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151 results on '"Casado P"'

1. Fostamatinib effectiveness and safety for immune thrombocytopenia in clinical practice

Author

González-López, Tomás José, Bermejo-Vega, Nuria, Cardesa-Cabrera, Rocío, Martínez-Robles, Violeta, Aguilar-Monserrate, Gerardo, Pérez-Segura, Gloria, Domingo, Abel, Luis-Navarro, Josefa, Lakhwani, Sunil, Acedo, Natalia, Lozano, María Luisa, Bernat, Silvia, Torres-Tienza, Ana, Ruano, Ana, Jarque, Isidro, Galán, Pilar, Benet, Carmen, Marcellini, Shally, Jimenez-Bárcenas, Reyes, Martínez-Carballeira, Daniel, De Miguel-Llorente, Dunia, Perona-Blázquez, Alvaro, Gonzalez-Gascón, Isabel, Lopez-Ansoar, Elsa, Alonso-Alonso, José María, Bengochea-Casado, María Luisa, Díaz-Gálvez, Francisco Javier, Moretó, Ana, Moreno-Jiménez, Gemma, Hernández-Martin, Roberto, de Cabo, Erik, Dávila-Valls, Julio, Cuesta, Amalia, Pastoriza, Carmen, Hermida-Fernández, Gerardo Julio, García, Covadonga, Pozas-Mañas, Miguel Angel, Aguilar, Carlos, Fernandez-Jimenez, Dolores, Navas-Elorza, Begoña, López-Santamaría Castro, Carolina, Lorenzo, Alvaro, Ortín, Xavier, García, Marta, Piernas, Sonia, Díaz-Santa, Johana, Soto, Inmaculada, Provan, Drew, and García-Donas Gabaldón, Gloria

Abstract

•Similar to clinical trial results, fostamatinib has demonstrated a high efficacy rate for ITP in daily clinical practice conditions.•Fostamatinib is a well-tolerated drug with a very low rate of thrombotic events associated with its use.

Published
2024
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2. Toxicity of Asciminib in Real Clinical Practice; Analysis of Side Effects and Cross-Intolerance with Tyrosine Kinase Inhibitors

Author

Pérez-Lamas, Lucía, Luna, Alejandro, Boque, Concepcion, Senin, María Alicia, Xicoy, Blanca, Giraldo, Pilar, Perez Lopez, Raul, Ruiz Nuño, Concepción, De las Heras, Natalia, Mora Casterá, Elvira, Garcia-Hernandez, Carmen, Segura Diaz, Adrian, Steegmann, Juan Luis, Velez Tenza, Patricia, Sanchez-Guijo, Fermin, Garcia-Noblejas Moya, Ana Maria, Juan Vera Goñi, Juan Antonio, Moreno Vega, Melania, Alvarez-Larran, Alberto, Cortes, Montse, Perez Encinas, Manuel, Serrano, Luis, Angona, Anna, Rosell, Ana, Lakhwani, Sunil, Colorado, Mercedes, Ramila, Elena, Cervero, Carlos, Cuevas, Beatriz, Villalon Blanco, Lucia, Hernandez Boluda, Juan Carlos, Paz Coll, Antonio, Gómez García de Soria, Valle, Fernández, Maria Jose, Casado, Luis Felipe, Alonso-Dominguez, Juan Manuel, Anguita Arance, Maria Magdalena, Carrascosa Mastell, Patricia, Salamanca Cuenca, Araceli, Jiménez-Velasco, Antonio, Ramírez, María José, López Esteban, Miguel, Sierra Pacho, Magdalena, Santaliestra, Marta, Alda Alvarez, Olga, de Paz, Raquel, and García Gutiérrez, Valentín

Published
2022
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3. Toxicity of Asciminib in Real Clinical Practice; Analysis of Side Effects and Cross-Intolerance with Tyrosine Kinase Inhibitors

