regions remains enigmatic. In this issue, Zovoilis et al. report that the polycomb protein EZH2, upon heat shock, facilitates transcription of stress-responsive genes by inducing the degradation of the ...
Supriya G, Prasanth   +1 more
openaire   +2 more sources

MYPT1/PP1‐Mediated EZH2 Dephosphorylation at S21 Promotes Epithelial–Mesenchymal Transition in Fibrosis through Control of Multiple Families of Genes

open access: yesAdvanced Science, 2022
The methyltransferase EZH2 plays an important role in regulating chromatin conformation and gene transcription. Phosphorylation of EZH2 at S21 by AKT kinase suppresses its function.
Lan Zhang   +24 more
doaj   +1 more source

EZH2 in normal and malignant hematopoiesis [PDF]

open access: yesLeukemia, 2013
The histone methyltransferase Enhancer of Zeste Homologue 2 (EZH2), a component of the polycomb group complex, is vital for stem cell development, including hematopoiesis. Its primary function, to deposit the histone mark H3K27me3, promotes transcriptional repression. The activity of EZH2 influences cell fate regulation, namely the balance between self-
K, Lund, P D, Adams, M, Copland
openaire   +2 more sources

Regulation of Tumor Angiogenesis by EZH2 [PDF]

open access: yesCancer Cell, 2010
Although VEGF-targeted therapies are showing promise, new angiogenesis targets are needed to make additional gains. Here, we show that increased Zeste homolog 2 (EZH2) expression in either tumor cells or in tumor vasculature is predictive of poor clinical outcome.
Lu, Chunhua   +37 more
openaire   +3 more sources

MicroRNA-365 Targets Multiple Oncogenes to Inhibit Proliferation, Invasion, and Self-Renewal of Aggressive Endometrial Cancer Cells [Retraction]

open access: yesCancer Management and Research, 2021
Wang C, Su K, Zhang Y, et al. Cancer Manag Res. 2018;10:5171–5185. At the authors request, the Editor and Publisher of Cancer Management and Research wish to retract the published article.
Wang C   +6 more
doaj  

Organoids in pediatric cancer research

open access: yesFEBS Letters, EarlyView.
Organoid technology has revolutionized cancer research, yet its application in pediatric oncology remains limited. Recent advances have enabled the development of pediatric tumor organoids, offering new insights into disease biology, treatment response, and interactions with the tumor microenvironment.
Carla Ríos Arceo, Jarno Drost
wiley   +1 more source

Epigenetic reprogramming of lineage switching in cancer

open access: yesFEBS Letters, EarlyView.
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı   +4 more
wiley   +1 more source

Home - About - Disclaimer - Privacy