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No. 79 (PMB 5) TGF-β-neutralization enhances cytarabine-induced apoptosis in AML cells in the bone marrow microenvironment Yoko Tabe 1,2 , Linhua Jin 1 , Yasuhito Hatanaka 1 , Takashi Miida 1 , Michael Andreeff 2 , Marina Konopleva 2 1, Department of Clinical Laboratory Medicine, Juntendo University School of Medicine, Tokyo, Japan 2, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA Aim: Hypoxia and interactions with bone marrow mesenchymal stromal cells (MSC) have emerged as essential components of the leukemic microenvironment in promoting leukemia cell survival. High levels of transforming growth factor beta 1 (TGF-β1) produced by stromal cells regulate cell proliferation, survival, and apoptosis, depending on the cellular context. In this study, we investigated the anti-leukemic effects and molecular mechanisms of action of TGF-β neutralizing antibody 1D11 under hypoxic conditions. We further investigated the anti-leukemic efficacy of 1D11 combined with CXCR4 antagonist plerixafor in the in vivo leukemia models. Design and Methods: The antileukemic effects and molecular mechanisms of action of monoclonal pan-TGF-β-neutralizing antibody 1D11 were determined utilizing flow cytometry, western blot, qPCR, and siRNA technology. The in vivo efficacy of 1D11 combined with CXCR4 antagonist Plerixafor was investigated in the Baf3/ITD model. Results: RhTGF-b1 induced accumulation of acute myeloid leukemia (AML) cells in a quiescent G0 state under MSC co-culture conditions, which was abrogated by 1D11. TGF-β1 upregulated p21 expression and the TGF-β target leukemia inhibitory factor (LIF) gene in AML cells which in turn promoted pro-survival phosphorylation of Stat3. 1D11 blocked these effects and enhanced Ara-C-induced apoptosis of AML cells in hypoxic and in normoxic conditions. Treatment with 1D11 combined with Plerixafor and Ara-C decreased leukemia burden in an in vivo leukemia model. Conclusions: Blockade of TGF-β by 1D11 and abrogation of CXCL12/CXCR4 signaling may enhance the efficacy of chemotherapy against AML cells in the hypoxic BM microenvironment. - 132 -
No. 80 (PMB 6) Introduction of HCV Quantification as a Diagnostic Tool in Mongolia: Significance and Lessons Learned Batmunkh Sayabold 1 , Nemekhbaatar Lkhaasuren 2 , Jazag Amarsanaa 1,5 , Jigjidsuren Chinburen 1,3 , Oidov Baatarkhuu 1,2 , Byambaa Suvd 1 , Tseveg Tsogtkhishig 2 , Bira Tsatsralt-Od 1,4 , Batmunkh Munkhbat 5 1) Mongolian Association for the Study of Liver Diseases, Mongolia; 2) Health Sciences University of Mongolia, Mongolia; 3) National Cancer Center, Mongolia; 4) National Center of Communicable Diseases, Mongolia; 5) Institute of Medical Sciences, Mongolia Background: The 17% of Mongolian population is infected with HCV, which makes the country one of the top HCV infected countries in the world. Though HCV quantification method was developed almost a decade ago, it was first introduced in Mongolia only in 2009. Methods: Total of HCV 212 patients were enrolled in the study. HCV quantification was performed at Happy Veritas clinical laboratory by Taqman real-time PCR method using ABI7000 from Applied Bio-systems, USA. Commercially available HCV quantification kit was used. Anti-HCV was purchased from ACON laboratories, USA. Results: Out of 212 patients who had HCV quantified, 35 were also checked for HCV antibody. Patients were divided in high viral load>2 million HCV copies/ml, and low-intermediate
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Program / Abstract Book
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Welcome Dear Friends and Colleagues
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ASCPaLM 2012 Executive Committee Pr
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Sponsors and supporters Abbott Japa
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Approximate Flight Times to Japan F
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The Kyoto City Subway system is eas
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Scientific Program Information Spea
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Event Hall is located by the confer
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Keynote Lecture (Chaired by Mitsuru
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FO 1 CLINICAL PATHOLOGY SCOPE IN CA
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FO 3 SUSTAINED EXPRESSION OF A NEUR
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FO 5 INDIAN STUDY OF LIVER FUNCTION