Author

Pérez-Lamas, Lucía, Luna, Alejandro, Boque, Concepcion, Senin, María Alicia, Xicoy, Blanca, Giraldo, Pilar, Perez Lopez, Raul, Ruiz Nuño, Concepción, De las Heras, Natalia, Mora Casterá, Elvira, Garcia-Hernandez, Carmen, Segura Diaz, Adrian, Steegmann, Juan Luis, Velez Tenza, Patricia, Sanchez-Guijo, Fermin, Garcia-Noblejas Moya, Ana Maria, Juan Vera Goñi, Juan Antonio, Moreno Vega, Melania, Alvarez-Larran, Alberto, Cortes, Montse, Perez Encinas, Manuel, Serrano, Luis, Angona, Anna, Rosell, Ana, Lakhwani, Sunil, Colorado, Mercedes, Ramila, Elena, Cervero, Carlos, Cuevas, Beatriz, Villalon Blanco, Lucia, Hernandez Boluda, Juan Carlos, Paz Coll, Antonio, Gómez García de Soria, Valle, Fernández, Maria Jose, Casado, Luis Felipe, Alonso-Dominguez, Juan Manuel, Anguita Arance, Maria Magdalena, Carrascosa Mastell, Patricia, Salamanca Cuenca, Araceli, Jiménez-Velasco, Antonio, Ramírez, María José, López Esteban, Miguel, Sierra Pacho, Magdalena, Santaliestra, Marta, Alda Alvarez, Olga, de Paz, Raquel, and García Gutiérrez, Valentín

Published
2022
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4. Real-World Data Analysis of the Molecular Response Kinetics within the Two First Years of the RELMC-NOVA Study in Newly Diagnosed Spanish CML-CP Patients Treated with Tirosin Kinasa Inhibitors (TKIs) in First Line

Author

Casado Montero, Luis Felipe, Garcia-Ormeña, Nuria, Perez Encinas, Manuel, Osorio-Prendes, Santiago, Ferrer Marin, Francisca, Sagüés, Miguel, Garcia-Gutiérrez, Valentín, Marco De Lucas, Fernando, Boque, Concepcion, Noya, Soledad, Gomez Casares, María Teresa, Estrada, Natalia, Goñi, Maria Angeles, Ramírez Payer, Angel, Requena, Maria Jose, Lakhwani, Sunil, Andrade Campos, Marcio Miguel, De las Heras, Natalia, Foncillas, María Ángeles, and Steegmann, Juan Luis

Published
2022
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5. Recovery of Uninvolved Heavy/Light Chain Pair Immunoparesis during Maintenance Is an Independent Prognostic Factor for Multiple Myeloma and Could Complement Prognosis Value of Minimal Residual Disease

Author

Lakhwani, Sunil, Rosinol Dachs, Laura, Puig, Noemi, Pico Picos, Miguel Angel, Medina-González, Laura, Martínez-López, Joaquín, Paiva, Bruno, Oriol, Albert, Rios, Rafael, Blanchard, María Jesús, Jarque, Isidro, Bargay, Joan, Moraleda, Jose Maria, Carrillo-Cruz, Estrella, Sureda, Anna, Krsnik, Isabel, Garcia, Esther González, Casado Montero, Luis Felipe, Marti, Josep M, Encinas, Cristina, De Arriba, Felipe, Palomera, Luis, Sampol, Antonia, Gonzalez-Montes, Yolanda, Motllo, Cristina, De La Cruz, Javier, Alonso Fernández, Rafael, Mateos, María-Victoria, Bladé Creixenti, Joan, Lahuerta, Juan-José, San-Miguel, Jesús, and Hernández, Miguel-Teodoro

Published
2022
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6. Thrombogenesis Mechanisms of High Doses of Ponatinib in Patients with Chronic Myeloid Leukemia (CML) Compared to Tyrosine Kinase Inhibitors

