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1. Identification by Real-time PCR of 13 mature microRNAs differentially expressed in colorectal cancer and non-tumoral tissues

Author

Moreno I, Navarro A, Abajo A, Ramirez N, Zárate R, Malumbres R, Agirre X, Cubedo E, Bandrés E, Monzó M, and García-Foncillas J

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract MicroRNAs (miRNAs) are short non-coding RNA molecules playing regulatory roles by repressing translation or cleaving RNA transcripts. Although the number of verified human miRNA is still expanding, only few have been functionally described. However, emerging evidences suggest the potential involvement of altered regulation of miRNA in pathogenesis of cancers and these genes are thought to function as both tumours suppressor and oncogenes. In our study, we examined by Real-Time PCR the expression of 156 mature miRNA in colorectal cancer. The analysis by several bioinformatics algorithms of colorectal tumours and adjacent non-neoplastic tissues from patients and colorectal cancer cell lines allowed identifying a group of 13 miRNA whose expression is significantly altered in this tumor. The most significantly deregulated miRNA being miR-31, miR-96, miR-133b, miR-135b, miR-145, and miR-183. In addition, the expression level of miR-31 was correlated with the stage of CRC tumor. Our results suggest that miRNA expression profile could have relevance to the biological and clinical behavior of colorectal neoplasia.

Published
2006
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2. Differentiation stage of myeloma plasma cells: biological and clinical significance

Author

Paiva, B, Puig, N, Cedena, M T, de Jong, B G, Ruiz, Y, Rapado, I, Martinez-Lopez, J, Cordon, L, Alignani, D, Delgado, J A, van Zelm, M C, Van Dongen, J J M, Pascual, M, Agirre, X, Prosper, F, Martín-Subero, J I, Vidriales, M-B, Gutierrez, N C, Hernandez, M T, Oriol, A, Echeveste, M A, Gonzalez, Y, Johnson, S K, Epstein, J, Barlogie, B, Morgan, G J, Orfao, A, Blade, J, Mateos, M V, Lahuerta, J J, and San-Miguel, J F

Published
2017
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3. Immunogenomic identification and characterization of granulocytic myeloid-derived suppressor cells in multiple myeloma

