BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
about
TWIST1 and BMI1 in Cancer Metastasis and ChemoresistanceSALL4, a novel marker for human gastric carcinogenesis and metastasisInhibition of histone deacetylase impacts cancer stem cells and induces epithelial-mesenchyme transition of head and neck cancerIntegration of DNA copy number alterations and transcriptional expression analysis in human gastric cancer.The Polycomb group protein RING1B is overexpressed in ductal breast carcinoma and is required to sustain FAK steady state levels in breast cancer epithelial cells.Aberrant upregulation of 14-3-3ơ expression serves as an inferior prognostic biomarker for gastric cancer.Oncogenic role of the chromobox protein CBX7 in gastric cancer.Expression and clinicopathological significance of Mel-18 and Bmi-1 mRNA in gastric carcinoma.Polycomb preferentially targets stalled promoters of coding and noncoding transcriptsBmi-1 promotes invasion and metastasis, and its elevated expression is correlated with an advanced stage of breast cancerSurgical treatment for patients with Krukenberg tumor of stomach origin: clinical outcome and prognostic factors analysis.MEL-18 loss mediates estrogen receptor-α downregulation and hormone independence.Downregulated miR-495 [Corrected] Inhibits the G1-S Phase Transition by Targeting Bmi-1 in Breast Cancer.DNA and histone methylation in gastric carcinogenesisAntitumor activity and inhibitory effects on cancer stem cell-like properties of Adeno-associated virus (AAV) -mediated Bmi-1 interference driven by Bmi-1 promoter for gastric cancer.Bmi-1 regulates stem cell-like properties of gastric cancer cells via modulating miRNAsGene silencing by the Polycomb group proteins and associations with cancer.Biomarkers for predicting future metastasis of human gastrointestinal tumors.Histone modifications: Targeting head and neck cancer stem cells.Context-dependent actions of Polycomb repressors in cancer.The evolutionary landscape of PRC1 core components in green lineage.Functional analysis and molecular characterization of spontaneously outgrown human lymphoblastoid cell lines.Expression patterns of microRNA-218 and its potential functions by targeting CIP2A and BMI1 genes in melanoma.The combination of RAD001 and MK-2206 exerts synergistic cytotoxic effects against PTEN mutant gastric cancer cells: involvement of MAPK-dependent autophagic, but not apoptotic cell death pathway.Low expression of Beclin 1, associated with high Bcl-xL, predicts a malignant phenotype and poor prognosis of gastric cancer.B-cell specific Moloney leukemia virus insert site 1 and peptidyl arginine deiminase IV positively regulate carcinogenesis and progression of esophageal squamous cell carcinoma.Expression and Clinicopathological Significance of Mel-18 and Bmi-1 in Esophageal Squamous Cell Carcinoma.BMI-1 Promotes Self-Renewal of Radio- and Temozolomide (TMZ)-Resistant Breast Cancer Cells.Mel-18 negatively regulates stem cell-like properties through downregulation of miR-21 in gastric cancer.Plasma Bmi1 mRNA as a potential prognostic biomarker for distant metastasis in colorectal cancer patientsThe nuclear receptor NR2E1/TLX controls senescence.Expression and clinicopathological significance of Mel-18 mRNA in colorectal cancer.In aggressive variants of non-Hodgkin lymphomas, Ezh2 is strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2.BRD4 regulates cellular senescence in gastric cancer cells via E2F/miR-106b/p21 axis.Stat6 cooperates with Sp1 in controlling breast cancer cell proliferation by modulating the expression of p21(Cip1/WAF1) and p27 (Kip1).Ubiquitin-specific protease 3 overexpression promotes gastric carcinogenesis and is predictive of poor patient prognosisOverexpression of CLC-3 is regulated by XRCC5 and is a poor prognostic biomarker for gastric cancerClinicopathological and Prognostic Significance of Expression of B-Cell-Specific Moloney Murine Leukemia Virus Insertion Site 1 (BMI-1) Gene and Protein in Gastrointestinal Stromal Tumors
P2860
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P2860
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
description
2010 nî lūn-bûn
@nan
2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@ast
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@en
type
label
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@ast
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@en
prefLabel
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@ast
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@en
P2093
P2860
P356
P1433
P1476
BMI1 and Mel-18 oppositely regulate carcinogenesis and progression of gastric cancer.
@en
P2093
Bing-Ya Liu
Feng-Chun Zhang
Goberdhan P Dimri
Wei-Jian Guo
Xiao-Wei Zhang
Ya-Ping Sheng
You-Wei Lu
P2860
P2888
P356
10.1186/1476-4598-9-40
P577
2010-02-21T00:00:00Z
P5875
P6179
1010684873