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oncogene addiction/tyrosine
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The plasticity of oncogene addiction: implications for targeted therapies directed to receptor tyrosine kinases.
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A common mutation of the epidermal growth factor receptor (EGFR) in glioblastoma multiforme (GBM) is an extracellular truncation known as the de2-7 EGFR (or EGFRvIII). Hepatocyte growth factor (HGF) is the ligand for the receptor tyrosine kinase (RTK) c-Met, and this signaling axis is often active
Oncogene addiction as a foundation of targeted cancer therapy: The paradigm of the MET receptor tyrosine kinase.
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Following nearly two decades of its conception, the phenomenon of oncogene addiction still represents a key concept of how progresses in basic research can translate to unprecedented translational breakthroughs. Coined by Bernard Weinstein, this term refers to the phenomenon by which cancer cells
KRAS in Non-Small-Cell Lung Cancer: Oncogenic Addiction and Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors.
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Targeting CK2-driven non-oncogene addiction in B-cell tumors.
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Genetic mutations of oncogenes often underlie deranged cell growth and altered differentiation pathways leading to malignant transformation of B-lymphocytes. However, addiction to oncogenes is not the only drive to lymphoid tumor pathogenesis. Dependence on non-oncogenes, which act by propelling
The RON receptor tyrosine kinase in pancreatic cancer pathogenesis and its potential implications for future targeted therapies.
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Pancreatic cancer remains a devastating disease with a mortality rate that has not changed substantially in decades. Novel therapies are therefore desperately needed. The RON receptor tyrosine kinase has been identified as an important mediator of KRAS oncogene addiction and is overexpressed in the
Oncogenic association of the Cbp/PAG adaptor protein with the Lyn tyrosine kinase in human B-NHL rafts.
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B-non-Hodgkin lymphomas (B-NHLs) use a raft-associated signalosome made of the constitutively active Lyn kinase, the tyrosine phosphorylated Cbp/PAG adaptor, and tyrosine phosphorylated STAT3 transcription factor. No such "signalosome" is found in rafts of ALK(+) T lymphoma and Hodgkin-derived cell
Generations of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors: Perils and Progress.
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UNASSIGNED
Epidermal growth factor receptor (EGFR) mutations have been detected in approximately 10 % of North American patients diagnosed with non-small cell lung cancer (NSCLC). Approximately 90 % of these mutations are exon 19 deletions or exon 21 L858R point mutations. First- and
Concise review: cancer cells escape from oncogene addiction: understanding the mechanisms behind treatment failure for more effective targeting.
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Oncogene addiction describes the dependence of some cancers on one or a few genes for their survival. Inhibition of the corresponding oncoproteins can lead to dramatic responses. However, in some cases, such as chronic myeloid leukemia (CML), a disease characterized by the presence of the abnormal
Differential Effects of Tyrosine Kinase Inhibitors on Normal and Oncogenic EGFR Signaling and Downstream Effectors.
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Constitutive activation of EGFR due to overexpression or mutation in tumor cells leads to dysregulated downstream cellular signaling pathways. Therefore, EGFR as well as its downstream effectors have been identified as important therapeutic targets. The FDA-approved small-molecule inhibitors of
Fusion tyrosine kinase mediated signalling pathways in the transformation of haematopoietic cells.
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The fusion tyrosine kinases (FTKs) are generated by chromosomal translocations creating bipartite proteins in which the kinase is hyperactivated by an adjoining oligomerization domain. Autophosphorylation of the FTK generates a 'signalosome', an ensemble of signalling proteins that transduce signals
Tyrosine kinases as molecular targets to inhibit cancer progression and metastasis.
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During the last decades, the improvement of our knowledge of the mechanisms responsible for cancer development has led to the introduction of new promising strategies of treatment, based on "molecular targeted" drugs. These drugs are designed to act on specific molecules, identified as major players
Only a subset of Met-activated pathways are required to sustain oncogene addiction.
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Tumor onset and progression require the accumulation of many genetic and epigenetic lesions. In some cases, however, cancer cells rely on only one of these lesions to maintain their malignant properties, and this dependence results in tumor regression upon oncogene inactivation ("oncogene
Cyclin-dependent kinase 7/9 inhibitor SNS-032 abrogates FIP1-like-1 platelet-derived growth factor receptor α and bcr-abl oncogene addiction in malignant hematologic cells.
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OBJECTIVE
The "gate-keeper" mutations T674I platelet-derived growth factor receptor α (PDGFRα) in hypereosinophilic syndrome (HES) and T315I Bcr-Abl in chronic myeloid leukemia (CML) are resistant to imatinib and the second-generation small-molecule tyrosine kinase inhibitors (TKI). However, to
Only a subset of Met-activated pathways are required to sustain oncogene addiction.
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Tumor onset and progression require the accumulation of many genetic and epigenetic lesions. In some cases, however, cancer cells rely on only one of these lesions to maintain their malignant properties, and this dependence results in tumor regression upon oncogene inactivation ("oncogene
"Oncogenic shock": explaining oncogene addiction through differential signal attenuation.
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"Oncogene addiction" describes the curious acquired dependence of tumor cells on an activated oncogene for their survival and/or proliferation, a phenomenon that has important implications for the success of targeted cancer therapies. However, the mechanisms explaining oncogene addiction remain
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