1.Plantar Keratoderma with Pachyonychia Likely Induced by Imatinib Mesylate.
Hyung Ok KIM ; Bo In LEE ; Jun Young LEE ; Young Min PARK
Annals of Dermatology 2013;25(4):526-528
No abstract available.
Benzamides
;
Mesylates*
;
Nails, Malformed*
;
Piperazines
;
Pyrimidines
;
Imatinib Mesylate
2.Lichenoid Drug Eruption after Low-Dose Imatinib Mesylate Treatment.
Jae Hyung LEE ; Jong Yoon CHUNG ; Mi Young JUNG ; Cho Rok KIM ; Ji Ho PARK ; Ji Hye PARK ; Jong Hee LEE ; Joo Heung LEE ; Jun Mo YANG ; Dong Youn LEE
Annals of Dermatology 2013;25(4):500-502
No abstract available.
Benzamides
;
Drug Eruptions*
;
Mesylates*
;
Piperazines
;
Pyrimidines
;
Imatinib Mesylate
3.Gastrointestinal Stromal Tumor.
The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2011;11(2):82-89
Gastrointestinal stromal tumor (GIST) is a relatively rare disease accounted for less than 1% of gastrointestinal tumors. In the past, surgery is the only reliable therapy for the locoregional GISTs. But with the development of the specific target agents such as imatinib or sunitinib, advanced metastatic GIST can be cured now. GISTs are incidentally found by endoscopic ultrasound or laparoscopic surgery for the abdominal mass and positive immunostain for KIT with characteristic histopathology is mandatory for the diagnosis. Mutational analyses for KIT and PDGFRA is helpful in the diagnosis and treatment of GISTs. Because most GISTs are potentially malignant and surgery itself has high recurrence rate, it should be treated at an early stage and chemotherapy should be considered aggressively. The tumor size, mitotic index, and the involved organs are important prognostic factors. In this paper, the pathogenesis of histopathology, clinical diagnosis and treatment of GISTs were reviewed.
Benzamides
;
Gastrointestinal Stromal Tumors
;
Indoles
;
Laparoscopy
;
Mitotic Index
;
Piperazines
;
Pyrimidines
;
Pyrroles
;
Rare Diseases
;
Recurrence
;
Imatinib Mesylate
4.Eosinophil disorders.
Korean Journal of Pediatrics 2009;52(6):643-648
Blood eosinophilia can be classified as either familial or acquired. Familial eosinophilia is a rare autosomal dominant disorder characterized by a stable eosinophil count. Acquired eosinophilia is classified further into a primary or secondary phenomenon depending on whether eosinophils are considered integral to the underlying disease. Primary eosinophilia is considered clonal in the presence of either a cytogenetic abnormality or bone marrow histological evidence of classified hematologic malignancies. Causes of secondary eosinophilia include infections, allergic or immunologic disorders, and drugs. Idiopathic eosinophilia belongs to a category of primary eosinophilia, and this is a diagnosis of exclusion. Cases with eosinophilia that lack evidence of clonality may be diagnosed as idiopathic hypereosinophilic syndrome after all causes of reactive eosinophilia have been eliminated. Genetic mutations involving the platelet-derived growth receptor genes (PDGFRA and PDGFRB) have been pathogenetically linked to clonal eosinophilia, and their presence predicts the treatment response to imatinib. In this review, I will present a clinical summary of both familial and acquired eosinophilia with emphasis on recent developments in molecular pathogenesis and treatment.
Benzamides
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Bone Marrow
;
Chromosome Aberrations
;
Eosinophilia
;
Eosinophils
;
Hematologic Neoplasms
;
Hypereosinophilic Syndrome
;
Piperazines
;
Pyrimidines
;
Imatinib Mesylate
5.Effect of ZD6474 on the proliferation of imatinib-resistant K562 cells.
