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Your search keyword '"Caligiuri, M."' showing total 13 results
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13 results on '"Caligiuri, M."'

1. Non-Hodgkin's lymphoma. Clinical practice guidelines in oncology

Author

Zelenetz, A. D., Advani, R. H., Buadi, F., Cabanillas, F., Caligiuri, M. A., Czuczman, M. S., Damon, L. E., Fayad, L., Flinn, I. W., Forero, A., Glenn, M. J., Gockerman, J. P., Leo Gordon, Harris, N. L., Hoppe, R. T., Kaminski, M. S., Lacasce, A. S., Nademanee, A., Porcu, P., Press, O., Prosnitz, L., Smith, M. R., Sotomayor, E. M., Vose, J. M., and Yahalom, J.

Subjects
Lymphoma, Non-Hodgkin, Humans
Published
2006

13. Identification of novel posttranscriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis

Author

Joshua J. Oaks, Guido Marcucci, Carlo Gambacorti-Passerini, Stefano Volinia, Anna M. Eiring, Michael A. Caligiuri, Gustavo Leone, William L. Willis, Ji Suk Chang, Ramasamy Santhanam, Mario Notari, Danilo Perrotti, Paolo Neviani, Eiring, A, Neviani, P, Santhanam, R, Oaks, J, Chang, J, Notari, M, Illis, W, GAMBACORTI PASSERINI, C, Volinia, S, Marcucci, G, Caligiuri, M, Leone, G, and Perrotti, D

Subjects
Male, Untranslated region, Cell Survival, Immunology, Fusion Proteins, bcr-abl, Antigens, CD34, Apoptosis, RNA-binding protein, Biology, Biochemistry, Heterogeneous-Nuclear Ribonucleoproteins, Mice, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, medicine, Animals, Humans, RNA, Neoplasm, Kinase activity, 3' Untranslated Regions, Bcr/abl, Mice, Knockout, ABL, Neoplasia, Gene Expression Regulation, Leukemic, breakpoint cluster region, RNA-Binding Proteins, Cell Biology, Hematology, Protein-Tyrosine Kinases, Hematopoietic Stem Cells, medicine.disease, Ribonomics, Cell Transformation, Neoplastic, E2F3 Transcription Factor, Cancer research, Female, Blast Crisis, K562 Cells, Chronic myelogenous leukemia, K562 cells
Abstract

Several RNA binding proteins (RBPs) have been implicated in the progression of chronic myelogenous leukemia (CML) from the indolent chronic phase to the aggressively fatal blast crisis. In the latter phase, expression and function of specific RBPs are aberrantly regulated at transcriptional or posttranslational levels by the constitutive kinase activity of the BCR/ABL oncoprotein. As a result, altered expression/function of RBPs leads to increased resistance to apoptotic stimuli, enhanced survival, growth advantage, and differentiation arrest of CD34+ progenitors from patients in CML blast crisis. Here, we identify the mRNAs bound to the hnRNP-A1, hnRNP-E2, hnRNP-K, and La/SSB RBPs in BCR/ABL-transformed myeloid cells. Interestingly, we found that the mRNA encoding the transcription factor E2F3 associates to hnRNP-A1 through a conserved binding site located in the E2F3 3′ untranslated region (UTR). E2F3 levels were upregulated in CML-BCCD34+ in a BCR/ABL kinase- and hnRNP-A1 shuttling-dependent manner. Moreover, by using shRNA-mediated E2F3 knock-down and BCR/ABL-transduced lineage-negative bone marrow cells from E2F3+/+ and E2F3-/- mice, we show that E2F3 expression is important for BCR/ABL clonogenic activity and in vivo leukemogenic potential. Thus, the complexity of the mRNA/RBP network, together with the discovery of E2F3 as an hnRNP-A1-regulated factor, outlines the relevant role played by RBPs in posttranscriptional regulation of CML development and progression. © 2008 by The American Society of Hematology.

Published
2008
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