Author

Perez C., Botta C., Zabaleta A., Puig N., Cedena M. -T., Goicoechea I., Alameda D., Jose-Eneriz E. S., Merino J., Rodriguez-Otero P., Maia C., Alignani D., Maiso P., Manrique I., Lara-Astiaso D., Vilas-Zornoza A., Sarvide S., Riillo C., Rossi M., Rosinol L., Oriol A., Blanchard M. -J., Rios R., Sureda A., Martin J., Martinez R., Bargay J., de la Rubia J., Hernandez M. -T., Martinez-Lopez J., Orfao A., Agirre X., Prosper F., Mateos M. -V., Lahuerta J. -J., Blade J., San-Miguel J. F., Paiva B., Espinosa M. C., Zamudio J. L. G., Herranz E. R., Tamayo R. R., Sanchez J. M., Bernal L. P., Rodriguez A. P. G., Garcia M. E. G., Mayol A. S., Lleonart J. B., Suarez A., Garcia M. T. H., Gaisan C. M., Ruiz B. H., Montero F. C., de Miguel Llorente D., Ramos F. S., Garcia A. I., Manteca M. M., Martin J. M. H., Barrigon F. E., Frade J. G., de Coca A. G., Franco C. A., Gomez J. L., Perez E. C., Creixenti J. B., Balari A. M. S., Montes Y. G., Teigell L. E., Guinon A. G., Monreal E. A., Campos J. A. S., Tutusaus J. M. M., Rocafiguera A. O., Gorrochategui M. G., Mesa M. G., Silva C. C., Perez M. S. G., Loureiro A. D., Sanchez J. A. M., Irazu M. J. N., Parraga F. J. P., Palacios J. J. L., Barahona P. B., Rodriguez C. E., Rivas J. A. H., de Oteyza J. P., del Barrio R. I., de la Guia A. L., Amor A. A., Pareja E. P., Castello I. K., Rodriguez M. J. B., Martinez R. M., Grau R. R., Mesa E. G., Sainz E. R., de Arriba F., Jimenez J. M. M., Romera M., Cardoso F. P., Perez J. M. A., Pomposo M. P., Persona E. P., Casasus A. I. T., Garcia P. R., Ramos I. J., Lor M. B. V., Garcia P. L. F., Chamorro C. M., Perez C., Botta C., Zabaleta A., Puig N., Cedena M.-T., Goicoechea I., Alameda D., Jose-Eneriz E.S., Merino J., Rodriguez-Otero P., Maia C., Alignani D., Maiso P., Manrique I., Lara-Astiaso D., Vilas-Zornoza A., Sarvide S., Riillo C., Rossi M., Rosinol L., Oriol A., Blanchard M.-J., Rios R., Sureda A., Martin J., Martinez R., Bargay J., de la Rubia J., Hernandez M.-T., Martinez-Lopez J., Orfao A., Agirre X., Prosper F., Mateos M.-V., Lahuerta J.-J., Blade J., San-Miguel J.F., Paiva B., Espinosa M.C., Zamudio J.L.G., Herranz E.R., Tamayo R.R., Sanchez J.M., Bernal L.P., Rodriguez A.P.G., Garcia M.E.G., Mayol A.S., Lleonart J.B., Suarez A., Garcia M.T.H., Gaisan C.M., Ruiz B.H., Montero F.C., de Miguel Llorente D., Ramos F.S., Garcia A.I., Manteca M.M., Martin J.M.H., Barrigon F.E., Frade J.G., de Coca A.G., Franco C.A., Gomez J.L., Perez E.C., Creixenti J.B., Balari A.M.S., Montes Y.G., Teigell L.E., Guinon A.G., Monreal E.A., Campos J.A.S., Tutusaus J.M.M., Rocafiguera A.O., Gorrochategui M.G., Mesa M.G., Silva C.C., Perez M.S.G., Loureiro A.D., Sanchez J.A.M., Irazu M.J.N., Parraga F.J.P., Palacios J.J.L., Barahona P.B., Rodriguez C.E., Rivas J.A.H., de Oteyza J.P., del Barrio R.I., de la Guia A.L., Amor A.A., Pareja E.P., Castello I.K., Rodriguez M.J.B., Martinez R.M., Grau R.R., Mesa E.G., Sainz E.R., de Arriba F., Jimenez J.M.M., Romera M., Cardoso F.P., Perez J.M.A., Pomposo M.P., Persona E.P., Casasus A.I.T., Garcia P.R., Ramos I.J., Lor M.B.V., Garcia P.L.F., and Chamorro C.M.

Subjects
Male, Transcription, Genetic, Neutrophils, T-Lymphocytes, Immunology, CD33, Biology, CD16, Biochemistry, Follow-Up Studie, Flow cytometry, Antigens, CD, medicine, Humans, Cytotoxic T cell, Lymphocyte Count, Tumor microenvironment, medicine.diagnostic_test, Myeloid-Derived Suppressor Cells, Cell Biology, Hematology, Middle Aged, Cell sorting, Neoplasm Proteins, medicine.anatomical_structure, T-Lymphocyte, Cancer research, Myeloid-derived Suppressor Cell, Female, Bone marrow, Multiple Myeloma, Human, Follow-Up Studies
Abstract

