CDK inhibitors (p16/p19/p21) induce senescence and autophagy in cancer-associated fibroblasts, "fueling" tumor growth via paracrine interactions, without an increase in neo-angiogenesis.
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Recapitulating the Tumor Ecosystem Along the Metastatic Cascade Using 3D Culture ModelsTumor and stromal-based contributions to head and neck squamous cell carcinoma invasionOncogenes induce the cancer-associated fibroblast phenotype: metabolic symbiosis and "fibroblast addiction" are new therapeutic targets for drug discoveryRole of oxidative stress and the microenvironment in breast cancer development and progressionRetinoids induce cellular senescence in breast cancer cells by RAR-β dependent and independent pathways: Potential clinical implications (Review)Longitudinal tracking of single live cancer cells to understand cell cycle effects of the nuclear export inhibitor, selinexor.Role of p62 in the suppression of inflammatory cytokine production by adiponectin in macrophages: Involvement of autophagy and p21/Nrf2 axis.CDK4/6 and autophagy inhibitors synergistically induce senescence in Rb positive cytoplasmic cyclin E negative cancers.Cellular senescence and protein degradation: breaking down cancerThe molecular balancing act of p16(INK4a) in cancer and aging.Palbociclib (PD 0332991) : targeting the cell cycle machinery in breast cancer.New targeted therapies for breast cancer: A focus on tumor microenvironmental signals and chemoresistant breast cancersStromal cells in tumor microenvironment and breast cancerChemotherapy induces the cancer-associated fibroblast phenotype, activating paracrine Hedgehog-GLI signalling in breast cancer cellsCellular senescence and autophagy of myoepithelial cells are involved in the progression of in situ areas of carcinoma ex-pleomorphic adenoma to invasive carcinoma. An in vitro modelTargeting multiple tyrosine kinase receptors with Dovitinib blocks invasion and the interaction between tumor cells and cancer-associated fibroblasts in breast cancer.Mitochondria "fuel" breast cancer metabolism: fifteen markers of mitochondrial biogenesis label epithelial cancer cells, but are excluded from adjacent stromal cellsCreating a tumor-resistant microenvironment: cell-mediated delivery of TNFα completely prevents breast cancer tumor formation in vivo.Cigarette smoke metabolically promotes cancer, via autophagy and premature aging in the host stromal microenvironment.Role of stress-activated OCT4A in the cell fate decisions of embryonal carcinoma cells treated with etoposide.Compartment-specific activation of PPARγ governs breast cancer tumor growth, via metabolic reprogramming and symbiosis.From Ancient Pathways to Aging Cells-Connecting Metabolism and Cellular Senescence.Negative control of CSL gene transcription by stress/DNA damage response and p53.Soluble egg antigens of Schistosoma japonicum induce senescence in activated hepatic stellate cells by activation of the STAT3/p53/p21 pathway1-(2-Hydroxy-5-methylphenyl)-3-phenyl-1,3-propanedione Induces G1 Cell Cycle Arrest and Autophagy in HeLa Cervical Cancer Cells.Selective disruption of rb-raf-1 kinase interaction inhibits pancreatic adenocarcinoma growth irrespective of gemcitabine sensitivity.Mesenchymal stroma: primary determinant and therapeutic target for epithelial cancer.Oncogenes and inflammation rewire host energy metabolism in the tumor microenvironment: RAS and NFκB target stromal MCT4.CDK4/6-inhibiting drug substitutes for p21 and p16 in senescence: duration of cell cycle arrest and MTOR activity determine geroconversion.Donor age negatively impacts adipose tissue-derived mesenchymal stem cell expansion and differentiation.Autophagy and the Cell Cycle: A Complex Landscape.The significance of the senescence pathway in breast cancer progression.Cellular senescence and its effector programs.Autophagy and cancer metabolism.Stress management by autophagy: Implications for chemoresistance.Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?Up-regulation of p21(WAF1/CIP1) by miRNAs and its implications in bladder cancer cells.Stromal Senescence By Prolonged CDK4/6 Inhibition Potentiates Tumor Growth.Characterization of early autophagy signaling by quantitative phosphoproteomicsTGF-β Family Signaling in Tumor Suppression and Cancer Progression.
P2860
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P2860
CDK inhibitors (p16/p19/p21) induce senescence and autophagy in cancer-associated fibroblasts, "fueling" tumor growth via paracrine interactions, without an increase in neo-angiogenesis.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@ast
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@en
type
label
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@ast
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@en
prefLabel
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@ast
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@en
P2093
P2860
P50
P356
P1433
P1476
CDK inhibitors (p16/p19/p21) i ...... increase in neo-angiogenesis.
@en
P2093
Anthony Howell
Barbara Chiavarina
Claudia Capparelli
James Hulit
Richard G Pestell
Sebastiano Andò
Timothy G Pestell
Ubaldo E Martinez-Outschoorn
P2860
P304
P356
10.4161/CC.21884
P577
2012-08-30T00:00:00Z