Publications by authors named "Daishi Kasai"

Purpose: The purposes of this study were to determine whether organic cation transporters (OCTs) can mediate platinum uptake, and whether OCT down-regulation confers resistance against cisplatin (CDDP) in cancer cells.

Methods: Two lung cancer cell lines, PC-6 and PC-14, and their CDDP-resistant derivatives, PC-6/CDDP and PC-14/CDDP, were analyzed. OCT expression levels were assayed using quantitative RT-PCR and Western blotting.

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The c-MET receptor tyrosine kinase is the receptor for hepatocyte growth factor. Recently, activation of the c-MET/hepatocyte growth factor signaling pathway was associated with poor prognosis in various solid tumors and was one of the mechanisms of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib. But the link between c-MET activation and the cytotoxic anticancer drug has not been fully examined.

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Background: Nestin is a class VI intermediate filament protein expressed in stem/progenitor cells during the development of the central nervous system. Nestin is detected in various types of tumors and is involved in malignant processes. This study investigated the expression and function of nestin in small-cell lung cancer (SCLC).

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Background: Pemetrexed is a key drug for therapy of non-small cell lung cancer (NSCLC).

Materials And Methods: In a search for biomarkers for study of the efficacy of pemetrexed treatment, we examined the thymidylate synthase (TYMS) copy number in NSCLC cell lines and in clinical NSCLC samples treated with pemetrexed, combined with platinum drugs.

Results: TYMS copy numbers in lung adenocarcinoma cell lines were significantly lower than in squamous cell carcinoma (p=0.

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Cytotoxic nucleoside analogues are widely used in cancer chemotherapy. We used the cytosine arabinoside (Ara-C)-resistant erythroleukaemia cell line K562 and the Ara-C-sensitive myeloid leukaemia cell line HL60 to examine the differential expression of molecular markers. We found increased expression levels of deoxycytidine kinase (dCK) and human equilibrative nucleoside transporter 1 (hENT1) and decreased levels of multidrug resistance protein 5 (ABCC5) and ribonucleoside reductase subunit M1 (RRM1) expression in Ara-C-sensitive HL60 cells.

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Introduction: Amrubicin is a promising agent in the treatment of lung cancer, but predictive biomarkers have not yet been described. NAD(P)H:quinone oxidoreductase 1 (NQO1) is an enzyme known to metabolize amrubicinol, the active metabolite of amrubicin, to an inactive compound. We examined the relationship between NQO1 and amrubicinol cytotoxicity.

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Purpose: Amrubicin, a totally synthetic 9-aminoanthracycline anticancer drug, has shown promising activity for lung cancer, but little is known about the mechanism of resistance for this agent. This study was aimed to clarify the role of P-glycoprotein (P-gp) in amrubicinol, an active metabolite of amrubicin, resistance in lung cancer cells.

Methods: Amrubicinol-resistant cell line PC-6/AMR-OH was developed by continuously exposing the small-cell lung cancer cell line PC-6 to amrubicinol.

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A 76-year-old woman was admitted to our hospital in October 2007 because of fever and anorexia. Chest computed tomography demonstrated consolidation and reticular shadows in the right middle lobe and left lingula. Pulmonary nontuberculous mycobacteriosis was diagnosed based on isolation of Mycobacterium intracellulare from her sputum.

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A 47-year-old man was admitted to our hospital because of dysarthric speech and high fever. His brain magnetic resonance imaging (MRI) showed high intensity in the splenium of the corpus callosum (SCC) on diffusion-weighted and FLAIR imaging. His chest CT showed ground-glass attenuation in bilateral lung upper lobes, and consolidation in the right lower lobe.

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Background: Although most patients of asthma can be controlled by inhaled corticosteroid (ICS), some patients remain uncontrolled even after the introduction of ICS treatment. In management of such difficult-to-treat asthma, systematic review including additional differential diagnosis and avoidance of exacerbating factors is very important.

Methods: Here we postulate a flow sheet presenting an algorithm which intends to achieve better asthma control following ATS refractory asthma guidance.

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