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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 01 Aug 2015.

BMI1 polycomb ring finger oncogene

Top mentioned proteins: Polycomb, CAN, p16, EZH2, Histone
Papers using Bmi-1 antibodies
The Polycomb group protein EZH2 impairs DNA repair in breast epithelial cells
Hendzel Michael J. et al., In The Journal of Cell Biology, 2004
... Control and one of two different BMI1 shRNA plasmids were obtained from OriGene.
Papers on Bmi-1
Near universal detection of alterations in CTNNB1 and Wnt pathway regulators in desmoid-type fibromatosis by whole-exome sequencing and genomic analysis.
Singer et al., Boston, United States. In Genes Chromosomes Cancer, 14 Aug 2015
Of the other five wild-type tumors sequenced, two had APC loss, two had chromosome 6 loss, and one had mutation of BMI1.
Human Umbilical Cord Lining Cells as Novel Feeder Layer for Ex Vivo Cultivation of Limbal Epithelial Cells.
Reza et al., Singapore, Singapore. In Invest Ophthalmol Vis Sci, 01 Aug 2015
We also compared the expression level of several putative limbal stem cell markers, such as HES1, ABCG2, ΔNP63, and BMI1, in the cultured limbal cells by immunostaining and quantitative (q)RT-PCR.
ALDH1A1-overexpressing cells are differentiated cells but not cancer stem or progenitor cells in human hepatocellular carcinoma.
Hara et al., Gifu, Japan. In Oncotarget, 22 Jul 2015
In double-staining IHC, ALDH1A1 was not co-expressed with BMI1, EpCAM, CD13, CD24, CD90 and CD133, which reported as cancer stem cell markers in HCC.
Clinical implications of intestinal stem cell markers in colorectal cancer.
Troelsen et al., Denmark. In Clin Colorectal Cancer, Jun 2015
This review provides an overview of the intestinal stem cell markers leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), Musashi1 (MSI1), and sex-determining region y-box 9 (SOX9) and their implications in human CRC.
Immunosuppressive plasma cells impede T-cell-dependent immunogenic chemotherapy.
Karin et al., San Diego, United States. In Nature, Jun 2015
Our previous studies revealed that B cells recruited by the chemokine CXCL13 into prostate cancer tumours promote the progression of castrate-resistant prostate cancer by producing lymphotoxin, which activates an IκB kinase α (IKKα)-BMI1 module in prostate cancer stem cells.
Cancer stem cells in oesophageal squamous cell carcinoma: Identification, prognostic and treatment perspectives.
Lam et al., Gold Coast, Australia. In Crit Rev Oncol Hematol, May 2015
It has also been demonstrated that stem cell markers like ALDH1, HIWI, Oct3/4, ABCG2, SOX2, SALL4, BMI-1, NANOG, CD133 and podoplanin are associated with patient's prognosis, pathological stages, cancer recurrence and therapy resistance.
Anticancer Effect of AntiMalarial Artemisinin Compounds.
Das, Dibrugarh, India. In Ann Med Health Sci Res, Mar 2015
Artemisinins seem to regulate key factors such as nuclear factor-kappa B, survivin, NOXA, hypoxia-inducible factor-1α, and BMI-1, involving multiple pathways that may affect drug response, drug interactions, drug resistance, and associated parameters upon normal cells.
High expression of carbonic anhydrase IX is significantly associated with glandular lesions in gastroesophageal junction and with tumorigenesis markers BMI1, MCM4 and MCM7.
Zhou et al., Rochester, United States. In Bmc Gastroenterol, Dec 2014
METHODS: In this study, we investigated CA9 expression in esophageal cancers and in precancerous lesions and explored the association of CA9 expression with prognostic factors and with stem cell and tumorigenesis-related markers including BMI1, cyclin E, ki67, MCM4 and MCM7 expression.
Different Effects of BORIS/CTCFL on Stemness Gene Expression, Sphere Formation and Cell Survival in Epithelial Cancer Stem Cells.
Benhattar et al., Lausanne, Switzerland. In Plos One, Dec 2014
Importantly, BORIS-silencing led to down-regulation of hTERT, stem cell (NANOG, OCT4, SOX2 and BMI1) and cancer stem cell markers (ABCG2, CD44 and ALDH1) genes.
FAL1ing inside an amplicon.
Huarte et al., Pamplona, Spain. In Cancer Cell, Oct 2014
FAL1 acts as an oncogene by stabilizing BMI1, which results in the repression of CDKN1A expression.
A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer.
Zhang et al., Philadelphia, United States. In Cancer Cell, Oct 2014
FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A.
Novel therapeutic targets for pancreatic cancer.
Chen et al., Hong Kong, Hong Kong. In World J Gastroenterol, Sep 2014
In order to give a better understanding of the current findings and to seek the direction in future pancreatic cancer research; in this review we will focus on targets suppressing tumour metastatsis and progression, KRAS activated downstream effectors, the relationship of Notch signaling and Nodal/Activin signaling with pancreatic cancer cells, the current findings of non-coding RNAs in inhibiting pancreatic cancer cell proliferation, brief discussion in transcription remodeling by epigenetic modifiers (e.g., HDAC, BMI1, EZH2) and the plausible therapeutic applications of cancer stem cell and hyaluronan in tumour environment.
Expandable megakaryocyte cell lines enable clinically applicable generation of platelets from human induced pluripotent stem cells.
Eto et al., Kyoto, Japan. In Cell Stem Cell, May 2014
This approach involves the establishment of stable immortalized megakaryocyte progenitor cell lines (imMKCLs) from PSC-derived hematopoietic progenitors through the overexpression of BMI1 and BCL-XL to respectively suppress senescence and apoptosis and the constrained overexpression of c-MYC to promote proliferation.
Self-renewal as a therapeutic target in human colorectal cancer.
O'Brien et al., Toronto, Canada. In Nat Med, 2014
Here we demonstrate that tumor formation and, more specifically, human colorectal CIC function are dependent on the canonical self-renewal regulator BMI-1.
The impact of microRNA-mediated PI3K/AKT signaling on epithelial-mesenchymal transition and cancer stemness in endometrial cancer.
Sakuragi et al., Sapporo, Japan. In J Transl Med, 2013
In endometrial cancer cells, miRNAs can activate or attenuate EMT and CSC by targeting PTEN and other EMT-associated genes, such as Twist1, ZEB1 and BMI-1.
Bmi1 is required for regeneration of the exocrine pancreas in mice.
Hebrok et al., San Francisco, United States. In Gastroenterology, 2012
Bmi1 contributes to regeneration of the exocrine pancreas after cerulein-induced injury through cell autonomous mechanisms, in part by regulating Cdkn2a expression, and non-cell autonomous mechanisms.
Prognostic relevance of c-Myc and BMI1 expression in patients with glioblastoma.
Larocca et al., Roma, Italy. In Am J Clin Pathol, 2012
We found that overexpression of c-Myc was significantly associated with that of BMI1, and that patients who harbored glioblastomas overexpressing c-Myc and BMI1 showed significantly longer overall survival.
Bmi1 facilitates primitive endoderm formation by stabilizing Gata6 during early mouse development.
Azuara et al., London, United Kingdom. In Genes Dev, 2012
Bmi1 overlaps with the nascent Gata6 and Nanog protein from the eight-cell stage onward before it preferentially cosegregates with Gata6 in primitive endoderm progenitors
Bmi1 confers resistance to oxidative stress on hematopoietic stem cells.
Iwama et al., Chiba, Japan. In Plos One, 2011
overexpression of Bmi1 confers resistance to stresses, particularly oxidative stress, onto hematopoietic stem cells. This enhances their regenerative capacity and suggests that Bmi1 is located downstream of ROS signaling and negatively regulated by it.
Bmi-1 siRNA inhibited ovarian cancer cell line growth and decreased telomerase activity.
Jin et al., Harbin, China. In Br J Biomed Sci, 2011
Bmi-1 siRNA has a role in inhibiting ovarian cancer cell line growth and decreasing telomerase activity
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