Mitf is the key molecular switch between mouse or human melanoma initiating cells and their differentiated progeny.
about
Melanoma: from melanocyte to genetic alterations and clinical optionsIn vitro evidence for senescent multinucleated melanocytes as a source for tumor-initiating cells.Alternative Treatments For Melanoma: Targeting BCL-2 Family Members to De-Bulk and Kill Cancer Stem CellsCell cycle gene networks are associated with melanoma prognosisThe novel gamma secretase inhibitor RO4929097 reduces the tumor initiating potential of melanomaDifferentiated melanocyte cell division occurs in vivo and is promoted by mutations in Mitf.A functional screen identifies specific microRNAs capable of inhibiting human melanoma cell viability.The soy-derived peptide Lunasin inhibits invasive potential of melanoma initiating cellsNovel roles for the MiTF/TFE family of transcription factors in organelle biogenesis, nutrient sensing, and energy homeostasisPGC-1 coactivators regulate MITF and the tanning response.Repression of genes involved in melanocyte differentiation in uveal melanoma.Regulatory and functional connection of microphthalmia-associated transcription factor and anti-metastatic pigment epithelium derived factor in melanomaMining gene expression signature for the detection of pre-malignant melanocytes and early melanomas with risk for metastasisChromatin barcodes as biomarkers for melanoma.PRMT5 is upregulated in malignant and metastatic melanoma and regulates expression of MITF and p27(Kip1.).MITF drives endolysosomal biogenesis and potentiates Wnt signaling in melanoma cells.Senescent cells develop a PARP-1 and nuclear factor-{kappa}B-associated secretome (PNAS)A novel hypoxia-associated subset of FN1 high MITF low melanoma cells: identification, characterization, and prognostic value.Loss of CITED1, an MITF regulator, drives a phenotype switch in vitro and can predict clinical outcome in primary melanoma tumours.Gene expression profiling identifies microphthalmia-associated transcription factor (MITF) and Dickkopf-1 (DKK1) as regulators of microenvironment-driven alterations in melanoma phenotypeMITF in melanoma: mechanisms behind its expression and activity.Methylation-dependent SOX9 expression mediates invasion in human melanoma cells and is a negative prognostic factor in advanced melanomaLow MITF/AXL ratio predicts early resistance to multiple targeted drugs in melanoma.microRNA-155, induced by interleukin-1ß, represses the expression of microphthalmia-associated transcription factor (MITF-M) in melanoma cells.MCL-1, BCL-XL and MITF Are Diversely Employed in Adaptive Response of Melanoma Cells to Changes in Microenvironment.Extrafollicular dermal melanocyte stem cells and melanomaUnderstanding melanoma stem cellsMITF and c-Jun antagonism interconnects melanoma dedifferentiation with pro-inflammatory cytokine responsiveness and myeloid cell recruitment.The emerging roles of Oct4 in tumor-initiating cells.Identification of the hypoxia-inducible factor 2α nuclear interactome in melanoma cells reveals master proteins involved in melanoma developmentAbsence of germline CDKN2A mutation in Sicilian patients with familial malignant melanoma: Could it be a population-specific genetic signature?Resveratrol inhibits alpha-melanocyte-stimulating hormone signaling, viability, and invasiveness in melanoma cells.The non-canonical functions of p27(Kip1) in normal and tumor biology.SOX10 ablation arrests cell cycle, induces senescence, and suppresses melanomagenesisInhibition of melanocortin 1 receptor slows melanoma growth, reduces tumor heterogeneity and increases survival.Differential mechanisms of tumor progression in clones from a single heterogeneous human melanoma.Microphthalmia-associated transcription factor suppresses invasion by reducing intracellular GTP pools.Hypoxia induces phenotypic plasticity and therapy resistance in melanoma via the tyrosine kinase receptors ROR1 and ROR2.Secretome from senescent melanoma engages the STAT3 pathway to favor reprogramming of naive melanoma towards a tumor-initiating cell phenotype.Translation reprogramming is an evolutionarily conserved driver of phenotypic plasticity and therapeutic resistance in melanoma.
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Mitf is the key molecular switch between mouse or human melanoma initiating cells and their differentiated progeny.
description
2011 nî lūn-bûn
@nan
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
2011年论文
@zh
2011年论文
@zh-cn
name
Mitf is the key molecular swit ...... their differentiated progeny.
@en
Mitf is the key molecular swit ...... their differentiated progeny.
@nl
type
label
Mitf is the key molecular swit ...... their differentiated progeny.
@en
Mitf is the key molecular swit ...... their differentiated progeny.
@nl
prefLabel
Mitf is the key molecular swit ...... their differentiated progeny.
@en
Mitf is the key molecular swit ...... their differentiated progeny.
@nl
P2093
P2860
P50
P356
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P1476
Mitf is the key molecular swit ...... d their differentiated progeny
@en
P2093
P2860
P2888
P304
P356
10.1038/ONC.2010.598
P407
P577
2011-01-31T00:00:00Z