Author

Aguila, Sonia, Cuenca, Ernesto J, Lys, Maria Jose, Garcia-Hernandez, Carmen, Fernández, Maria Jose, Noya, Maria, García Gutiérrez, Valentín, Palomera, Luis, Senín, Alicia, Perez Lopez, Raul, Pérez-Encinas, Manuel, Angona, Anna, Puerta, Jose M, Vallansot, Rolando, Conesa, Venancio, Hernandez Boluda, Juan Carlos, Rosell, Ana, Cortes, Montse, Ortí, Guillermo, Xicoy, Blanca, Carreño, Gonzalo, Mora Castera, Elvira, Giraldo, Pilar, Lozano, Maria Luisa, Casado, Luis Felipe, Ferrer Marin, Francisca, and Gelmc, on Behalf Of

Published
2022
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7. Immunoparesis Recovery in Transplant-Ineligible Newly Diagnosis Multiple Myeloma Patients: An Independent Prognosis Factor That Could Complement Prognostic Value of Minimal Residual Disease

Author

Lakhwani, Sunil, Mateos, María Victoria, Martínez-López, Joaquín, Paiva, Bruno, Rosinol Dachs, Laura, Martínez, Rafael, Oriol, Albert, Bargay, Joan, Gonzalez-Montes, Yolanda, Gironella, Mercedes, Encinas, Cristina, Martin, Jesus, Jarque, Isidro, Granell, Miquel, Abella, Eugenia, García Mateo, Aránzazu, Hernández-Rivas, José Ángel, Ramila, Elena, Krsnik, Isabel, Casado Montero, Luis Felipe, De Arriba, Felipe, Palomera, Luis, Sampol, Antonia, Moraleda, Jose Maria, Casanova, Maria, Delgado, Pilar, Lafuente, Ana, Amutio, Elena, Martínez, Aurelio Lopez, Altés, Albert, Ruíz, M. Ángeles, Lopez-Anglada, Lucia, Bladé Creixenti, Joan, Lahuerta, Juan-José, San-Miguel, Jesús, and Hernández, Miguel-Teodoro

Published
2022
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8. Real-World Data Analysis of the Molecular Response Kinetics within the Two First Years of the RELMC-NOVA Study in Newly Diagnosed Spanish CML-CP Patients Treated with Tirosin Kinasa Inhibitors (TKIs) in First Line

Author

Casado Montero, Luis Felipe, Garcia-Ormeña, Nuria, Perez Encinas, Manuel, Osorio-Prendes, Santiago, Ferrer Marin, Francisca, Sagüés, Miguel, Garcia-Gutiérrez, Valentín, Marco De Lucas, Fernando, Boque, Concepcion, Noya, Soledad, Gomez Casares, María Teresa, Estrada, Natalia, Goñi, Maria Angeles, Ramírez Payer, Angel, Requena, Maria Jose, Lakhwani, Sunil, Andrade Campos, Marcio Miguel, De las Heras, Natalia, Foncillas, María Ángeles, and Steegmann, Juan Luis

Published
2022
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9. Thrombogenesis Mechanisms of High Doses of Ponatinib in Patients with Chronic Myeloid Leukemia (CML) Compared to Tyrosine Kinase Inhibitors

Author

Aguila, Sonia, Cuenca, Ernesto J, Lys, Maria Jose, Garcia-Hernandez, Carmen, Fernández, Maria Jose, Noya, Maria, García Gutiérrez, Valentín, Palomera, Luis, Senín, Alicia, Perez Lopez, Raul, Pérez-Encinas, Manuel, Angona, Anna, Puerta, Jose M, Vallansot, Rolando, Conesa, Venancio, Hernandez Boluda, Juan Carlos, Rosell, Ana, Cortes, Montse, Ortí, Guillermo, Xicoy, Blanca, Carreño, Gonzalo, Mora Castera, Elvira, Giraldo, Pilar, Lozano, Maria Luisa, Casado, Luis Felipe, Ferrer Marin, Francisca, and Gelmc, on Behalf Of

Published
2022
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10. Deep Multi-Omics Profiling in Cytogenetically Poor-Risk AML

