Multiple oncogenic changes (K-RAS(V12), p53 knockdown, mutant EGFRs, p16 bypass, telomerase) are not sufficient to confer a full malignant phenotype on human bronchial epithelial cells. - Wikidata - awgldk - TriplyDB

Multiple oncogenic changes (K-RAS(V12), p53 knockdown, mutant EGFRs, p16 bypass, telomerase) are not sufficient to confer a full malignant phenotype on human bronchial epithelial cells.

Multiple oncogenic changes (K-RAS(V12), p53 knockdown, mutant EGFRs, p16 bypass, telomerase) are not sufficient to confer a full malignant phenotype on human bronchial epithelial cells.

http://www.wikidata.org/entity/Q46952752

about

Intratumoral epiregulin is a marker of advanced disease in non-small cell lung cancer patients and confers invasive properties on EGFR-mutant cells Molecular biology of lung cancer: clinical implications Replacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responses Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas H-REV107-1 stimulates growth in non-small cell lung carcinomas via the activation of mitogenic signaling Smoking, p53 mutation, and lung cancer Expression of sirtuin 1 and 2 is associated with poor prognosis in non-small cell lung cancer patients Effect of KRAS oncogene substitutions on protein behavior: implications for signaling and clinical outcome Oncogenic K-Ras regulates proliferation and cell junctions in lung epithelial cells through induction of cyclooxygenase-2 and activation of metalloproteinase-9 Akt activation is responsible for enhanced migratory and invasive behavior of arsenic-transformed human bronchial epithelial cells A genome-wide screen for promoter methylation in lung cancer identifies novel methylation markers for multiple malignancies CDDO-Me protects normal lung and breast epithelial cells but not cancer cells from radiation Identification of a candidate therapeutic autophagy-inducing peptide Polymorphisms, mutations, and amplification of the EGFR gene in non-small cell lung cancers The biological sense of cancer: a hypothesis Multiple cancer testis antigens function to support tumor cell mitotic fidelity.Two subunits of human ORC are dispensable for DNA replication and proliferation.Inhibition of breast cancer metastasis suppressor 1 promotes a mesenchymal phenotype in lung epithelial cells that express oncogenic K-RasV12 and loss of p53.Transcriptional profiling of non-small cell lung cancer cells with activating EGFR somatic mutations.Molecular profiling of breast cancer cell lines defines relevant tumor models and provides a resource for cancer gene discovery.Oncogene mutations, copy number gains and mutant allele specific imbalance (MASI) frequently occur together in tumor cells.Ras regulates kinesin 13 family members to control cell migration pathways in transformed human bronchial epithelial cells.Integrative genomic analyses identify BRF2 as a novel lineage-specific oncogene in lung squamous cell carcinoma NeuroD1 mediates nicotine-induced migration and invasion via regulation of the nicotinic acetylcholine receptor subunits in a subset of neural and neuroendocrine carcinomas.AURKA mRNA expression is an independent predictor of poor prognosis in patients with non-small cell lung cancer Cytoglobin, the newest member of the globin family, functions as a tumor suppressor gene Epidermal growth factor receptors with tyrosine kinase domain mutations exhibit reduced Cbl association, poor ubiquitylation, and down-regulation but are efficiently internalized Mechanisms of Cancer Induction by Tobacco-Specific NNK and NNN.PIK3CA mutations and copy number gains in human lung cancers.Mechanisms promoting escape from mitotic stress-induced tumor cell death.Phosphoproteomics identifies oncogenic Ras signaling targets and their involvement in lung adenocarcinomas.Branching morphogenesis of immortalized human bronchial epithelial cells in three-dimensional culture.Multipotent capacity of immortalized human bronchial epithelial cells Ras transformation uncouples the kinesin-coordinated cellular nutrient response MicroRNA expression distinguishes SCLC from NSCLC lung tumor cells and suggests a possible pathological relationship between SCLCs and NSCLCs Epidermal growth factor receptor in glioma: signal transduction, neuropathology, imaging, and radioresistance SMAC mimetic (JP1201) sensitizes non-small cell lung cancers to multiple chemotherapy agents in an IAP-dependent but TNF-α-independent manner hnRNP L regulates the tumorigenic capacity of lung cancer xenografts in mice via caspase-9 pre-mRNA processing Suppression of TET1-dependent DNA demethylation is essential for KRAS-mediated transformation.Alternative splicing of caspase 9 is modulated by the phosphoinositide 3-kinase/Akt pathway via phosphorylation of SRp30a.

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P2860

Multiple oncogenic changes (K-RAS(V12), p53 knockdown, mutant EGFRs, p16 bypass, telomerase) are not sufficient to confer a full malignant phenotype on human bronchial epithelial cells.

http://www.wikidata.org/entity/Q46952752

description

2006 nî lūn-bûn

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2006年の論文

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2006年学术文章

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Multiple oncogenic changes (K- ...... an bronchial epithelial cells.

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Multiple oncogenic changes (K- ...... an bronchial epithelial cells.

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Multiple oncogenic changes (K- ...... an bronchial epithelial cells.

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Multiple oncogenic changes (K- ...... an bronchial epithelial cells.

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Multiple oncogenic changes (K- ...... an bronchial epithelial cells.

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Multiple oncogenic changes (K- ...... an bronchial epithelial cells.

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0008-5472.CAN-05-2521

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Cancer Research

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Multiple oncogenic changes (K- ...... man bronchial epithelial cells

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Adi F Gazdar

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David S Shames

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Jerry W Shay

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John D Minna

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Luc Girard

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Mitsuo Sato

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Noriaki Sunaga

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Ruben D Ramirez

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Woochang Lee

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2116-2128

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10.1158/0008-5472.CAN-05-2521

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Melville B Vaughan

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2006-02-01T00:00:00Z

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