C-MYC overexpression is required for continuous suppression of oncogene-induced senescence in melanoma cells. - Wikidata - awgldk - TriplyDB

C-MYC overexpression is required for continuous suppression of oncogene-induced senescence in melanoma cells.

C-MYC overexpression is required for continuous suppression of oncogene-induced senescence in melanoma cells.

http://www.wikidata.org/entity/Q39954044

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MYC, Metabolism, and Cancer Small-molecule inhibitors of the Myc oncoprotein Polycomb group protein Bmi1 is required for growth of RAF driven non-small-cell lung cancer Raf kinases in cancer-roles and therapeutic opportunities Liver-specific expressions of HBx and src in the p53 mutant trigger hepatocarcinogenesis in zebrafish Pseudo-DNA damage response in senescent cells MYC on the path to cancer RAB7 counteracts PI3K-driven macropinocytosis activated at early stages of melanoma development The relative contributions of the p53 and pRb pathways in oncogene-induced melanocyte senescence.Phosphorylation by Cdk2 is required for Myc to repress Ras-induced senescence in cotransformation.MYC and the control of DNA replication.Epstein-Barr virus (EBV) Rta-mediated EBV and Kaposi's sarcoma-associated herpesvirus lytic reactivations in 293 cells.Cellular senescence and protein degradation: breaking down cancer p27Kip1 mediates addiction of ovarian cancer cells to MYCC (c-MYC) and their dependence on MYC paralogs.MYC Inactivation Elicits Oncogene Addiction through Both Tumor Cell-Intrinsic and Host-Dependent Mechanisms.Dabrafenib and its potential for the treatment of metastatic melanoma.Transcriptome profiling identifies HMGA2 as a biomarker of melanoma progression and prognosis.Melanoma proliferation and chemoresistance controlled by the DEK oncogene TGF-beta signaling engages an ATM-CHK2-p53-independent RAS-induced senescence and prevents malignant transformation in human mammary epithelial cells.Senescent cells develop a PARP-1 and nuclear factor-{kappa}B-associated secretome (PNAS)The profile of tumor antigens which can be targeted by immunotherapy depends upon the tumor's anatomical site.BCYRN1, a c-MYC-activated long non-coding RNA, regulates cell metastasis of non-small-cell lung cancer.PP2A-B56α controls oncogene-induced senescence in normal and tumor human melanocytic cells Comparative metabolic flux profiling of melanoma cell lines: beyond the Warburg effect.New Perspectives of "omics" Applications in Melanoma Research.Cellular senescence and cancer chemotherapy resistance.A prognostic signature of defective p53-dependent G1 checkpoint function in melanoma cell lines B-Raf activation cooperates with PTEN loss to drive c-Myc expression in advanced prostate cancer Functional characterization of RAD52 as a lung cancer susceptibility gene in the 12p13.33 locus Recent progress in genetics of aging, senescence and longevity: focusing on cancer-related genes.The role of senescence and prosurvival signaling in controlling the oncogenic activity of FGFR2 mutants associated with cancer and birth defects.A genomic screen identifies TYRO3 as a MITF regulator in melanoma.Activities of multiple cancer-related pathways are associated with BRAF mutation and predict the resistance to BRAF/MEK inhibitors in melanoma cells.Epigenetics in human melanoma.ERK and cell death: mechanisms of ERK-induced cell death--apoptosis, autophagy and senescence.Cancer stem cells: a reality, a myth, a fuzzy concept or a misnomer? An analysis.Cdk2: a key regulator of the senescence control function of Myc.Resistance to transforming growth factor β-mediated tumor suppression in melanoma: are multiple mechanisms in place?Pathways of oncogene-induced senescence in human melanocytic cells Advances in melanoma senescence and potential clinical application.

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C-MYC overexpression is required for continuous suppression of oncogene-induced senescence in melanoma cells.

http://www.wikidata.org/entity/Q39954044

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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name

C-MYC overexpression is requir ...... senescence in melanoma cells.

@en

C-MYC overexpression is requir ...... senescence in melanoma cells.

@nl

type

label

C-MYC overexpression is requir ...... senescence in melanoma cells.

@en

C-MYC overexpression is requir ...... senescence in melanoma cells.

@nl

prefLabel

C-MYC overexpression is requir ...... senescence in melanoma cells.

@en

C-MYC overexpression is requir ...... senescence in melanoma cells.

@nl

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C-MYC overexpression is requir ...... senescence in melanoma cells.

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A E Berman

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D Zhuang

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E V Prochownik

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J A Wawrzyniak

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M A Nikiforov

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M S Soengas

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V Grachtchouk

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W-H Tang

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P2860

TRRAP-dependent and TRRAP-independent transcriptional activation by Myc family oncoproteins.

WAF1, a potential mediator of p53 tumor suppression

A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage

Determinants of BRAF mutations in primary melanomas

Extra c-myc oncogene copies in high risk cutaneous malignant melanoma and melanoma metastases

ARF functions as a melanoma tumor suppressor by inducing p53-independent senescence

Distinct sets of genetic alterations in melanoma

p53-dependent apoptosis modulates the cytotoxicity of anticancer agents

Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas

Restoration of p53 function leads to tumour regression in vivo

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Thomas Giordano

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