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Advanced Technical Seminar Sekisui
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Measurement of Albuminuria (Siemens
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The current status of the diagnosis
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Establishment of Reference Interval
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Innovative Lipid Biomarkers (Denka
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Scientific Innovation Seminar (Abbo
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PLEX-ID Technology as a Single Tool
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POSTER SESSION 1. Clinical Chemistr
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Naoko Yamaguchi, Tomohiro Takeda, C
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in Type 2 Diabetes Mellitus First D
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No. 36. Identification of autoantib
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Okamura 1) , Masahumi Takata 2) , M
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Hunsuk Suh 1 MD, PhD, Jonghee Shin
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Department of Pathology, Kansai Med
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No. 80. Introduction of HCV Quantif
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No. 91. Genome-wide association ana
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Abstracts - 53 -
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No. 2 (PC2) Soluble FcγRIIIa Mφ l
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No. 4 (PC 4) Detection of hereditar
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No. 6 (PC 6) Analysis of cholestery
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No. 8 (PC 8) Development of the enz
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No. 10 (PC 10) Direct analysis of c
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No. 12 (PC 12) Reference value for
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No. 14 (PC 14) Detection of autoant
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No. 16 (PC 16) Temporal changes in
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No. 18 (PC 18) IODINE STATUS AMONG
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No. 20 (PC 20) Plasma free Fatty Ac
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No. 22 (PE 1) Two-Step Biochemical
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No. 24 (PE 3) Adiponectin HMW Level
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No. 26 (PE 5) Analysis of von Wille
Page 85 and 86: No. 28 (PI 2) Diagnostic value of A
Page 87 and 88: No. 30 (PI 4) Evaluation of Hepatri
Page 89 and 90: No. 32 (PI 6) Discrepancy between s
Page 91 and 92: No. 34 (PI 8) Inhibition of the NF-
Page 93 and 94: No. 36 (PH 2) Identification of aut
Page 95 and 96: No. 38 (PH 4) Contribution of uncon
Page 97 and 98: No. 40 (PH 6) Red Blood Cells absor
Page 99 and 100: No. 42 (PH 8) Great impact of the b
Page 101 and 102: No. 44 (PH 10) Relation between VKO
Page 103 and 104: No. 46 (PH 12) Suspect of malaria i
Page 105 and 106: No. 48 (PH 14) Intravascular large
Page 107 and 108: No. 50 (PH 16) Calculation of Measu
Page 109 and 110: No. 52 (PM 1) High seroprevalence o
Page 111 and 112: No. 54 (PM 3) Epidemiological and m
Page 113 and 114: No. 56 (PM 5) Tuberculosis screenin
Page 115 and 116: No. 58 (PM 7) Mycobacterium Kyorine
Page 117 and 118: No. 60 (PM 9) Sensitive, one, two-d
Page 119 and 120: No. 62 (PM 11) Simultaneous inhibit
Page 121 and 122: No. 64 (PM 13) Measurement of Proca
Page 123 and 124: No. 66 (PF 1) Comparison of four po
Page 125 and 126: No. 68 (PP 1) The expressions of O
Page 127 and 128: No. 70 (PP 3) Poorly differentiated
Page 129 and 130: No. 72 (PP 5) The morphological cha
Page 131 and 132: No. 74 (PP 7) Neuropathological fin
Page 133 and 134: No. 76 (PMB 2) Diagnostic strategie
Page 135: No. 78 (PMB 4) Study of essential o
Page 139 and 140: No. 82 (PMB 8) Analysis of Fas exon
Page 141 and 142: No. 84 (PMB 10) A rapid and automat
Page 143 and 144: No. 86 (PMB 12) Increased expressio
Page 145 and 146: No 88 (PO 2) Assessment of early ma
Page 147 and 148: No. 90 (PO 4) The role of Rb2/p130
Page 149 and 150: No. 92 (PO 6) Molecular analysis of
Page 151 and 152: No. 94 (PO 8) The genealogical stud
Page 153 and 154: No. 96 (P0 10) Regulatory and pro-i
Page 155 and 156: No. 98 (PO 12) Chaotic Nature of My
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