Granulocytic myeloid-derived suppressor cells (G-MDSCs) promote tumor growth and immunosuppression in multiple myeloma (MM). However, their phenotype is not well established for accurate monitoring or clinical translation. We aimed to provide the phenotypic profile of G-MDSCs based on their prognostic significance in MM, immunosuppressive potential, and molecular program. The preestablished phenotype of G-MDSCs was evaluated in bone marrow samples from controls and MM patients using multidimensional flow cytometry; surprisingly, we found that CD11b+CD14−CD15+CD33+HLADR− cells overlapped with common eosinophils and neutrophils, which were not expanded in MM patients. Therefore, we relied on automated clustering to unbiasedly identify all granulocytic subsets in the tumor microenvironment: basophils, eosinophils, and immature, intermediate, and mature neutrophils. In a series of 267 newly diagnosed MM patients (GEM2012MENOS65 trial), only the frequency of mature neutrophils at diagnosis was significantly associated with patient outcome, and a high mature neutrophil/T-cell ratio resulted in inferior progression-free survival (P < .001). Upon fluorescence-activated cell sorting of each neutrophil subset, T-cell proliferation decreased in the presence of mature neutrophils (0.5-fold; P = .016), and the cytotoxic potential of T cells engaged by a BCMA×CD3-bispecific antibody increased notably with the depletion of mature neutrophils (fourfold; P = .0007). Most interestingly, RNA sequencing of the 3 subsets revealed that G-MDSC–related genes were specifically upregulated in mature neutrophils from MM patients vs controls because of differential chromatin accessibility. Taken together, our results establish a correlation between the clinical significance, immunosuppressive potential, and transcriptional network of well-defined neutrophil subsets, providing for the first time a set of optimal markers (CD11b/CD13/CD16) for accurate monitoring of G-MDSCs in MM.

Published
2020

7. Preclinical activity of LBH589 alone or in combination with chemotherapy in a xenogeneic mouse model of human acute lymphoblastic leukemia

Author

Vilas-Zornoza, A, Agirre, X, Abizanda, G, Moreno, C, Segura, V, De Martino Rodriguez, A, José-Eneriz, E S, Miranda, E, Martín-Subero, J I, Garate, L, Blanco-Prieto, M J, García de Jalón, J A, Rio, P, Rifón, J, Cigudosa, J C, Martinez-Climent, J A, Román-Gómez, J, Calasanz, M J, Ribera, J M, and Prósper, F

Published
2012
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19. Generation of a High Number of Healthy Erythroid Cells from Gene-Edited Pyruvate Kinase Deficiency Patient-Specific Induced Pluripotent Stem Cells

Author

Garate, Z, Quintana-Bustamante, O, Crane, AM, Olivier, E, Poirot, L, Galetto, R, Kosinski, P, Hill, C, Kung, C, Agirre, X, Orman, I, Cerrato, L, Alberquilla, O, Rodriguez-Fornes, F, Fusaki, N, Garcia-Sanchez, F, Maia, TM, Ribeiro, ML, Sevilla, J, Prosper, F, Jin, S, Mountford, J, Guenechea, G, Gouble, A, Bueren, JA, Davis, BR, and Segovia, JC

Subjects
Células Eritroides, Recombination, Genetic, Anemia Hemolítica Congénita não Esferocítica, lcsh:R5-920, DNA, Complementary, Base Sequence, Induced Pluripotent Stem Cells, Pyruvate Kinase, Cell Count, Anemia, Hemolytic, Congenital Nonspherocytic, Genetic Therapy, Pyruvate Metabolism, Inborn Errors, Article, Erythroid Cells, lcsh:Biology (General), Gene Targeting, Leukocytes, Mononuclear, Piruvato Quinase, Humans, Erros Inatos do Metabolismo dos Piruvatos, lcsh:Medicine (General), lcsh:QH301-705.5, Alleles, Células-Tronco Pluripotentes Induzidas
Abstract

