Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with cancer commonly experience seizures. Combined therapy with anticonvulsant drugs (AEDs) and chemotherapeutic drugs or tyrosine kinase inhibitors carries inherent risks on drug-drug interactions (DDIs). In this review, pharmacokinetic studies of AEDs with chemotherapeutic drugs, tyrosine kinase inhibitors, and glucocorticoids are discussed, including data on maximum tolerated dose, drug clearance, elimination half-life, and organ exposure. Enzyme-inducing AEDs (EIAEDs) cause about a 2-fold to 3-fold faster clearance of concurrent chemotherapeutic drugs metabolized along the same pathway, including cyclophosphamide, irinotecan, paclitaxel, and teniposide, and up to 4-fold faster clearance with the tyrosine kinase inhibitors crizotinib, dasatinib, imatinib, and lapatinib. The use of tyrosine kinase inhibitors, particularly imatinib and crizotinib, may lead to enzyme inhibition of concurrent therapy. Many of the newer generation AEDs do not induce or inhibit drug metabolism, but they can alter enzyme activity by other drugs including AEDs, chemotherapeutics and tyrosine kinase inhibitors. Glucocorticoids can both induce and undergo metabolic change. Quantitative data on changes in drug metabolism help to apply the appropriate dose regimens. Because the large individual variability in metabolic activity increases the risks for undertreatment and/or toxicity, we advocate routine plasma drug monitoring. There are insufficient data available on the effects of tyrosine kinase inhibitors on AED metabolism.
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PMID:Seizures and cancer: drug interactions of anticonvulsants with chemotherapeutic agents, tyrosine kinase inhibitors and glucocorticoids. 3138 88

Microtubule-associated protein tau associates with Src family tyrosine kinase Fyn and is tyrosine phosphorylated by Fyn. The presence of tyrosine phosphorylated tau in AD and the involvement of Fyn in AD has drawn attention to the tau-Fyn complex. In this study, a tau-Fyn double knockout (DKO) mouse was generated to investigate the role of the complex. DKO mice resembled Fyn KO in novel object recognition and contextual fear conditioning tasks and resembled tau KO mice in the pole test and protection from pentylenetetrazole-induced seizures. In glutamate-induced Ca²⁺ response, Fyn KO was decreased relative to WT and DKO had a greater reduction relative to Fyn KO, suggesting that tau may have a Fyn-independent role. Since tau KO resembled WT in its Ca²⁺ response, we investigated whether microtubule-associated protein 2 (MAP2) served to compensate for tau, since the MAP2 level was increased in tau KO but decreased in DKO mice. We found that like tau, MAP2 increased Fyn activity. Moreover, tau KO neurons had increased density of dendritic MAP2-Fyn complexes relative to WT neurons. Therefore, we hypothesize that in the tau KO, the absence of tau would be compensated by MAP2, especially in the dendrites, where tau-Fyn complexes are of critical importance. In the DKO, decreased levels of MAP2 made compensation more difficult, thus revealing the effect of tau in the Ca²⁺ response.
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PMID:Loss of tau and Fyn reduces compensatory effects of MAP2 for tau and reveals a Fyn-independent effect of tau on calcium. 3145 42

Apatinib, a novel tyrosine kinase inhibitor, has anti-angiogenetic effect just as bevacizumab. Although bevacizumab has been used successfully in treating cerebral radiation necrosis, there has yet not any report on that apatinib can treat pseudoprogression with symptoms. Here we report a case of glioblastoma multiforme (GBM) patient with pseudoprogression after receiving the concurrent chemoradiotherapy, which was successfully treated by apatinib. A 51-year-old woman had multiple intracranial lesions (left parietal and right frontal), the primary left parietal lesion was surgically removed and was pathologically confirmed as glioblastoma (WHO grade IV). Then the patient received postoperative temozolomide with concurrent chemoradiotherapy. Three weeks after the radiotherapy, the patient experienced increased intracranial pressure and seizure. Magnetic resonance imaging (MRI) T1 enhancement examination showed an increase of abnormal enhancement range in the area of irradiation. After multiple disciplinary team (MDT) discussion, the patient was diagnosed with pseudoprogression after radiotherapy. Then she was given apatinib for 8 weeks at a dose of 500 mg qd. During the treatment period, the clinical symptoms and corresponding nerve images of the patient have been rapidly improved. In 12 months after the radiotherapy, progression of tumor in the primary site has not been discovered. Apatinib showed a good therapeutic effect and tolerance for the development of pseudoprogression advances with obvious symptoms.
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PMID:Apatinib treatment for symptomatic pseudoprogression after standard treatment for glioblastoma multiforme: a case report. 3186 35

We report here a rare case of atypical posterior reversible encephalopathy syndrome (PRES) due to oral tyrosine kinase inhibitor cabozantinib. No case reports of such have been found in our literature search. The patient, a 70-year-old female with metastatic renal cell cancer on oral tyrosine kinase inhibitor cabozantinib, was brought into the emergency room because of confusion and seizures, found to have elevated blood pressure and atypical MRI findings consistent with PRES due to cabozantinib.
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PMID:Atypical Posterior Reversible Encephalopathy Syndrome due to Oral Tyrosine Kinase Inhibitor Cabozantinib: First Case Report. 3299 65


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