A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes. - Wikidata - wikimedia - TriplyDB

A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes.

A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes.

http://www.wikidata.org/entity/Q37169157

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A novel pro-apoptotic function of RACK1: suppression of Src activity in the intrinsic and Akt pathways PME-1 protects extracellular signal-regulated kinase pathway activity from protein phosphatase 2A-mediated inactivation in human malignant glioma FoxM1, a critical regulator of oxidative stress during oncogenesis Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanisms The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas Oncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer Cells The double face of Morgana in tumorigenesis MYC activation is a hallmark of cancer initiation and maintenance Mechanisms of disseminated cancer cell dormancy: an awakening field One more stem cell niche: how the sensitivity of chronic myeloid leukemia cells to imatinib mesylate is modulated within a "hypoxic" environment.Role of Werner syndrome gene product helicase in carcinogenesis and in resistance to genotoxins by cancer cells c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells AST1306, a novel irreversible inhibitor of the epidermal growth factor receptor 1 and 2, exhibits antitumor activity both in vitro and in vivo Lapatinib-binding protein kinases in the African trypanosome: identification of cellular targets for kinase-directed chemical scaffolds BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with oncogenic EGFR mutations Noisy-threshold control of cell death.Survival and death signals can predict tumor response to therapy after oncogene inactivation Computational delineation of tyrosyl-substrate recognition and catalytic landscapes by the epidermal growth factor receptor tyrosine kinase domain.Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas.Single cell cytometry of protein function in RNAi treated cells and in native populations ERK2, but not ERK1, mediates acquired and "de novo" resistance to imatinib mesylate: implication for CML therapy Role of network branching in eliciting differential short-term signaling responses in the hypersensitive epidermal growth factor receptor mutants implicated in lung cancer Molecular systems biology of ErbB1 signaling: bridging the gap through multiscale modeling and high-performance computing.Dormancy of metastatic melanoma CD44 attenuates activation of the hippo signaling pathway and is a prime therapeutic target for glioblastoma Inactivation of MYC reverses tumorigenesis.Structural and mechanistic underpinnings of the differential drug sensitivity of EGFR mutations in non-small cell lung cancer.Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase.Response and resistance to MEK inhibition in leukaemias initiated by hyperactive Ras The mitogen-activated protein kinase kinase 4 has a pro-oncogenic role in skin cancer.Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance.Systems biology modeling reveals a possible mechanism of the tumor cell death upon oncogene inactivation in EGFR addicted cancers.What are we learning from the cancer genome?Clinical implications of novel activating EGFR mutations in malignant peritoneal mesothelioma.Drug-repositioning screening identified piperlongumine as a direct STAT3 inhibitor with potent activity against breast cancer.MEK-dependent negative feedback underlies BCR-ABL-mediated oncogene addiction THOC5 spliceosome protein: a target for leukaemogenic tyrosine kinases that affects inositol lipid turnover.Analysis of Somatic Mutations in Cancer: Molecular Mechanisms of Activation in the ErbB Family of Receptor Tyrosine Kinases.c-Myc dependent expression of pro-apoptotic Bim renders HER2-overexpressing breast cancer cells dependent on anti-apoptotic Mcl-1

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A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes.

http://www.wikidata.org/entity/Q37169157

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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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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2006年學術文章

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name

A common signaling cascade may ...... L, and EGF receptor oncogenes.

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A common signaling cascade may ...... L, and EGF receptor oncogenes.

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type

label

A common signaling cascade may ...... L, and EGF receptor oncogenes.

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A common signaling cascade may ...... L, and EGF receptor oncogenes.

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prefLabel

A common signaling cascade may ...... L, and EGF receptor oncogenes.

@en

A common signaling cascade may ...... L, and EGF receptor oncogenes.

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J.CCR.2006.09.014

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A common signaling cascade may ...... L, and EGF receptor oncogenes.

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Daniel A Haber

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Diana Y Lee

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Inna P Way

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Jane Jiang

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Jeffrey Settleman

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Marie Classon

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Patrycja Gajowniczek

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Sreenath V Sharma

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Yuki Yuza

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P2860

Akt phosphorylates and negatively regulates apoptosis signal-regulating kinase 1

Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways

Negative feedback regulation of ASK1 by protein phosphatase 5 (PP5) in response to oxidative stress

SU6656, a selective src family kinase inhibitor, used to probe growth factor signaling

EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib

EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

The pro-apoptotic Ras effector Nore1 may serve as a Ras-regulated tumor suppressor in the lung

Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells

Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis

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