Summary Pyruvate kinase deficiency (PKD) is a rare erythroid metabolic disease caused by mutations in the PKLR gene. Erythrocytes from PKD patients show an energetic imbalance causing chronic non-spherocytic hemolytic anemia, as pyruvate kinase defects impair ATP production in erythrocytes. We generated PKD induced pluripotent stem cells (PKDiPSCs) from peripheral blood mononuclear cells (PB-MNCs) of PKD patients by non-integrative Sendai viral vectors. PKDiPSCs were gene edited to integrate a partial codon-optimized R-type pyruvate kinase cDNA in the second intron of the PKLR gene by TALEN-mediated homologous recombination (HR). Notably, we found allele specificity of HR led by the presence of a single-nucleotide polymorphism. High numbers of erythroid cells derived from gene-edited PKDiPSCs showed correction of the energetic imbalance, providing an approach to correct metabolic erythroid diseases and demonstrating the practicality of this approach to generate the large cell numbers required for comprehensive biochemical and metabolic erythroid analyses., Highlights • Patient-specific PKDiPSCs are generated from PB-MNCs by a non-integrative system • PKDiPSCs are gene edited to insert a partial co-RPK in the PKLR locus mediated by TALEN • An SNP in the homology arm leads to allele-specific homologous recombination • Gene-edited PKDiPSCs generate a high number of metabolically corrected erythroid cells, Patient-specific induced pluripotent stem cells (iPSCs) are the perfect platform to study erythroid metabolic diseases and test innovative treatments. Segovia, Quintana-Bustamante, and colleagues showed the correction of pyruvate kinase deficiency (PKD) by combining iPSC and gene-editing technologies and provide an approach to generate the large number of erythroid cells required for comprehensive biochemical and metabolic analyses of this disease and its treatment.

Published
2015

20. PF583 COMPREHENSIVE ANALYSIS OF THE COMPLEXITY AND HETEROGENEITY OF THE LNCRNAS TRANSCRIPTOME IN MULTIPLE MYELOMA

Author

Carrasco-Leon, A., primary, Ezponda, T., additional, Meydan, C., additional, Valcárcel, L.V., additional, Ordoñez, R., additional, Kulis, M., additional, Garate, L., additional, Miranda, E., additional, Segura, V., additional, Guruceaga, E., additional, Vilas-Zornoza, A., additional, Alignani, D., additional, Castro-Labrador, L., additional, Pascual, M., additional, Amundarain, A., additional, El-Omri, H., additional, Taha, R. Y, additional, Calasanz, M.J., additional, Planes, F.J., additional, Mason, C., additional, Miguel, J. San, additional, Subero, J.I. Martin, additional, Melnick, A., additional, Prosper, F., additional, and Agirre, X., additional

Published
2019
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21. S843 THE PROLIFERATIVE HISTORY SHAPES THE DNA METHYLOME OF B-CELL TUMORS AND PREDICTS CLINICAL OUTCOME

Author

Duran-Ferrer, M., primary, Clot, G., additional, Nadeu, F., additional, Beekman, R., additional, Baumann, T., additional, Nordlund, J., additional, Marincevic-Zuniga, Y., additional, Rivas-Delgado, A., additional, Ordoñez, R., additional, Castellano, G., additional, Kulis, M., additional, Queirós, A., additional, Seung-Tae, L., additional, Wiemels, J., additional, Royo, R., additional, Puiggrós, M., additional, Torrents, D., additional, Giné, E., additional, Beà, S., additional, Jares, P., additional, Agirre, X., additional, Prosper, F., additional, López-Otín, C., additional, Puente, X.S., additional, Delgado, J., additional, López-Guillermo, A., additional, Campo, E., additional, and Martín-Subero, J.I., additional

Published
2019
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22. PF567 CHROMATIN ACTIVATION AS A UNIFYING PRINCIPLE UNDERLYING PATHOGENIC MECHANISMS IN MULTIPLE MYELOMA

Author

Ordoñez, R., primary, Kulis, M., additional, Russiñol, N., additional, Chapaprieta, V., additional, Beekman, R., additional, Meydan, C., additional, Duran-Ferrer, M., additional, Verdaguer-Dot, N., additional, Clot, G., additional, Vilarrasa-Blasi, R., additional, Garate, L., additional, Miranda, E., additional, Carrasco, A., additional, Ezponda, T., additional, Martens, J.H.A., additional, El-Omri, H., additional, Taha, R.Y., additional, Calasanz, M.J., additional, Paiva, B., additional, Miguel, J. San, additional, Flicek, P., additional, Gut, I., additional, Melnick, A., additional, Mitsiades, C.S., additional, Licht, J.D., additional, Campo, E., additional, Stunnenberg, H.G., additional, Agirre, X., additional, Martin-Subero, J.I., additional, and Prósper, F., additional

