Oncogenic protein tyrosine kinases

@article{Santoro2004OncogenicPT,
  title={Oncogenic protein tyrosine kinases},
  author={Massimo Santoro and Francesca Carlomagno and Rosa Marina Melillo and Alfredo Fusco},
  journal={Cellular and Molecular Life Sciences CMLS},
  year={2004},
  volume={61},
  pages={2954-2964}
}
Abstract.RET is the receptor for glial-derived neurotrophic factor growth factors. It is a paradigm of a single gene that causes different types of human cancer when targeted by different genetic alterations. Like other receptor tyrosine kinases, once activated, RET recruits a variety of signaling molecules that mediate biological responses. Here we review data on the signaling pathways that lead to RET-mediated cell transformation and recent evidence that manipulation of RET holds promise for… 
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A Series of RET Fusion Spitz Neoplasms With Plaque-Like Silhouette and Dyscohesive Nesting of Epithelioid Melanocytes.
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5 cases of RET fusion Spitz neoplasms are identified and characteristics features which can help with recognition of the RET subgroup of Spitz are described which include plaque-like silhouette and monotonous epithelioid cytology with expansile and dyscohesive nesting.
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This study demonstrates that the Ret Gly691Ser mutation is associated with pVUR and may be one of the genetic causes of this condition in the French‐Canadian population in Quebec.
Array CGH demonstrates characteristic aberration signatures in human papillary thyroid carcinomas governed by RET/PTC
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The array CGH data presented serve as a starting point for further studies on gene expression and function of genes identified in this study and should be considered as a basis for future studies on RET/PTC-positive and-negative tumours.

References

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Ret-mediated mitogenesis requires Src kinase activity.
TLDR
Activated Ret is able to bind and stimulate c-Src kinase and that Src activation is essential for the mitogenic activity of Ret, and it is shown that Ret is ability to associate with the SH2 domain of Src in a phosphotyrosine-dependent fashion.
Tyrosine 981, a Novel Ret Autophosphorylation Site, Binds c-Src to Mediate Neuronal Survival*
TLDR
It is shown by multiple approaches that Ret tyrosine 981 constitutes the major binding site of the Src homology 2 domain of Src and therefore the primary residue responsible for Src activation upon Ret engagement, and becomes phosphorylated in dissociated sympathetic neurons after ligand stimulation.
The kinase inhibitor PP1 blocks tumorigenesis induced by RET oncogenes.
TLDR
Targeting RET oncogenes with PP1 or related compounds as a novel treatment strategy for RET-associated neoplasms is suggested.
Grap-2, a novel RET binding protein, is involved in RET mitogenic signaling
TLDR
Results suggest that besides being involved in tyrosine kinase signaling in hematopoietic cells, Grap-2 plays a tissue-specific role as an inhibitor of RET mitogenic signaling.
ZD6474, an orally available inhibitor of KDR tyrosine kinase activity, efficiently blocks oncogenic RET kinases.
TLDR
ZD6474, a low molecular weight tyrosine kinase inhibitor, blocks the enzymatic activity of RET-derived oncoproteins at a one-half maximal inhibitory concentration of 100 nM and might offer a potential treatment strategy for carcinomas sustaining oncogenic activation of RET.
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TLDR
It is suggested that the RAS and PI3-K pathways activated by GDNF bifurcate mainly through SHC bound to tyrosine 1062 in RET, which is important for activation of CREB and NF-κB in GDNF-treated cells, respectively.
The GDNF family: Signalling, biological functions and therapeutic value
Members of the nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) families — comprising neurotrophins and GDNF-family ligands (GFLs), respectively — are crucial for the…
Docking Protein FRS2 Links the Protein Tyrosine Kinase RET and Its Oncogenic Forms with the Mitogen-Activated Protein Kinase Signaling Cascade
TLDR
It is demonstrated that FRS2 couples both ligand-regulated and oncogenic forms of RET, with the MAP kinase signaling cascade as part of the response of RET under normal biological conditions and pathological conditions, such as MEN 2 and papillary thyroid carcinomas.
The Neuron-Specific Rai (ShcC) Adaptor Protein Inhibits Apoptosis by Coupling Ret to the Phosphatidylinositol 3-Kinase/Akt Signaling Pathway
TLDR
It is proposed that Rai potentiates the MAPK and PI3K signaling pathways and regulates Ret-dependent and -independent survival signals.
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