Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
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Compound
Query: UNIPROT:P10721 (
c-kit
)
6,575
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Tyrosine kinase
inhibitors (TKIs) have significantly improved the clinical outcomes of patients with chronic myeloid leukemia (CML). However, patients with CML need to receive TKI therapy for several years. Hence, the safety of long-term TKI treatment warrants utmost attention. Among various adverse events caused by TKI therapy, cardiovascular events (CVEs), such as acute myocardial infarction, cerebral infarction, and pulmonary hypertension, are the most serious with high mortality. TKIs inhibit various off-target molecules involved in the occurrence of CVEs such as
c-Kit
, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor (VEGFR), and Tie-2/Tec. At present, nilotinib, dasatinib, and ponatinib, but not bosutinib, have been demonstrated to increase the risk of CVEs in patients with CML compared with imatinib. Conversely, patients with CML have also been shown to have high CVE risks regardless of the TKI treatment compared with non-cancer population. Hence, further analyses are required to deduce the influence of TKI treatment on CVEs. Whatever the cause may be, to prevent CVEs in patients with CML, we need to appropriately screen and monitor CVE risks such as hypertension, serum glucose, lipid levels, ankle-brachial index (ABI), Electrocardiography (ECG), and echocardiography before and during TKI treatment.
...
PMID:[Management of cardiovascular complications in CML patients treated with tyrosine kinase inhibitors]. 2941 32
Gastrointestinal stromal tumor (GIST) is a rare but an important clinical entity seen in our clinical practice. It is the most common mesenchymal tumor of the gastrointestinal tract and most common malignancy of the small intestine. Although the exact prevalence of GIST is not known, the incidence of GIST has been increasing. GISTs arise from interstitial cells of Cajal. Most of the GISTs occur due to mutation in
c-kit
gene or platelet derived growth factor receptor alpha gene. 15% of GISTs do not have these mutations and they are called wild-type GISTs. Almost all GISTs express KIT receptor tyrosine kinase. Histologically, GISTs look like spindle cell tumors most of the time but they can be epitheloid or mixed type. The median size of GISTs varies from 2.7 cm to 8.9 cm. Clinically, patients with small GISTs remain asymptomatic but as the GIST size increases, patients present with various symptoms depending on the location of the GIST. Most of GISTs are located in the stomach or small bowel. Diagnosis is suspected on imaging and endoscopic studies, and confirmed by tissue acquisition with immunohistochemical staining. The aggressiveness of GISTs depends on the size, mitotic index and location. Surgical resection is the treatment of choice. But various endoscopic modalities of resection are increasingly being tried.
Tyrosine kinase
inhibitors are extremely useful in the management of large GISTs, unresectable GISTs and metastatic GISTs. Treatment options for metastatic GISTs also include radiotherapy, chemotherapy, hepatic artery embolization, chemoembolization and radiofrequency ablation.
...
PMID:Recent advances in the management of gastrointestinal stromal tumor. 3287 69
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