Published
2019
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25. THE ANALYSIS OF EPIGENOE OF MULTIPE MYELOMA REVEALS A HYPERMETHYLATION OF THE DNA IN SPECIFIC ENHANCER REGIONS OF B CELLS

Author

Agirre, X., Castellano, G., Pascual, M., Heath, S., Kulis, M., Segura, V., Bergmann, A., Russinol, N., Queiros, A. C., Beekman, R., Rodriguez-Madoz Juan, R., San Jose-Eneriz, E., Gutierrez Norma, C., Garcia-Verdugo, J. M., Schirmer Eric, C., Gut, M., MJ Calasanz, Flicek, P., Siebert, R., Campo, E., San Miguel Jesus, F., Melnick, A., Stunnenberg Hendrik, G., Gut Ivo, G., Prosper, F., and Martin-Subero, J.

Subjects
GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), Molecular Biology
Abstract

Contains fulltext : 150476.pdf (Publisher’s version ) (Open Access)

Published
2015

26. Use of human pharyngeal and palatine tonsils as a reservoir for the analysis of B-cell ontogeny in 10 paired samples

Author

Pascual, M., primary, Alignani, D., additional, Vilas-Zornoza, A., additional, Delgado, J.A., additional, Vázquez, I., additional, Malumbres, R., additional, Rodriguez, I., additional, Barriuso, R., additional, Calasanz, M.J., additional, Paiva, B., additional, Agirre, X., additional, Prósper, F., additional, and Cervera-Paz, F.J., additional

Published
2016
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27. Down-regulated expression of hsa-miR-181c in Fanconi anemia patients: implications in TNF alpha regulation and proliferation of hematopoietic progenitor cells

Author

Rio, P, Agirre, X, Garate, L, Banos, R, Alvarez, L, San Jose-Eneriz, E, Badell, I, Casado, JA, Garin, M, Prosper, F, and Bueren, JA

Abstract

Fanconi anemia (FA) is an inherited genetic disorder associated with BM failure and cancer predisposition. In the present study, we sought to elucidate the role of microRNAs (miRNAs) in the hematopoietic defects observed in FA patients. Initial studies showed that 3 miRNAs, hsa-miR-133a, hsa-miR-135b, and hsa-miR181c, were significantly down-regulated in lymphoblastoid cell lines and fresh peripheral blood cells from FA patients. In vitro studies with cells expressing the luciferase reporter fused to the TNF alpha 3'-untranslated region confirmed in silico predictions suggesting an interaction between hsa-miR-181c and TNF alpha mRNA. These observations were consistent with the down-regulated expression of TNF alpha mediated by hsa-miR-181c in cells from healthy donors and cells from FA patients. Because of the relevance of TNF alpha in the hematopoietic defects of FA patients, in the present study, we transfected BM cells from FA patients with hsa-miR-181c to evaluate the impact of this miRNA on their clonogenic potential. hsa-miR-181c markedly increased the number and size of the myeloid and erythroid colonies generated by BM cells from FA patients. Our results offer new clues toward understanding the biologic basis of BM failure in FA patients and open new possibilities for the treatment of the hematologic dysfunction in FA patients based on miRNA regulation. (Blood. 2012;119(13):3042-3049)

Published
2012

28. Whole-epigenome analysis in multiple myeloma reveals DNA hypermethylation of B cell-specific enhancers

Author

Agirre, X., primary, Castellano, G., additional, Pascual, M., additional, Heath, S., additional, Kulis, M., additional, Segura, V., additional, Bergmann, A., additional, Esteve, A., additional, Merkel, A., additional, Raineri, E., additional, Agueda, L., additional, Blanc, J., additional, Richardson, D., additional, Clarke, L., additional, Datta, A., additional, Russiñol, N., additional, Queirós, A.C., additional, Beekman, R., additional, Rodríguez-Madoz, J.R., additional, San José-Enériz, E., additional, Fang, F., additional, Gutiérrez, N.C., additional, García-Verdugo, J.M., additional, Robson, M.I., additional, Schirmer, E.C., additional, Guruceaga, E., additional, Martens, J.H.A., additional, Gut, M., additional, Calasanz, M.J., additional, Flicek, P., additional, Siebert, R., additional, Campo, E., additional, San Miguel, J.F., additional, Melnick, A., additional, Stunnenberg, H.G., additional, Gut, I.G., additional, Prosper, F., additional, and Martín-Subero, J.I., additional

