Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gliomas are a diverse group of brain tumors of glial origin. Most are characterized by diffuse infiltrative growth in the surrounding brain. In combination with their refractive nature to chemotherapy this makes it almost impossible to cure patients using combinations of conventional therapeutic strategies. The drastically increased knowledge about the molecular underpinnings of gliomas during the last decade has elicited high expectations for a more rational and effective therapy for these tumors. Most studies on the molecular pathways involved in glioma biology thus far had a strong focus on growth factor receptor protein tyrosine kinase (PTK) and phosphatidylinositol phosphatase signaling pathways. Except for the tumor suppressor PTEN, much less attention has been paid to the PTK counterparts, the protein tyrosine phosphatase (PTP) superfamily, in gliomas. PTPs are instrumental in the reversible phosphorylation of tyrosine residues and have emerged as important regulators of signaling pathways that are linked to various developmental and disease-related processes. Here, we provide an overview of the current knowledge on PTP involvement in gliomagenesis. So far, the data point to the potential implication of receptor-type (RPTPdelta, DEP1, RPTPmicro, RPTPzeta) and intracellular (PTP1B, TCPTP, SHP2, PTPN13) classical PTPs, dual-specific PTPs (MKP-1, VHP, PRL-3, KAP, PTEN) and the CDC25B and CDC25C PTPs in glioma biology. Like PTKs, these PTPs may represent promising targets for the development of novel diagnostic and therapeutic strategies in the treatment of high-grade gliomas.
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PMID:Protein tyrosine phosphatases in glioma biology. 1993 68

Pediatric glioma is a devastating brain tumor. Serine threonine tyrosine kinase 1 (STYK1) is a member of the protein tyrosine kinase family and plays a significant role in the formation of several malignant tumors. However, the expression pattern and role of STYK1 in glioma are not yet clear. The aim of this study was to investigate the role and molecular mechanism of STYK1 in glioma. The results showed that STYK1 was highly expressed in glioma cell lines. We also found that knockdown of STYK1 inhibited cell proliferation, migration, and invasion in vitro as well as tumorigenesis in vivo. Furthermore, knockdown of STYK1 significantly decreased the expression levels of phosphorylation of PI3K and Akt in glioma cells. Taken together, our data suggest that STYK1 plays an important role in the development and progression of glioma. Therefore, STYK1 may represent a novel therapeutic target for the treatment of glioma.
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PMID:Knockdown of Serine Threonine Tyrosine Kinase 1 (STYK1) Inhibits the Migration and Tumorigenesis in Glioma Cells. 2798 28


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