"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
about
At the crossroads: EGFR and PTHrP signaling in cancer-mediated diseases of boneSignaling cross-talk in the resistance to HER family receptor targeted therapyEffective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers.PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFRImproved overall survival following tyrosine kinase inhibitor treatment in advanced or metastatic non-small-cell lung cancer-the Holy Grail in cancer treatment?Survival and death signals can predict tumor response to therapy after oncogene inactivationCombined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas.Effective and selective targeting of leukemia cells using a TORC1/2 kinase inhibitorBMS-536924 reverses IGF-IR-induced transformation of mammary epithelial cells and causes growth inhibition and polarization of MCF7 cellsApoptosis induced by JAK2 inhibition is mediated by Bim and enhanced by the BH3 mimetic ABT-737 in JAK2 mutant human erythroid cells.Trastuzumab Sensitizes Ovarian Cancer Cells to EGFR-targeted Therapeutics.Rational combination of dual PI3K/mTOR blockade and Bcl-2/-xL inhibition in AML.Oncogenic mutant forms of EGFR: lessons in signal transduction and targets for cancer therapy.Potential clinical implications of BRAF mutations in histiocytic proliferations.Systems biology modeling reveals a possible mechanism of the tumor cell death upon oncogene inactivation in EGFR addicted cancers.Activation of oncogenic pathways in idiopathic pulmonary fibrosis.Notch-EGFR/HER2 Bidirectional Crosstalk in Breast CancerSynergistic antitumor effect between gefitinib and fractionated irradiation in anaplastic oligodendrogliomas cannot be predicted by the Egfr signaling activity.From Hen House to Bedside: Tracing Hanafusa's Legacy from Avian Leukemia Viruses to SRC to ABL and BeyondAurora kinase inhibitors as anticancer molecules.Epidermal Growth Factor Receptor Mutation Enhances Expression of Cadherin-5 in Lung Cancer CellsAntitumor activity of a monoclonal antibody targeting major histocompatibility complex class I-Her2 peptide complexes.Urokinase-type Plasminogen Activator (uPA) is Inhibited with QLT0267 a Small Molecule Targeting Integrin-linked Kinase (ILK)Overcoming resistance to molecularly targeted anticancer therapies: Rational drug combinations based on EGFR and MAPK inhibition for solid tumours and haematologic malignanciesRAS oncogene suppression induces apoptosis followed by more differentiated and less myelosuppressive disease upon relapse of acute myeloid leukemia.The plasticity of oncogene addiction: implications for targeted therapies directed to receptor tyrosine kinases.A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes.Characterization of a Dual CDC7/CDK9 Inhibitor in Multiple Myeloma Cellular ModelsOvercoming resistance in chronic myelogenous leukemia.Selection criteria for c-Met-targeted therapies: emerging evidence for biomarkers.Validating cancer drug targets through chemical geneticsClinical challenges in targeting anaplastic lymphoma kinase in advanced non-small cell lung cancer.Identifying novel targets of oncogenic EGF receptor signaling in lung cancer through global phosphoproteomics.KRAS and HRAS mutations confer resistance to MET targeting in preclinical models of MET-expressing tumor cells.Proteomic profiling identified multiple short-lived members of the central proteome as the direct targets of the addicted oncogenes in cancer cells.A systematic approach to therapeutic target selection in oesophago-gastric cancer.Gene silencing for epidermal growth factor receptor variant III induces cell-specific cytotoxicitySuppression of v-Src transformation by andrographolide via degradation of the v-Src protein and attenuation of the Erk signaling pathway.The Therapeutic Potential of CRISPR/Cas9 Systems in Oncogene-Addicted Cancer Types: Virally Driven Cancers as a Model System.Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis.
P2860
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P2860
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@ast
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@en
type
label
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@ast
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@en
prefLabel
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@ast
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@en
P2093
P1476
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
@en
P2093
Daniel A Haber
Jeffrey Settleman
Michael A Fischbach
Sreenath V Sharma
P304
4392s-4395s
P356
10.1158/1078-0432.CCR-06-0096
P407
P433
P577
2006-07-01T00:00:00Z