Published
2015
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30. NUP98 is fused to adducin 3 in a patient with T-cell acute lymphoblastic leukemia and myeloid markers, with a new translocation t(10;11)(q25;p15)

Author

Lahortiga, I., Vizmanos, Jl, Agirre, X., Vazquez, I., Cigudosa, Jc, Larrayoz, Mj, Sala, F., Gorosquieta, A., Perez-Equiza, K., Calasanz, Mj, and Maria D. Odero

Subjects
Chromosomes, Human, Pair 11/ultrastructure, Chromosomes, Human, Pair 10/ultrastructure, Oncogene Proteins, Fusion/genetics, Translocation, Genetic, Leukemia-Lymphoma, Adult T-Cell/genetics
Abstract

The nucleoporin 98 gene (NUP98) has been reported to be fused to 13 partner genes in hematological malignancies with 11p15 translocations. Twelve of them have been identified in patients with myeloid neoplasias and only 1, RAP1GDS1 (4q21), is fused with NUP98 in five patients with T-cell acute lymphoblastic leukemia (T-ALL). Three of these patients coexpressed T and myeloid markers, suggesting the specific association of t(4;11)(q21;p15) with a subset of T-ALL originating from an early progenitor, which has the potential to express mature T-cell antigens as well as myeloid markers. We describe here a new NUP98 partner involved in a t(10;11)(q25;p15) in a patient with acute biphenotypic leukemia, showing coexpression of mature T and myeloid markers. The gene involved, located in 10q25, was identified as ADD3 using 3'-RACE. ADD3 codes for the ubiquitous expressed subunit gamma of the adducin protein, and it seems to play an important role in the skeletal organization of the cell membrane. Both NUP98-ADD3 and ADD3-NUP98 fusion transcripts are expressed in the patient. This is the second partner of NUP98 described in T-ALL. Adducin shares with the product of RAP1GDS1, and with all of the nonhomeobox NUP98 partners, the presence of a region with significant probability of adopting a coiled-coil conformation. This region is always retained in the fusion transcript with the NH(2) terminus FG repeats of NUP98, suggesting an important role in the mechanism of leukemogenesis.

Published
2003

33. Aberrant DNA methylation profile of chronic and transformed classic Philadelphia-negative myeloproliferative neoplasms

Author

Perez, C., primary, Pascual, M., additional, Martin-Subero, J. I., additional, Bellosillo, B., additional, Segura, V., additional, Delabesse, E., additional, Alvarez, S., additional, Larrayoz, M. J., additional, Rifon, J., additional, Cigudosa, J. C., additional, Besses, C., additional, Calasanz, M. J., additional, Cross, N. C. P., additional, Prosper, F., additional, and Agirre, X., additional

Published
2013
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34. Downregulation of specific miRNAs in hyperdiploid multiple myeloma mimics the oncogenic effect of IgH translocations occurring in the non-hyperdiploid subtype

Author

Rio-Machin, A, primary, Ferreira, B I, additional, Henry, T, additional, Gómez-López, G, additional, Agirre, X, additional, Alvarez, S, additional, Rodriguez-Perales, S, additional, Prosper, F, additional, Calasanz, M J, additional, Martínez, J, additional, Fonseca, R, additional, and Cigudosa, J C, additional

Published
2012
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37. Down-regulation of EVI1 is associated with epigenetic alterations and good prognosis in patients with acute myeloid leukemia

