Artículos de revistas
Identification Of Target Genes Using Gene Expression Profile Of Granulocytes From Patients With Chronic Myeloid Leukemia Treated With Tyrosine Kinase Inhibitors
Registro en:
Leukemia And Lymphoma. Informa Healthcare, v. 55, n. 8, p. 1861 - 1869, 2014.
10428194
10.3109/10428194.2013.855311
2-s2.0-84904900099
Autor
Mascarenhas C.D.C.
Ferreira Da Cunha A.
Brugnerotto A.F.
Gambero S.
De Almeida M.H.
Carazzolle M.F.
Pagnano K.B.B.
Traina F.
Costa F.F.D.
De Souza C.A.
Institución
Resumen
Differential gene expression analysis by suppression subtractive hybridization with correlation to the metabolic pathways involved in chronic myeloid leukemia (CML) may provide a new insight into the pathogenesis of CML. Among the overexpressed genes found in CML at diagnosis are SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were decreased when compared to healthy volunteers. Some genes were identified and involved in CML for the first time, including TOB1, which showed a low expression in patients with CML during tyrosine kinase inhibitor treatment with no complete cytogenetic response. In agreement, reduced expression of TOB1 was also observed in resistant patients with CML compared to responsive patients. This might be related to the deregulation of apoptosis and the signaling pathway leading to resistance. Most of the identified genes were related to the regulation of nuclear factor κB (NF-κB), AKT, interferon and interleukin-4 (IL-4) in healthy cells. The results of this study combined with literature data show specific gene pathways that might be explored as markers to assess the evolution and prognosis of CML as well as identify new therapeutic targets. © 2014 Informa UK, Ltd. 55 8 1861 1869 Luatti, S., Additional chromosomal abnormalities in Philadelphia-positive clone: Adverse prognostic influence on frontline imatinib therapy: A GIMEMA Working Party on CML analysis (2012) Blood, 120, pp. 761-767 Deininger, M.W., Goldman, J.M., Melo, J.V., The molecular biology of chronic myeloid leukemia (2000) Blood, 96, pp. 3343-3356 Baran, Y., Saydam, G., Cumulative clinical experience from a decade of use: Imatinib as first-line treatment of chronic myeloid leukemia (2012) J Blood Med, 3, pp. 139-150 Melo, J.V., Hughes, T.P., Apperley, J.F., Chronic myeloid leukemia (2003) Hematology Am Soc Hematol Educ Program, pp. 132-152 Mascarenhas, C.C., New mutations detected by denaturing high performance liquid chromatography during screening of exon 6 bcr-abl mutations in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors (2009) Leuk Lymphoma, 50, pp. 1148-1154 Wong, S., Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations (2004) Proc Natl Acad Sci USA, 101, pp. 17456-17461 Inokuchi, K., Chronic myelogenous leukemia: From molecular biology to clinical aspects and novel targeted therapies (2006) J Nippon Med Sch, 73, pp. 178-192 Park, S., Application of array comparative genomic hybridization in chronic myeloid leukemia (2013) Methods Mol Biol, 973, pp. 55-68 Remsing Rix, L.L., Global target profile of the kinase inhibitor bosutinib in primary chronic myeloid leukemia cells (2009) Leukemia, 23, pp. 477-485 Canalli, A.A., Granulocytic adhesive interactions and their role in sickle cell vaso-occlusion (2005) Hematology, 10, pp. 419-425 Diatchenko, L., Suppression subtractive hybridization: A method for generating diff erentially regulated or tissue-specific cDNA probes and libraries (1996) Proc Natl Acad Sci USA, 93, pp. 6025-6030 Diatchenko, L., Suppression subtractive hybridization: A versatile method for identifying diff erentially expressed genes (1999) Methods Enzymol, 303, pp. 349-380 Hillmann, A., Dunne, E., Kenny, D., CDNA amplification by SMARTPCR and suppression subtractive hybridization (SSH)-PCR (2009) Methods Mol Biol, 496, pp. 223-243 Ewing, B., Base-calling of automated sequencer traces using phred I. Accuracy assessment (1998) Genome Res, 8, pp. 175-185 Ghosh, S., Global gene expression and Ingenuity biological functions analysis on PCBs 153 and 138 induced human PBMC in vitro reveals diff erential mode(s) of action in developing toxicities (2011) Environ Int, 37, pp. 838-857 Gilmore, T.D., The Rel/NF-kappaB signal transduction pathway: Introduction (1999) Oncogene, 18, pp. 6842-6844 Samy, R.P., Identification of a novel Calotropis procera protein that can suppress tumor growth in breast cancer through the suppression of NF-kappaB pathway (2012) PLoS One, 7, pp. e48514 Albensi, B.C., Mattson, M.P., Evidence for the involvement of TNF and NF-kappaB in hippocampal synaptic plasticity (2000) Synapse, 35, pp. 151-159 Li, F., Sethi, G., Targeting transcription factor NF-kappaB to overcome chemoresistance and radioresistance in cancer therapy (2010) Biochim Biophys Acta, 1805, pp. 167-180 Pezzolesi, M.G., Comparative genomic and functional analyses reveal a novel cis-acting PTEN regulatory element as a highly conserved functional E-box motif deleted in Cowden syndrome (2007) Hum Mol Genet, 16, pp. 1058-1071 Bidere, N., Casein kinase 1alpha governs antigen-receptorinduced NF-kappaB activation and human lymphoma cell survival (2009) Nature, 458, pp. 92-96 Cerveira, N., Bizarro, S., Teixeira, M.R., MLL-SEPTIN gene fusions in hematological malignancies (2011) Biol Chem, 392, pp. 713-724 Zhao, L.J., Functional features of RUNX1 mutants in acute transformation of chronic myeloid leukemia and their contribution to inducing murine full-blown leukemia (2012) Blood, 119, pp. 2873-2882 Ichikawa, M., AML-1 is required for megakaryocytic maturation and lymphocytic diff erentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis (2004) Nat Med, 10, pp. 299-304 Blackmore, T.M., The transcriptional cofactor MIER1-beta negatively regulates histone acetyltransferase activity of the CREBbinding protein (2008) BMC Res Notes, 1, p. 68 Kohler, M., Evidence for distinct substrate specificities of importin alpha family members in nuclear protein import (1999) Mol Cell Biol, 19, pp. 7782-7791 Murati, A., Myeloid malignancies: Mutations, models and management (2012) BMC Cancer, 12, p. 304 Daver, N., FLT3 mutations in myelodysplastic syndrome and chronic myelomonocytic leukemia (2013) Am J Hematol, 88, pp. 56-59 Bai, Y., Itch E3 ligase-mediated regulation of TGF-beta signaling by modulating smad2 phosphorylation (2004) Mol Cell, 15, pp. 825-831 Tzachanis, D., Tob is a negative regulator of activation that is expressed in anergic and quiescent T cells (2001) Nat Immunol, 2, pp. 1174-1182 Naka, K., TGF-beta-FOXO signalling maintains leukaemiainitiating cells in chronic myeloid leukaemia (2010) Nature, 463, pp. 676-680 Ezzeddine, N., Human TOB, an antiproliferative transcription factor, is a poly(A)-binding protein-dependent positive regulator of cytoplasmic mRNA deadenylation (2007) Mol Cell Biol, 27, pp. 7791-7801 Kundu, J., Tob1 induces apoptosis and inhibits proliferation, migration and invasion of gastric cancer cells by activating Smad4 and inhibiting betacatenin signaling (2012) Int J Oncol, 41, pp. 839-848