http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Chen, Jen-Shi,Chao, Yee,Bang, Yung-Jue,Roca, Enrique,Chung, Hyun C.,Palazzo, Felipe,Kim, Yeul H.,Myrand, Scott P.,Mullaney, Brian P.,Shen, Li J.,Linn, Carlos Lippincott Williams Wilkins, Inc. 2010 ANTICANCER DRUGS Vol.21 No.8
This phase I/II study was conducted to determine the maximum recommended dose of pemetrexed when given in combination with a fixed dose of cisplatin, and the efficacy, toxicity and association of 5,10-methylenetetrahydrofolate reductase (MTHFR) variants with this pemetrexed--cisplatin combination, in patients with unresectable, advanced gastric carcinoma. Patients 18–70 years of age, with stage IV disease or post-surgery recurrence, no earlier palliative chemotherapy, 0 or 1 Eastern Cooperative Oncology Group performance status, were included. The cisplatin dose was 75 mg/m. In phase I, the initial dose of pemetrexed was 600 mg/m, escalated in 100 mg/m increments. In phase II, efficacy, including overall response rate, overall survival, as well as toxicity and MTHFR pharmacogenetics were investigated. Phase I enrolled 16 patients; 700 mg/m was defined as pemetrexed recommended dose. Thirteen serious adverse events were reported; the most common grade 3/4 toxicities were haematologic (10 of 13, 76.9%). Phase II enrolled 73 patients, 69 qualified for safety and 68 for efficacy analysis; 65 for pharmacogenomic analysis. Overall response rate was 23.5% (14.1%, 35.4%), disease control rate 55.9%, median overall survival 11.8 months (95% confidence interval, 7.2–18.5 months), progression-free survival 4.9 months (95% confidence interval, 2.8–7.1 months), and median response duration 5.4 months. Patients with MTHFR A1298C variants had median overall survival of 6.6 months, significantly shorter than patients with the wild type (median 18.5 months, P=0.001). The pemetrexed--cisplatin combination in patients with advanced gastric cancer generates modest efficacy and a manageable toxicity profile. The reduced overall survival in patients with MTHFR A1298C polymorphism variants deserves further investigation.
Loh, Tiing Jen,Moon, Heegyum,Cho, Sunghee,Jang, Hana,Liu, Yong Chao,Tai, Hongmei,Jung, Da-Woon,Williams, Darren R,Kim, Hey-Ran,Shin, Myung-Geun,Liao, D Joshua,Zhou, Jianhua,Shi, Wei,Zheng, Xuexiu,Shen National Hellenic Research Foundation 2015 ONCOLOGY REPORTS Vol.34 No.3
<P>CD44 is a transmembrane receptor for hyaluronic acid. CD44 pre-mRNA contains 19?exons, 9?of which are alternatively spliced. Among the CD44 spliced variants, the v4-7 variant, one of the v6?exon-containing isoforms that contains variable exon?4, 5, 6 and?7, confers metastatic potential to non-metastatic cells. Splicing of CD44 and the function of CD44 isoforms are different in breast cancer cells. hnRNP?A1 is a ubiquitously expressed protein with an inhibitory function in pre-mRNA splicing. We showed that CD44v6 isoform, which includes all of the v6-containing mRNA isoforms, had the highest expression level in non-metatatic breast cancer cells (MCF7) when compared to the level in metastatic breast cancer cells (MDA-MB-231) and normal breast cells (MCF10A). Furthermore we showed that hnRNP?A1 knockdown regulated splicing of CD44 differently in breast cancer cells. We showed here that CD44 isoform expression is completely different in MDA-MB-231 cells than that in MCF7 and MCF10A cells, whereas MCF7 and MCF10A cells had a similar expression pattern of CD44 isoforms. RT-PCR analysis of CD44v6 showed that MCF7 and MCF10A cells predominantly expressed the c5v6v7v8v9v10c6 isoform. However, in addition to this isoform, MDA-MB-231 cells also expressed the c5v6v8v9v10c6 and c5v6c6 isoforms. We also found that knockdown of hnRNP?A1 significantly reduced the expression of c5v6v7v8v9v10c6 and c5v6v8v9v10c6, and promoted the expression of c5v6c6. hnRNP?A1 knockdown significantly induced cell death. In addition, hnRNP?A1 knockdown induced a decrease in cell invasion in the MDA-MB-231 cells. Our results indicate that the knockdown of hnRNP A1 has a specific function on the splicing of CD44 in breast cancer cells.</P>
Li, Chunling,Shi, Yimin,Wang, Weidong,Sardeli, Chrysanthi,Kwon, Tae-Hwan,Thomsen, Klaus,Jonassen, Thomas,Djurhuus, Jens Christian,Knepper, Mark A,Nielsen, Soren,Frokiaer, Jorgen American Physiological Society 2006 American Journal of Physiology Vol.290 No.2