Author

Vazquez, I., primary, Maicas, M., additional, Cervera, J., additional, Agirre, X., additional, Marin-Bejar, O., additional, Marcotegui, N., additional, Vicente, C., additional, Lahortiga, I., additional, Gomez-Benito, M., additional, Carranza, C., additional, Valencia, A., additional, Brunet, S., additional, Lumbreras, E., additional, Prosper, F., additional, Gomez-Casares, M. T., additional, Hernandez-Rivas, J. M., additional, Calasanz, M. J., additional, Sanz, M. A., additional, Sierra, J., additional, and Odero, M. D., additional

Published
2011
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38. LMO2 expression reflects the different stages of blast maturation and genetic features in B-cell acute lymphoblastic leukemia and predicts clinical outcome

Author

Malumbres, R., primary, Fresquet, V., additional, Roman-Gomez, J., additional, Bobadilla, M., additional, Robles, E. F., additional, Altobelli, G. G., additional, Calasanz, M.{ a. } J., additional, Smeland, E. B., additional, Aznar, M. A., additional, Agirre, X., additional, Martin-Palanco, V., additional, Prosper, F., additional, Lossos, I. S., additional, and Martinez-Climent, J. A., additional

Published
2011
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40. R15 – Oral miR-16 participe à l’angiogenèse des tumeurs exprimant l’oncogène de fusion X-ALK

Author

Dejean, E., primary, Rénalier, M.H., additional, Foisseau, M., additional, Agirre, X., additional, De Paiva, G.R., additional, Al Saati, T., additional, Soulier, J., additional, Desjobert, C., additional, Lamant, L., additional, Felsher, D.W., additional, Cavaillé, J., additional, Prats, H., additional, Delsol, G., additional, Giuriato, S., additional, and Meggetto, F., additional

Published
2010
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47. Identification by Real-time PCR of 13 mature microRNAs differentially expressed in colorectal cancer and non-tumoral tissues.

Author

Bandrés, E., Cubedo, E., Agirre, X., Malumbres, R., Zàrate, R., Ramirez, N., Abajo, A., Navarro, A., Moreno, I., Monzó, M., and Garcia-Foncillas, J.

Subjects
COLON cancer, ONCOGENES, CARCINOGENESIS, TUMOR suppressor genes, CANCER cells, CANCER research
Abstract

MicroRNAs (miRNAs) are short non-coding RNA molecules playing regulatory roles by repressing translation or cleaving RNA transcripts. Although the number of verified human miRNA is still expanding, only few have been functionally described. However, emerging evidences suggest the potential involvement of altered regulation of miRNA in pathogenesis of cancers and these genes are thought to function as both tumours suppressor and oncogenes. In our study, we examined by Real-Time PCR the expression of 156 mature miRNA in colorectal cancer. The analysis by several bioinformatics algorithms of colorectal tumours and adjacent nonneoplastic tissues from patients and colorectal cancer cell lines allowed identifying a group of 13 miRNA whose expression is significantly altered in this tumor. The most significantly deregulated miRNA being miR-31, miR-96, miR-133b, miR-135b, miR-145, and miR-183. In addition, the expression level of miR-31 was correlated with the stage of CRC tumor. Our results suggest that miRNA expression profile could have relevance to the biological and clinical behavior of colorectal neoplasia. [ABSTRACT FROM AUTHOR]

Published
2006
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48. The normal epithelial cell-specific 1 (NES1) gene, a candidate tumor suppressor gene on chromosome 19q13.3-4, is downregulated by hypermethylation in acute lymphoblastic leukemia.

Author

J. Roman-Gomez, C., Jimenez-Velasco, A., Agirre, X., Castillejo, J.A., Barrios, M., Andreu, E.J., Prosper, F., Heiniger, A., and Torres, A.

Subjects
EPITHELIAL cells, GENES, METHYLATION, LYMPHOBLASTIC leukemia, EPITHELIUM, LYMPHOCYTIC leukemia
Abstract

Studies the downregulation of the normal epithelial cell-specific 1 (NES1) gene by hypermethylation in acute lymphoblastic leukemia. Transcriptional silencing due to abnormal methylation of CpG islands within gene promoters; Presence of normal NES1 gene in chromosomes 19q; Physiological function of NES1; Epigenetic inactivation of NES1 gene.

Published
2004
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