Merkerova M, Bruchova H, Brdicka R (2005) Specific silencing of PCNA gene expression in leukemic cell lines using siRNA.
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Sancéau J, Truchet S, Bauvois B (2003) Matrix metalloproteinase-9 silencing by RNA interference triggers the migratory-adhesive switch in Ewing´s sarcoma cells. Sherr M, Battmer K, Winkler T et al (2003) Specific inhibition of bcr-abl gene expression by small interfering RNA. Withey JM, Marley SB, Kaeda J et al (2005) Targeting primary human leukaemia cells with RNA interference: Bcr-Abl targeting inhibits myeloid progenitor self-renewal in chronic myeloid leukaemia cells. Proc Natl Acad Sci USA 92(25):11746–11750ĭykxhoorn DM, Novina CD, Sharp PA (2003) Killing the messenger: short RNAs that silence gene expression. Raitano AB, Halpern JR, Hambuch TM et al (1995) The Bcr-Abl leukemia oncogene activates Jun kinase and requires Jun for transformation. Mayer IA, Verma A, Grumbach IM et al (2001) The p38 MAPK pathway mediates the growth inhibitory effects of interferon-alpha in BCR-ABL-expressing cells. Br J Haematol 125:128–140ĭeininger MW, Goldman JM, Melo JV (2000) The molecular biology of chronic myeloid leukemia. Kamiguti AS, Lee ES, Till KJ et al (2004) The role of matrix metalloproteinase 9 in the pathogenesis of chronic lymphocytic leukaemia. Pegahi R, Poyer F, Legrand E et al (2005) Spontaneous and cytokine-evoked production of matrix metalloproteinases by bone marrow and peripheral blood pre-B cells in childhood acute lymphoblastic leukaemia. Hiratsuka S, Nakamura K, Iwai S et al (2002) MMP9 induction by vascular endothelial growth factor receptor-1 is involved in lung-specific metastasis. Kossakowska AE, Urbanski SJ, Watson A et al (1993) Patterns of expression of metalloproteinases and their inhibitors in human malignant lymphomas. O-charoenrat P, Rhys-Evans P, Court WJ et al (1999) Differential modulation of proliferation, matrix metalloproteinase expression and invasion of human head and neck squamous carcinoma cells by c-erbB ligands. An immunofluorescent laser confocal scanning microscopical study.
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#3dlabprint p38 normal or high mod#
Mod Pathol 10:91-97īall LM, Pope J, Howard CV et al (1994) PCNA Ki-67 dissociation in childhood acute lymphoblastic leukaemia. O’Reilly PE, Raab SS, Niemann TH, et al (1197) p53, proliferating cell nuclear antigen, and Ki-67 expression in extrauterine leiomyosarcomas.
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J Cell Sci 116:3051–3060ĭel Giglio A, O’Brien S, Ford RJ Jr et al (1993) Proliferating cell nuclear antigen (PCNA) expression in chronic lymphocytic leukemia (CLL). Maga G, Hubscher U (2003) Proliferating cell nuclear antigen (PCNA): a dancer with many partner. BIOforum Int 5:259–261īruchova H, Borovanova T, Klamova H, Brdicka R (2002) Gene expression profiling in chronic myeloid leukemia patients treated with hydroxyurea. Cas Lek Cesk 139:655–659īruchova H, Borovanova T, Brdicka R (2001) Gene expression in patients with chronic myeloid leukemia. According to our results, nucleofection appears to be the only suitable non-viral method for siRNA delivery into the hard-to-transfect CML primary cells.īruchova H, Klamova H, Brdicka R (2000) Gene expression in chronic myeloid leukemia patients at time of diagnosis. Gene expressions ranged 22–37% that remained from original levels. In the study we obtained the best transfection efficiency using nucleofector technology. Electroporation achieved better results (suppression to 63%) but it was associated with high degree of cell death (more than 60%).
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Chemical transfection reagents (Oligofectamine, Metafectene, siPORT Amine) commonly used to transfect siRNAs in CML cell lines showed very low siRNA delivery in CML primary cells-mRNA levels decreased at the most to 76%. Chemically synthesized siRNAs against mentioned genes were transfected into the cells and level of knockdown was determined by real time RT-PCR. Using fluorescein-labeled siRNAs we systematically tested a variety of physical and chemical non-vector based transfection methods in order to evaluate which of them gave the most suitable transfer. One of the crucial requirements for this purpose is a high efficiency of siRNA delivery into CML primary cells. We suppose that the genes may be implicated in the disease development and a siRNA-suppression can elucidate their functions in leukemogenesis. Our array-based analyses of gene expression in patients with chronic myeloid leukemia (CML) revealed several genes (MMP8, MMP9, PCNA, JNK2, MAPK p38) with significant increased expression. Development of array methods contributes to elucidation of many genes expressed during oncogenesis.