<P>The purpose of this study was to evaluate the effects of the anti-inflammatory hormone alpha-melanocyte-stimulating hormone (alpha-MSH) treatment on renal function and expression of aquaporins (AQPs) and Na-K-ATPase in the kidney in response to 24 h of bilateral ureteral obstruction (BUO) or release of BUO (BUO-R). In rats with 24-h BUO, immunoblotting revealed that downregulation of AQP2 and AQP3 was attenuated (AQP2: 38 +/- 5 vs. 13 +/- 4%; AQP3: 44 +/- 3 vs. 19 +/- 4% of sham levels; P < 0.05), whereas downregulation of Na-K-ATPase was prevented by alpha-MSH treatment (Na-K-ATPase: 94 +/- 7 vs. 35 +/- 5% of sham levels; P < 0.05). Immunocytochemistry confirmed the changes in AQP1 and Na-K-ATPase expression. Renal tubular cell apoptosis was confirmed in BUO kidneys, and alpha-MSH treatment virtually completely abolished apoptosis. Furthermore, we measured glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively. Forty-eight hours after BUO-R demonstrated that alpha-MSH treatment almost completely prevented the decrease in GFR (nontreated: 271 +/- 50; alpha-MSH: 706 +/- 85; sham: 841 +/- 105 microl x min(-1).100 g body wt(-1), P < 0.05) and ERPF (nontreated: 1,139 +/- 217; alpha-MSH: 2,598 +/- 129; sham: 2,633 +/- 457 microl x min(-1).100 g body wt(-1), P < 0.05). alpha-MSH treatment also partly prevented the downregulation of AQP1 and Na-K-ATPase expression in rats after BUO-R for 48 h. In conclusion, alpha-MSH treatment significantly prevents impairment in renal function and also prevents downregulation of AQP2, AQP3, and Na-K-ATPase during BUO or AQP1 and Na-K-ATPase after BUO-R, demonstrating a marked renoprotective effect of alpha-MSH treatment in conditions with urinary tract obstruction.</P>
Liu, Chi-Jen,Wang, Chang-Hai,Chien, Chia-Chi,Yang, Tsung-Yeh,Chen, Shin-Tai,Leng, Wei-Hua,Lee, Cheng-Feng,Lee, Kuen-Ho,Hwu, Y,Lee, Yao-Chang,Cheng, Chia-Liang,Yang, Chung-Shi,Chen, Y J,Je, J H,Margari IOP Pub 2008 Nanotechnology Vol.19 No.29
<P>We explored a very interesting gold nanoparticle system—pegylated gold in colloidal solution—and analyzed its uptake by mice colorectal adenocarcinoma CT26 tumor cells and the impact on the cell’s response to x-ray irradiation. We found that exposure to polyethylene glycol (PEG) modified (‘pegylated’) 4.7 ± 2.6 nm gold nanoparticles synthesized by a novel synchrotron-based method enhances the response of CT26 cells to x-ray irradiation. Transmission electron microscopy (TEM) and confocal microscopy revealed that substantial amounts of such nanoparticles are taken up and absorbed by the cells and this conclusion is supported by quantitative induced coupled plasma (ICP) results. Standard tests indicated that the internalized particles are highly biocompatible but strongly enhance the cell damage induced by x-ray irradiation. Synchrotron radiation Fourier transform infrared (SR-FTIR) spectromicroscopy analyzed the chemical aspects of this phenomenon: the appearance of C = O stretching bond spectral features could be used as a marker for cell damage and confirmed the enhancement of the radiation-induced toxicity for cells.</P>
Gemcitabine Plus Cisplatin for Advanced Biliary Tract Cancer: A Systematic Review
박준오,오도연,Chiun Hsu,Jen-Shi Chen,Li-Tzong Chen,Mauro Orlando,김종석,임호영 대한암학회 2015 Cancer Research and Treatment Vol.47 No.3
Evidence suggests that combined gemcitabine-cisplatin chemotherapy extends survival in patients with advanced biliary tract cancer (BTC). We conducted a systematic review in order to collate this evidence and assess whether gemcitabine-cisplatin efficacy is influenced by primary tumor site, disease stage, or geographic region, and whether associated toxicities are related to regimen. MEDLINE (1946-search date), EMBASE (1966-search date), ClinicalTrials. gov (2008-search date), and abstracts from major oncology conferences (2009- search date) were searched (5 Dec 2013) using terms for BTC, gemcitabine, and cisplatin. All study types reporting efficacy (survival, response rates) or safety (toxicities) outcomes of gemcitabine-cisplatin in BTC were eligible for inclusion; efficacy data were extracted from prospective studies only. Evidence retrieved from one meta-analysis (abstract), four randomized controlled trials, 12 nonrandomized prospective studies, and three retrospective studies supported the efficacy and safety of gemcitabine-cisplatin for BTC. Median overall survival ranged from 4.6 to 11.7 months, and response rate ranged from 17.1% to 36.6%. Toxicities were generally acceptable and manageable. Heterogeneity in study designs and data collected prevented formal meta-analysis, however exploratory assessments suggested that efficacy did not vary with primary tumor site (gallbladder vs. others), disease stage (metastatic vs. locally advanced), or geographic origin (Asia vs. other). Incidence of grade 3/4 toxicities was not related to gemcitabine dose or cisplatin frequency. Despite individual variation in study designs, the evidence presented suggests that gemcitabine-cisplatin is effective in patients from a diverse range of countries and with heterogeneous disease characteristics. No substantial differences in toxicity were observed among the different dosing schedules of gemcitabine and cisplatin.