Hong-Yun JIA ; Xiao-Man WU ; Zhong-Ying WANG ; Xiao-Yan DENG ; Zhen LIN ; Gui-Ling FENG ; Wen-Lin HUANG
Chinese Journal of Hematology 2010;31(6):371-375
<p>OBJECTIVETo investigate the effect of tyrosine kinase inhibitor ZD6474 (Vandetanib) on the proliferative inhibition of K562 cells and its derived imatinib-resistant K562/G cells and its mechanism.p><p>METHODSImatinib-resistant K562/G cells were obtained by culturing cells in gradually increasing concentrations of imatinib. The changed factors related to drug-resistance were tested by Western blot. ZD6474 and imatinib affected K562/G and parental K562 cells proliferation were analyzed by WST assay. Flow cytometry was used to analyze cell cycle. Direct inhibition of Src activity by ZD6474 was measured by a colorimetric ELISA assay with recombinant human Src kinase.p><p>RESULTS10 µmol/L imatinib failed to inhibit K562/G cells proliferation or induce cell cycle arrest. Compared with that in parental K562 cells, there were marked high levels of p-Src and Src protein in K562/G cells. The expression of Bcl-2 and p-STAT3 also increased in K562/G cells. After 48 hours incubation, the IC(50) values of ZD6474 in K562 and K562/G cells were 1.61 µmol/L and 3.18 µmol/L, respectively. ZD6474 treatment caused accumulation of cells in the G(0)/G(1) fraction and cell apoptosis in K562 and K562/G cells. ZD6474 decreased the expression of p-Src and Src at post-transcriptional level. Moreover, ZD6474 increased the ratio of Bax/Bcl-2 and decreased the expression of p-STAT3 at the same concentration for inducing apoptosis.p><p>CONCLUSIONSZD6474 is effective in inhibiting the proliferation of imatinib-resistant K562/G cells and parental K562 cells, and induces their apoptasis by significant inhibition of Src kinase activity. Our study provides a reliable experimental basis for chronic myeloid leukemia treatment with ZD6474.p>
Apoptosis
;
drug effects
;
Benzamides
;
pharmacology
;
Humans
;
Imatinib Mesylate
;
K562 Cells
;
Piperazines
;
pharmacology
;
Pyrimidines
;
pharmacology
6.Bladder interstitial cells and pathophysiology.
Journal of Central South University(Medical Sciences) 2014;39(6):644-648
Bladder interstitial cell (IC) is a cell, which lacks thick filaments and dense bodies but with incomplete basement membrane, rough endoplasmic reticulum and golgi apparatus. IC is divided into 4 subtypes: lamina propria IC, intramuscular IC, IC between the detrusor bundles and perivascular IC. There are different ion currents and related activation pathways in the lamina propria IC and intramuscular IC. Ca2+ signaling pathways play an important role in the communication between IC and detrusor. Any bladder lesions affecting the ion current and Ca2+ signaling pathways can lead to bladder dysfunction. The bladder lesions include bladder outlet obstruction, bladder pain syndrome, interstitial cystitis, neurogenic bladder and diabetes. Imatinib mesylate is currently an available treatment target in IC, and electrical stimulation of acupuncture therapy is a new direction.
Benzamides
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Cystitis, Interstitial
;
pathology
;
Electric Stimulation
;
Humans
;
Imatinib Mesylate
;
Mucous Membrane
;
pathology
;
Piperazines
;
Pyrimidines
;
Signal Transduction
7.Role of Sodium Ion in Renal Transport of p-Aminohippurate in vitro.
Yang Saeng PARK ; Seung Mook LEE
Yonsei Medical Journal 1980;21(2):123-128
The effect of sodium on p-aminohippurate (PAH) transport kinetics was studied in isolated rat kidney slices in an attempt to define the role of sodium ion in renal organic acid transport. 1. In normally metabolizing renal slices, Na+ increased the Vmax of PAH influx without changing the Michaelis constant (Km). On the other hand, the effIux of preaccumulated PAH was reduced as the Na+ concentration increased. 2. In metabolically impaired renal slices, Na+ had no apparent effect on the influx and efflux of PAH. These results may indicate that Na+ is important for the energy transducing reaction in the PAH transport process.
Aminohippuric Acids/metabolism*
;
Animal
;
Biological Transport, Active/drug effects
;
Culture Media
;
Female
;
In Vitro
;
Kidney/metabolism*
;
Kinetics
;
Male
;
Organ Culture
;
Rats
;
Sodium/pharmacology*
;
p-Aminohippuric Acid/metabolism*
8.Changes in Rena1 Na-K-ATPase Activity and PAH Transport Kinetics in Uninephrectomized Rats and Cold Exposed Hamsters.
