A closely homologous tyrosine kinase PDGFRA is observed in 5% to 7% of GISTs.
The patient responded to Imatinib remedy without any recurrence right after six months. More than 80% of PDGFRA mutations arise in exon 18. They are largely missense mutations top to substitution of Asp to Val.
5% to 15% of GISTs tend not to harbor either kit or PDGFRA mutations and are known as wild kind GISTs. These tumors might be beneficial for CD117 and might be mistakenly labeled as an Imitanib susceptible GIST. Nevertheless, these tumors are regarded as less responsive VEGF to imatinib treatment with a poorer prognosis. It has been suggested that these tumors harbor the insulin growth factor 1 receptor mutation, which is highly expressed in both adult and pediatric wild type GIST. The downregulation of IGF1R activity would lead to cytotoxicity or induced apoptosis in experimental studies. The spectrum of clinical presentation in GIST is broad. It is largely dependent on tumor size and location. GIST causing symptoms are usually larger in size, more than 6 cm in diameter. The most common presentation of GIST is abdominal pain and/or GI bleeding.
The most common metastatic sites include the abdominal cavity, liver, and rarely bones and soft tissues. GISTs very rarely, if not, metastasize to the lymph nodes and the skin.
Neurobromatosis type I can also harbor multiple GISTs in approximately 7% of patients. This results from germline mutation of NF 1 gene that encodes neurobromin.
Thursday, March 28, 2013
Quickly Fixes For the AG-1478 ALK Inhibitor Problems
Labels:
AG-1478,
ALK Inhibitor,
Alogliptin,
Celecoxib
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