Intense X-ray induced formation of silver nanoparticles stabilized by biocompatible polymers
Wang, Chang-Hai,Liu, Chi-Jen,Wang, Cheng-Liang,Chien, Chia-Chi,Hwu, Y.,Liu, Ru-Shi,Yang, Chung-Shi,Je, Jung-Ho,Lin, Hong-Ming,Margaritondo, G. Springer-Verlag 2009 Applied physics. A, Materials science & processing Vol.97 No.2
Cheng, Wei-Hong,Kao, Chen-Yi,Hung, Yu-Shin,Su, Po-Jung,Hsieh, Chia-Hsun,Chen, Jen-Shi,Wang, Hung-Ming,Chou, Wen-Chi Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.6
Background: The aim of our study was to assess the practical utility of the palliative prognostic index (PPI) as a prognostic tool used by nurse specialists in a hospice consultation setting in Taiwan. Methods: In total, 623 terminal cancer patients under hospice consultation care from one medical center in northern Taiwan were enrolled between January 1 and June 30, 2011. PPI was assessed by a nurse specialist at first hospice consultation and patients categorized into groups by prognosis (good, intermediate, poor). Patient survival was analyzed retrospectively to determine significance of between-group differences. Results: By PPI sum score, 37.2% of patients were in the good prognosis group, 18% in the intermediate prognosis group and 44.8% in the poor prognosis group. The death rates were 56%, 81.2% and 89.6% and median survivals were 76, 18 and 7 days, respectively. The hazard ratio was 0.19 (95% confidence interval [CI] 0.10-0.24, p<0.001) for the poor versus good prognosis group and 0.54 (95% CI 0.43-0.69, p<0.001) for the poor versus intermediate prognosis group. The sensitivity and specificity for the poor prognosis group was 66% and 71%; the positive predictive value and negative predictive value were 81% and 52%, respectively, to predict patient death within 21 days (area under the curve of the receiver operating characteristic was 0.68). Conclusions: Assessment by PPI can accurately predict survival of terminal cancer patients receiving hospice consultation care. PPI is a simple tool and can be administered by nurse members of hospice consultation teams.
Phase II study of sunitinib as second-line treatment for advanced gastric cancer
Bang, Yung-Jue,Kang, Yoon-Koo,Kang, Won K.,Boku, Narikazu,Chung, Hyun C.,Chen, Jen-Shi,Doi, Toshihiko,Sun, Yan,Shen, Lin,Qin, Shukui,Ng, Wai-Tong,Tursi, Jennifer M.,Lechuga, Maria J.,Lu, Dongrui Ray,R Springer US 2011 Investigational new drugs Vol.29 No.6
<P><B>Summary</B></P><P><I>Purpose.</I> This phase II, open-label, multicenter study assessed the oral, multitargeted, tyrosine kinase inhibitor sunitinib in patients with advanced gastric or gastroesophageal junction adenocarcinoma who had received prior chemotherapy. <I>Experimental design</I>. Patients received sunitinib 50 mg/day on Schedule 4/2 (4 weeks on treatment, followed by 2 weeks off treatment). The primary endpoint was objective response rate; secondary endpoints included clinical benefit rate, duration of response, progression-free survival (PFS), overall survival (OS), pharmacokinetics, pharmacodynamics, safety and tolerability, and quality of life. <I>Results</I>. Of 78 patients enrolled, most had gastric adenocarcinoma (93.6%) and metastatic disease (93.6%). All were evaluable for safety and efficacy. Two patients (2.6%) had partial responses and 25 patients (32.1%) had a best response of stable disease for ≥6 weeks. Median PFS was 2.3 months (95% confidence interval [CI], 1.6–2.6 months) and median OS was 6.8 months (95% CI, 4.4–9.6 months). Grade ≥3 thrombocytopenia and neutropenia were reported in 34.6% and 29.4% of patients, respectively, and the most common non-hematologic adverse events were fatigue, anorexia, nausea, diarrhea, and stomatitis. Pharmacokinetics of sunitinib and its active metabolite were consistent with previous reports. There were no marked associations between baseline soluble protein levels, or changes from baseline, and measures of clinical outcome. <I>Conclusions</I>. The progression-delaying effect and manageable toxicity observed with sunitinib in this study suggest that although single-agent sunitinib has insufficient clinical value as second-line treatment for advanced gastric cancer, its role in combination with chemotherapy merits further study.</P>