Enhancer of Zeste Homolog 2 Protein
-
Subject Areas on Research
- Acute myeloid leukemia ontogeny is defined by distinct somatic mutations.
- Alternative Splicing of EZH2 pre-mRNA by SF3B3 Contributes to the Tumorigenic Potential of Renal Cancer.
- An integrative model of pathway convergence in genetically heterogeneous blast crisis chronic myeloid leukemia.
- An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation.
- CRISPR-SID: Identifying EZH2 as a druggable target for desmoid tumors via in vivo dependency mapping.
- Cell autonomous role of PTEN in regulating castration-resistant prostate cancer growth.
- EZH2 expression is associated with inferior overall survival in mantle cell lymphoma.
- EZH2 regulates the transcription of estrogen-responsive genes through association with REA, an estrogen receptor corepressor.
- Environmental estrogens differentially engage the histone methyltransferase EZH2 to increase risk of uterine tumorigenesis.
- Epigenetic Switch-Induced Viral Mimicry Evasion in Chemotherapy-Resistant Breast Cancer.
- Epigenetic silencing of tumor suppressor Par-4 promotes chemoresistance in recurrent breast cancer.
- High-grade neuroendocrine carcinomas of the lung highly express enhancer of zeste homolog 2, but carcinoids do not.
- Loss of tumor suppressor IGFBP4 drives epigenetic reprogramming in hepatic carcinogenesis.
- Loss of tumor suppressor KDM6A amplifies PRC2-regulated transcriptional repression in bladder cancer and can be targeted through inhibition of EZH2.
- Mantle Cell Lymphoma Involving Skin: A Clinicopathologic Study of 37 Cases.
- Reprogrammed marrow adipocytes contribute to myeloma-induced bone disease.
- TP53 genomic status regulates sensitivity of gastric cancer cells to the histone methylation inhibitor 3-deazaneplanocin A (DZNep).
- Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation.
- The Genetic Basis of Hepatosplenic T-cell Lymphoma.