Drug-induced senescence generates chemoresistant stemlike cells with low reactive oxygen species.
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Redox Modulating NRF2: A Potential Mediator of Cancer Stem Cell ResistanceAnti-inflammatory/antioxidant use in long-term maintenance cancer therapy: a new therapeutic approach to disease progression and recurrenceChemotherapy targeting cancer stem cellsDocetaxel-induced polyploidization may underlie chemoresistance and disease relapseERO1α-dependent endoplasmic reticulum-mitochondrial calcium flux contributes to ER stress and mitochondrial permeabilization by procaspase-activating compound-1 (PAC-1).Chronic oxidative stress increases growth and tumorigenic potential of MCF-7 breast cancer cells.Circulating Tumor Cells in Early-Stage Breast Cancer.C10ORF10/DEPP-mediated ROS accumulation is a critical modulator of FOXO3-induced autophagy.Chemotherapeutics-induced Oct4 expression contributes to drug resistance and tumor recurrence in bladder cancer.Cdt1 is differentially targeted for degradation by anticancer chemotherapeutic drugs.Vascular endothelial growth factor C promotes breast cancer progression via a novel antioxidant mechanism that involves regulation of superoxide dismutase 3.Activation of NRF2 by p62 and proteasome reduction in sphere-forming breast carcinoma cells.Dynamic equilibrium between cancer stem cells and non-stem cancer cells in human SW620 and MCF-7 cancer cell populations.Polyploidy Formation in Doxorubicin-Treated Cancer Cells Can Favor Escape from Senescence.Senescence-associated secretory phenotype favors the emergence of cancer stem-like cells.A multi-stage process including transient polyploidization and EMT precedes the emergence of chemoresistent ovarian carcinoma cells with a dedifferentiated and pro-inflammatory secretory phenotypeSuppression of RAF/MEK or PI3K synergizes cytotoxicity of receptor tyrosine kinase inhibitors in glioma tumor-initiating cells.Repopulation of ovarian cancer cells after chemotherapyExpression of aldehyde dehydrogenase after neoadjuvant chemotherapy is associated with expression of hypoxia-inducible factors 1 and 2 alpha and predicts prognosis in locally advanced breast cancerConnecting the Dots: Therapy-Induced Senescence and a Tumor-Suppressive Immune Microenvironment.The autophagy inhibitor chloroquine targets cancer stem cells in triple negative breast cancer by inducing mitochondrial damage and impairing DNA break repair.Different administration strategies with paclitaxel induce distinct phenotypes of multidrug resistance in breast cancer cellsIs it time for a new paradigm for systemic cancer treatment? Lessons from a century of cancer chemotherapyReactive oxygen species in eradicating acute myeloid leukemic stem cellsRole of SUMO activating enzyme in cancer stem cell maintenance and self-renewal.Involvement of NRF2 Signaling in Doxorubicin Resistance of Cancer Stem Cell-Enriched Colonospheres.Low-dose triptolide in combination with idarubicin induces apoptosis in AML leukemic stem-like KG1a cell line by modulation of the intrinsic and extrinsic factors.Another facet to the anticancer response to lamellarin D: induction of cellular senescence through inhibition of topoisomerase I and intracellular Ros productionPregnane X-receptor promotes stem cell-mediated colon cancer relapseThe senescence-associated secretory phenotype induces cellular plasticity and tissue regeneration.Mitotic catastrophe and cell cycle arrest are alternative cell death pathways executed by bortezomib in rituximab resistant B-cell lymphoma cellsMetabolic enzymes: key modulators of functionality in cancer stem-like cells.Chemotherapy enriches for an invasive triple-negative breast tumor cell subpopulation expressing a precursor form of N-cadherin on the cell surface.In vitro long-term treatment with MAPK inhibitors induces melanoma cells with resistance plasticity to inhibitors while retaining sensitivity to CD8 T cells.A nucleolytic lupus autoantibody is toxic to BRCA2-deficient cancer cells.MicroRNAs regulate both epithelial-to-mesenchymal transition and cancer stem cells.Constitutive expression and activation of stress response genes in cancer stem-like cells/tumour initiating cells: potent targets for cancer stem cell therapy.EZH2 inhibition re-sensitizes multidrug resistant B-cell lymphomas to etoposide mediated apoptosis.Modulation of SOX2 expression delineates an end-point for paclitaxel-effectiveness in breast cancer stem cells.Role of "oncogenic nexus" of CIP2A in breast oncogenesis: how does it work?
P2860
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P2860
Drug-induced senescence generates chemoresistant stemlike cells with low reactive oxygen species.
description
2011 nî lūn-bûn
@nan
2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Drug-induced senescence genera ...... h low reactive oxygen species.
@ast
Drug-induced senescence genera ...... h low reactive oxygen species.
@en
type
label
Drug-induced senescence genera ...... h low reactive oxygen species.
@ast
Drug-induced senescence genera ...... h low reactive oxygen species.
@en
prefLabel
Drug-induced senescence genera ...... h low reactive oxygen species.
@ast
Drug-induced senescence genera ...... h low reactive oxygen species.
@en
P2093
P2860
P356
P1476
Drug-induced senescence genera ...... h low reactive oxygen species.
@en
P2093
Jem Prabhakar
M Radhakrishna Pillai
S Asha Nair
Santhi Achuthan
Thankayyan R Santhoshkumar
P2860
P304
37813-37829
P356
10.1074/JBC.M110.200675
P407
P577
2011-08-30T00:00:00Z