Yang Saeng PARK ; Seung Mook LEE ; Ae Ran HWANG
Yonsei Medical Journal 1979;20(1):8-16
Renal Na+, K+-activated adenosinetriphosphatase (Na-K-ATPase) activity and the p-aminohippurate (PAH) transport kinetics were studied in uninephrectomized rats and cold exposed hamsters. In rats, the specific activity of renal Na-K-ATPase increased by approximately 50% in one week after uninephrectomy and remained more or less constant during the next three weeks. The capacity (Jmax) of PAH influx into the renal cortical slice was sharply increased in one week after nephrectomy, but after which it returned to the control level. In cold exposed hamsters, the specific activity of renal Na-K-ATPase did not increase until 48 days of cold exposure at which time it reached approximately 50% above the control level. On the other hand, the Jmax of PAH influx increased by about 80% in 10 days of co1d exposure and somewhat declined thereafter. These results suggest that PAH active transport in the renal slice is not ratelimited by the activity of Na-K-ATPase under physiological conditions.
Aminohippuric Acids/metabolism*
;
Animal
;
Biological Transport, Active
;
Female
;
Hamsters
;
Hibernation
;
Kidney/enzymology*
;
Male
;
Na(+)-K(+)-Exchanging ATPase/metabolism*
;
Nephrectomy
;
Rats
;
p-Aminohippuric Acid/metabolism*
9.Pityriasis rosea-like Drug Eruption Induced by Imatinib Mesylate (Gleevec(TM)).
Ah Young CHO ; Dae Hun KIM ; Myung IM ; Young LEE ; Young Joon SEO ; Jeung Hoon LEE
Annals of Dermatology 2011;23(Suppl 3):S360-S363
Imatinib mesylate (Gleevec(TM), STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors. Although its use has been associated with various adverse cutaneous reactions, pityriasis rosea-like drug eruptions are rare. Here, we report a case of pityriasis rosea-like drug eruption that developed following the administration of imatinib mesylate to treat CML.
Benzamides
;
Drug Eruptions
;
Gastrointestinal Stromal Tumors
;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
;
Mesylates
;
Piperazines
;
Pityriasis
;
Pityriasis Rosea
;
Pyrimidines
;
Imatinib Mesylate
10.The 10 Years of Experiences with GISTs.
Kyung Ha LEE ; In Sang SONG ; Ji Young SUL ; Ji Yeon KIM ; Kwang Sik CHUN ; Sang Il LEE ; Dae Young KANG ; Song I CHOI ; Seung Moo NOH
Journal of the Korean Surgical Society 2010;78(6):376-384
PURPOSE: Gastrointestinal stromal tumors (GISTs) possess highly variable clinical behaviors and the study thereof is insufficient. There are no standard guidelines for diagnosis and treatment of GISTs, so it is difficult to predict recurrences and conduct appropriate treatments. Throughout the last 10 years of experiences with GIST patients, we have identified the variables predicting recurrences and classified the risk groups by NIH classification, Fletcher risk stratification and UICC TNM stage. METHODS: From January 1998 to December 2007, 88 patients with pathologic confirm and surgical resection were diagnosed with GISTs. GISTs were diagnosed when the tumor had characteristic histologic features and confirmed positive by KIT, CD34, or PDGFRA. RESULTS: The size, mitotic index, existence of symptoms, and origins of tumor correlate statistically with recurrence (0.002, <0.001, 0.027, 0.011). The NIH classification, Fletcher risk stratification and UICC TNM stage are correlated with recurrence (0.001, <0.001, <0.001) and 5 year disease free survival, statistically (0.009, <0.001, <0.001). Fifteen patients experienced recurrences. 14 patients were treated with imatinib, and 6 of them showed a response to the treatment. All 4 patients who had R1 resection did not survived due to the progression of the disease. CONCLUSION: The patients with large, high mitotic index, symptomatic, or extra-gastric tumor require strict surveillance. Also, patients with low risk must be under surveillance due to the possibility of recurrence. It is important to perform R0, en bloc resection. Although the imatinib is the treatment of choice with recurred or metastatic GISTs, the disease is likely to develop resistance, further studies on newly targeted therapy is in need.
Benzamides
;
Disease-Free Survival
;
Gastrointestinal Stromal Tumors
;
Humans
;
Imatinib Mesylate
;
Mitotic Index
;
Piperazines
;
Pyrimidines
;
Recurrence
;
Survival Rate