Author

Rio-Machin, Ana, Bewicke-Copley, Findlay, Zheng, Jiexin, Casado Izquierdo, Pedro, Miettinen, Juho J., Khan, Naeem, Demeulemeester, Jonas, Krizsán, Szilvia, Middleton, Christopher, Benkwitz-Bedford, Sam, Saad, Joseph, Vilas-Zornoza, Amaia, Ezponda, Teresa, Grey, William, Lavallée, Vincent-Philippe, Nolin-Lapalme, Alexis, Miraki-Moud, Farideh, Matthews, Janet, Grantham, Marianne, Colm, Ryan J, Bond, Jonathan, Di Bella, Doriana, Wennerberg, Krister, Parsons, Alun, Zeng, Andy G.X., Armes, Hannah, Close, Karina, Kaya, Fadimana, Rouault-Pierre, Kevin, Gribben, John G., Prosper, Felipe, Cavenagh, James, Dick, John E., Freeman, Sylvie D, Van Loo, Peter, Bödör, Csaba, Sauvageau, Guy, Porkka, Kimmo, Heckman, Caroline A., Wang, Jun, Cazier, Jean-Baptiste, Taussig, David, Bonnet, Dominique, Cutillas, Pedro, and Fitzgibbon, Jude

Published
2022
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11. Immunoparesis Recovery in Transplant-Ineligible Newly Diagnosis Multiple Myeloma Patients: An Independent Prognosis Factor That Could Complement Prognostic Value of Minimal Residual Disease

Author

Lakhwani, Sunil, Mateos, María Victoria, Martínez-López, Joaquín, Paiva, Bruno, Rosinol Dachs, Laura, Martínez, Rafael, Oriol, Albert, Bargay, Joan, Gonzalez-Montes, Yolanda, Gironella, Mercedes, Encinas, Cristina, Martin, Jesus, Jarque, Isidro, Granell, Miquel, Abella, Eugenia, García Mateo, Aránzazu, Hernández-Rivas, José Ángel, Ramila, Elena, Krsnik, Isabel, Casado Montero, Luis Felipe, De Arriba, Felipe, Palomera, Luis, Sampol, Antonia, Moraleda, Jose Maria, Casanova, Maria, Delgado, Pilar, Lafuente, Ana, Amutio, Elena, Martínez, Aurelio Lopez, Altés, Albert, Ruíz, M. Ángeles, Lopez-Anglada, Lucia, Bladé Creixenti, Joan, Lahuerta, Juan-José, San-Miguel, Jesús, and Hernández, Miguel-Teodoro

Published
2022
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12. Recovery of Uninvolved Heavy/Light Chain Pair Immunoparesis during Maintenance Is an Independent Prognostic Factor for Multiple Myeloma and Could Complement Prognosis Value of Minimal Residual Disease

Author

Lakhwani, Sunil, Rosinol Dachs, Laura, Puig, Noemi, Pico Picos, Miguel Angel, Medina-González, Laura, Martínez-López, Joaquín, Paiva, Bruno, Oriol, Albert, Rios, Rafael, Blanchard, María Jesús, Jarque, Isidro, Bargay, Joan, Moraleda, Jose Maria, Carrillo-Cruz, Estrella, Sureda, Anna, Krsnik, Isabel, Garcia, Esther González, Casado Montero, Luis Felipe, Marti, Josep M, Encinas, Cristina, De Arriba, Felipe, Palomera, Luis, Sampol, Antonia, Gonzalez-Montes, Yolanda, Motllo, Cristina, De La Cruz, Javier, Alonso Fernández, Rafael, Mateos, María-Victoria, Bladé Creixenti, Joan, Lahuerta, Juan-José, San-Miguel, Jesús, and Hernández, Miguel-Teodoro

Published
2022
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13. Inhibition of Stearoyl-CoA Desaturase Has Anti-Leukemic Properties in Acute Myeloid Leukemia

Author

Dembitz, Vilma, Lawson, Hannah, Philippe, Celine, Burt, Richard J., James, Sophie, Magee, Aoife S.M., Woodley, Keith, Durko, Jozef, Campos, Joana, Austin, Michael James, Rio-Machin, Ana, Casado Izquierdo, Pedro, Bewicke-Copley, Findlay, Rodriguez Blanco, Giovanny, Patel, Bela, Hazlehurst, Lori, Peck, Barrie, Finch, Andrew, Cutillas, Pedro, Fitzgibbon, Jude, Yuneva, Mariia, Rouault-Pierre, Kevin, Copland, John, Kranc, Kamil, and Gallipoli, Paolo

Published
2022
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14. Inhibition of Stearoyl-CoA Desaturase Has Anti-Leukemic Properties in Acute Myeloid Leukemia

Author

Dembitz, Vilma, Lawson, Hannah, Philippe, Celine, Burt, Richard J., James, Sophie, Magee, Aoife S.M., Woodley, Keith, Durko, Jozef, Campos, Joana, Austin, Michael James, Rio-Machin, Ana, Casado Izquierdo, Pedro, Bewicke-Copley, Findlay, Rodriguez Blanco, Giovanny, Patel, Bela, Hazlehurst, Lori, Peck, Barrie, Finch, Andrew, Cutillas, Pedro, Fitzgibbon, Jude, Yuneva, Mariia, Rouault-Pierre, Kevin, Copland, John, Kranc, Kamil, and Gallipoli, Paolo

Published
2022
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15. Deep Multi-Omics Profiling in Cytogenetically Poor-Risk AML

Author

Rio-Machin, Ana, Bewicke-Copley, Findlay, Zheng, Jiexin, Casado Izquierdo, Pedro, Miettinen, Juho J., Khan, Naeem, Demeulemeester, Jonas, Krizsán, Szilvia, Middleton, Christopher, Benkwitz-Bedford, Sam, Saad, Joseph, Vilas-Zornoza, Amaia, Ezponda, Teresa, Grey, William, Lavallée, Vincent-Philippe, Nolin-Lapalme, Alexis, Miraki-Moud, Farideh, Matthews, Janet, Grantham, Marianne, Colm, Ryan J, Bond, Jonathan, Di Bella, Doriana, Wennerberg, Krister, Parsons, Alun, Zeng, Andy G.X., Armes, Hannah, Close, Karina, Kaya, Fadimana, Rouault-Pierre, Kevin, Gribben, John G., Prosper, Felipe, Cavenagh, James, Dick, John E., Freeman, Sylvie D, Van Loo, Peter, Bödör, Csaba, Sauvageau, Guy, Porkka, Kimmo, Heckman, Caroline A., Wang, Jun, Cazier, Jean-Baptiste, Taussig, David, Bonnet, Dominique, Cutillas, Pedro, and Fitzgibbon, Jude

Published
2022
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16. Conditional expression of HGAL leads to the development of diffuse large B-cell lymphoma in mice

Author

Raboso-Gallego, Javier, Casado-García, Ana, Jiang, Xiaoyu, Isidro-Hernández, Marta, Gentles, Andrew J., Zhao, Shuchun, Natkunam, Yaso, Blanco, Oscar, Domínguez, Verónica, Pintado, Belén, Alonso-López, Diego, De Las Rivas, Javier, Vicente-Dueñas, Carolina, Lossos, Izidore S., and Sanchez-Garcia, Isidro

Abstract

Diffuse large B-cell lymphomas (DLBCLs) are clinically and genetically heterogeneous tumors. Deregulation of diverse biological processes specific to B cells, such as B-cell receptor (BCR) signaling and motility regulation, contribute to lymphomagenesis. Human germinal center associated lymphoma (HGAL) is a B-cell–specific adaptor protein controlling BCR signaling and B lymphocyte motility. In normal B cells, it is expressed in germinal center (GC) B lymphocytes and promptly downregulated upon further differentiation. The majority of DLBCL tumors, primarily GC B-cell types, but also activated types, express HGAL. To investigate the consequences of constitutive expression of HGAL in vivo, we generated mice that conditionally express human HGAL at different stages of hematopoietic development using 3 restricted Cre-mediated approaches to initiate expression of HGAL in hematopoietic stem cells, pro-B cells, or GC B cells. Following immune stimulation, we observed larger GCs in mice in which HGAL expression was initiated in GC B cells. All 3 mouse strains developed DLBCL at a frequency of 12% to 30% starting at age 13 months, leading to shorter survival. Immunohistochemical studies showed that all analyzed tumors were of the GC B-cell type. Exon sequencing revealed mutations reported in human DLBCL. Our data demonstrate that constitutive enforced expression of HGAL leads to DLBCL development.

Published
2021
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17. Conditional expression of HGAL leads to the development of diffuse large B-cell lymphoma in mice

Author

Raboso-Gallego, Javier, Casado-García, Ana, Jiang, Xiaoyu, Isidro-Hernández, Marta, Gentles, Andrew J., Zhao, Shuchun, Natkunam, Yaso, Blanco, Oscar, Domínguez, Verónica, Pintado, Belén, Alonso-López, Diego, De Las Rivas, Javier, Vicente-Dueñas, Carolina, Lossos, Izidore S., and Sanchez-Garcia, Isidro

Abstract

Diffuse large B-cell lymphomas (DLBCLs) are clinically and genetically heterogeneous tumors. Deregulation of diverse biological processes specific to B cells, such as B-cell receptor (BCR) signaling and motility regulation, contribute to lymphomagenesis. Human germinal center associated lymphoma (HGAL) is a B-cell–specific adaptor protein controlling BCR signaling and B lymphocyte motility. In normal B cells, it is expressed in germinal center (GC) B lymphocytes and promptly downregulated upon further differentiation. The majority of DLBCL tumors, primarily GC B-cell types, but also activated types, express HGAL. To investigate the consequences of constitutive expression of HGAL in vivo, we generated mice that conditionally express human HGAL at different stages of hematopoietic development using 3 restricted Cre-mediated approaches to initiate expression of HGAL in hematopoietic stem cells, pro-B cells, or GC B cells. Following immune stimulation, we observed larger GCs in mice in which HGAL expression was initiated in GC B cells. All 3 mouse strains developed DLBCL at a frequency of 12% to 30% starting at age 13 months, leading to shorter survival. Immunohistochemical studies showed that all analyzed tumors were of the GC B-cell type. Exon sequencing revealed mutations reported in human DLBCL. Our data demonstrate that constitutive enforced expression of HGAL leads to DLBCL development.

Published
2021
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18. An intact gut microbiome protects genetically predisposed mice against leukemia

Author

Vicente-Dueñas, Carolina, Janssen, Stefan, Oldenburg, Marina, Auer, Franziska, González-Herrero, Inés, Casado-García, Ana, Isidro-Hernández, Marta, Raboso-Gallego, Javier, Westhoff, Philipp, Pandyra, Aleksandra A., Hein, Daniel, Gössling, Katharina L., Alonso-López, Diego, De Las Rivas, Javier, Bhatia, Sanil, García-Criado, Francisco Javier, García-Cenador, María Begoña, Weber, Andreas P. M., Köhrer, Karl, Hauer, Julia, Fischer, Ute, Sánchez-García, Isidro, and Borkhardt, Arndt

Abstract

The majority of childhood leukemias are precursor B-cell acute lymphoblastic leukemias (pB-ALLs) caused by a combination of prenatal genetic predispositions and oncogenic events occurring after birth. Although genetic predispositions are frequent in children (>1% to 5%), fewer than 1% of genetically predisposed carriers will develop pB-ALL. Although infectious stimuli are believed to play a major role in leukemogenesis, the critical determinants are not well defined. Here, by using murine models of pB-ALL, we show that microbiome disturbances incurred by antibiotic treatment early in life were sufficient to induce leukemia in genetically predisposed mice, even in the absence of infectious stimuli and independent of T cells. By using V4 and full-length 16S ribosomal RNA sequencing of a series of fecal samples, we found that genetic predisposition to pB-ALL (Pax5 heterozygosity or ETV6-RUNX1 fusion) shaped a distinct gut microbiome. Machine learning accurately (96.8%) predicted genetic predisposition using 40 of 3983 amplicon sequence variants as proxies for bacterial species. Transplantation of either wild-type (WT) or Pax5+/– hematopoietic bone marrow cells into WT recipient mice revealed that the microbiome is shaped and determined in a donor genotype–specific manner. Gas chromatography-mass spectrometry (GC-MS) analyses of sera from WT and Pax5+/– mice demonstrated the presence of a genotype-specific distinct metabolomic profile. Taken together, our data indicate that it is a lack of commensal microbiota rather than the presence of specific bacteria that promotes leukemia in genetically predisposed mice. Future large-scale longitudinal studies are required to determine whether targeted microbiome modification in children predisposed to pB-ALL could become a successful prevention strategy.

Published
2020
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19. An intact gut microbiome protects genetically predisposed mice against leukemia

Author

Vicente-Dueñas, Carolina, Janssen, Stefan, Oldenburg, Marina, Auer, Franziska, González-Herrero, Inés, Casado-García, Ana, Isidro-Hernández, Marta, Raboso-Gallego, Javier, Westhoff, Philipp, Pandyra, Aleksandra A., Hein, Daniel, Gössling, Katharina L., Alonso-López, Diego, De Las Rivas, Javier, Bhatia, Sanil, García-Criado, Francisco Javier, García-Cenador, María Begoña, Weber, Andreas P.M., Köhrer, Karl, Hauer, Julia, Fischer, Ute, Sánchez-García, Isidro, and Borkhardt, Arndt

Abstract

The majority of childhood leukemias are precursor B-cell acute lymphoblastic leukemias (pB-ALLs) caused by a combination of prenatal genetic predispositions and oncogenic events occurring after birth. Although genetic predispositions are frequent in children (>1% to 5%), fewer than 1% of genetically predisposed carriers will develop pB-ALL. Although infectious stimuli are believed to play a major role in leukemogenesis, the critical determinants are not well defined. Here, by using murine models of pB-ALL, we show that microbiome disturbances incurred by antibiotic treatment early in life were sufficient to induce leukemia in genetically predisposed mice, even in the absence of infectious stimuli and independent of T cells. By using V4 and full-length 16S ribosomal RNA sequencing of a series of fecal samples, we found that genetic predisposition to pB-ALL (Pax5heterozygosity or ETV6-RUNX1fusion) shaped a distinct gut microbiome. Machine learning accurately (96.8%) predicted genetic predisposition using 40 of 3983 amplicon sequence variants as proxies for bacterial species. Transplantation of either wild-type (WT) or Pax5+/–hematopoietic bone marrow cells into WT recipient mice revealed that the microbiome is shaped and determined in a donor genotype–specific manner. Gas chromatography-mass spectrometry (GC-MS) analyses of sera from WT and Pax5+/–mice demonstrated the presence of a genotype-specific distinct metabolomic profile. Taken together, our data indicate that it is a lack of commensal microbiota rather than the presence of specific bacteria that promotes leukemia in genetically predisposed mice. Future large-scale longitudinal studies are required to determine whether targeted microbiome modification in children predisposed to pB-ALL could become a successful prevention strategy.

Published
2020
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20. Predictors of unsustained measurable residual disease negativity in transplant-eligible patients with multiple myeloma

Author

Guerrero, Camila, Puig, Noemi, Cedena, María-Teresa, Calasanz, María-José, Gutierrez, Norma C., Fernandez, Manuela, Oriol, Albert, Ríos-Tamayo, Rafael, Hernandez, Miguel-Teodoro, Martínez-Martínez, Rafael, Bargay, Joan, de Arriba, Felipe, Palomera, Luis, Gonzalez-Rodriguez, Ana Pilar, Gonzalez Perez, Marta-Sonia, Orfao, Alberto, Mateos, María-Victoria, Martinez-Lopez, Joaquin, Rosiñol, Laura, Bladé, Joan, Lahuerta, Juan-Jose, San-Miguel, Jesus F., Paiva, Bruno, Casanova Espinosa, María, Zamudio, José Luís Guzman, Ríos Herranz, Eduardo, Rios Tamayo, Rafael, Martín Sánchez, Jesús, Palomera Bernal, Luís, González Rodríguez, Ana Pilar, González García, María Esther, Mayol, Antonia Sampol, Bargay Lleonart, Joan, Suárez, Alexia, Hernández García, Miguel Teodoro, Gaisán, Carmen Montes, Hernández Ruiz, Belén, Casado Montero, Felipe, Miguel Llorente, Dunia de, Ramos, Fernando Solano, Ibañez Garcia, Ángela, Manteca, Mariví Mateos, Mariano Hernández Martín, José, Escalante Barrigón, Fernando, García Frade, Javier, de Coca, Alfonso García, Franco, Carlos Aguilar, Labrador Gómez, Jorge, Cabezudo Pérez, Elena, Bladé Creixentí, Joan, Balari, Ana MaSureda, González Montes, Yolanda, Teigell, Lourdes Escoda, García Guiñón, Antonio, Abella Monreal, Eugenia, Alfonso Soler Campos, Juan, Martí Tutusaus, Josep Ma, Rocafiguera, Albert Oriol, Gorrochategui, Miquel Granell, Mesa, Mercedes Gironella, Silva, Carmen Cabrera, González Pérez, Marta Sonia, Loureiro, Ana Dios, Méndez Sánchez, José Angel, Irazu, María Josefa Nájera, Párraga, Francisco Javier Peñalver, Lahuerta Palacios, Juan José, Barahona, Pilar Bravo, Rodríguez, Cristina Encinas, Hernández Rivas, José Ángel, Oteyza, Jaime Pérez de, Iglesias del Barrio, Rebeca, López de la Guia, Ana, Amor, Adrián Alegre, Prieto Pareja, Elena, Castelló, Isabel Krsnik, Blanchard Rodríguez, MaJesús, Martínez Martínez, Rafael, Riaza Grau, Rosalía, Mesa, Eugenio Giménez, Ruiz Sainz, Elena, Arriba, Felipe de, Moraleda Jiménez, Jose María, Romera, Marta, Cardoso, Felipe Prósper, Arguiñano Pérez, José Ma, Pomposo, María Puente, Pérez Persona, Ernesto, Teruel Casasús, Ana Isabel, García, Paz Ribas, Jarque Ramos, Isidro, Villarrubia Lor, María Blanca, Fernández García, Pedro Luis, Fernández García, Pedro Luis, and Martínez Chamorro, Carmen

Abstract

•ISS 3, high CTC levels, and a longer time to first MRD negativity are significant predictors of MRD resurgence and/or progressive disease.

Published
2024
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21. Bortezomib, lenalidomide, and dexamethasone as induction therapy prior to autologous transplant in multiple myeloma

Author

Rosiñol, Laura, Oriol, Albert, Rios, Rafael, Sureda, Anna, Blanchard, María Jesús, Hernández, Miguel Teodoro, Martínez-Martínez, Rafael, Moraleda, Jose M., Jarque, Isidro, Bargay, Juan, Gironella, Mercedes, de Arriba, Felipe, Palomera, Luis, González-Montes, Yolanda, Martí, Josep M., Krsnik, Isabel, Arguiñano, Jose M., González, Maria Esther, González, Ana Pilar, Casado, Luis Felipe, López-Anglada, Lucia, Paiva, Bruno, