Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer - Wikidata - awgldk - TriplyDB

Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

http://www.wikidata.org/entity/Q34704011

about

TWIST1 and BMI1 in Cancer Metastasis and Chemoresistance Yin Yang 1 is associated with cancer stem cell transcription factors (SOX2, OCT4, BMI1) and clinical implication An overview of long non-coding RNAs in ovarian cancers A Novel Aspect of Tumorigenesis-BMI1 Functions in Regulating DNA Damage Response Emerging role of cancer stem cells in the biology and treatment of ovarian cancer: basic knowledge and therapeutic possibilities for an innovative approach B-cell-specific Moloney murine leukemia virus integration site 1: potential stratification factor and therapeutic target for epithelial ovarian cancer Cystathionine beta-synthase (CBS) contributes to advanced ovarian cancer progression and drug resistance Ubiquitination and degradation of ribonucleotide reductase M1 by the polycomb group proteins RNF2 and Bmi1 and cellular response to gemcitabine Validation of Bmi1 as a therapeutic target of hepatocellular carcinoma in mice.BMI1 polycomb group protein acts as a master switch for growth and death of tumor cells: regulates TCF4-transcriptional factor-induced BCL2 signaling.BMI-1, a promising therapeutic target for human cancer.Role of TGF-β signaling in uterine carcinosarcoma.Bmi-1: At the crossroads of physiological and pathological biology.Overexpression and lack of copy number variation in the BMI-1 gene in human glioma Inhibition of BMI1 induces autophagy-mediated necroptosis.Therapeutic evaluation of microRNA-15a and microRNA-16 in ovarian cancer.VEGFA activates an epigenetic pathway upregulating ovarian cancer-initiating cells.Overcoming challenges of ovarian cancer stem cells: novel therapeutic approaches.Ovarian cancer stem cells: elusive targets for chemotherapy.miR-15a/miR-16 down-regulates BMI1, impacting Ub-H2A mediated DNA repair and breast cancer cell sensitivity to doxorubicin Auraptene Attenuates Malignant Properties of Esophageal Stem-Like Cancer Cells.Knockdown of Bmi1 inhibits bladder cancer cell growth both in vitro and in vivo by blocking cell cycle at G1 phase and inducing apoptosis.BMI1 attenuates etoposide-induced G2/M checkpoints via reducing ATM activation.Andrographolide impedes cancer stemness and enhances radio-sensitivity in oral carcinomas via miR-218 activation.MDR1 mediated chemoresistance: BMI1 and TIP60 in action Effect of shRNA-Mediated Gene Silencing of Bmi-1 Expression on Chemosensitivity of CD44+ Nasopharyngeal Carcinoma Cancer Stem-Like Cells.Ovarian cancer stem cells: a new target for cancer therapy.BMI-1 is a potential therapeutic target in diffuse intrinsic pontine glioma.Mitochondrial BMI1 maintains bioenergetic homeostasis in cells.Pluripotency transcription factors and Metabolic reprogramming of mitochondria in tumor-initiating stem-like cells.Role of BMI1 in epithelial ovarian cancer: investigated via the CRISPR/Cas9 system and RNA sequencing.Cancer Stem Cells (CSCs) in Drug Resistance and their Therapeutic Implications in Cancer Treatment.Evaluating the Mechanism and Therapeutic Potential of PTC-028, a Novel Inhibitor of BMI-1 Function in Ovarian Cancer.Predicting clinical outcome in feline oral squamous cell carcinoma: tumour initiating cells, telomeres and telomerase.Etoposide-resistance in a neuroblastoma model cell line is associated with 13q14.3 mono-allelic deletion and miRNA-15a/16-1 down-regulation

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

http://www.wikidata.org/entity/Q34704011

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2011 nî lūn-bûn

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2011 թուականի Մարտին հրատարակուած գիտական յօդուած

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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JOURNAL.PONE.0017918

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Enhancing chemotherapy response with Bmi-1 silencing in ovarian cancer

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Anil K Sood

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Annamaria Szabolcs

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Enfeng Wang

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Gabriel Lopez-Berestein

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Nicholas B Jennings

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Priyabrata Mukherjee

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Resham Bhattacharya

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Sanjib Bhattacharyya

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P2860

Microarray analysis identifies a death-from-cancer signature predicting therapy failure in patients with multiple types of cancer

Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways.

MiR-15a and MiR-16 control Bmi-1 expression in ovarian cancer

BMI1-mediated histone ubiquitylation promotes DNA double-strand break repair

Identification and characterization of ovarian cancer-initiating cells from primary human tumors

Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation

The polycomb group gene Bmi1 regulates antioxidant defenses in neurons by repressing p53 pro-oxidant activity

Analyzing real-time PCR data by the comparative C(T) method

Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells

bmi-1 transgene induces lymphomas and collaborates with myc in tumorigenesis

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10.1371/JOURNAL.PONE.0017918

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Cristian Rodriguez-Aguayo

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2011-03-21T00:00:00Z

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50892358

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3061867

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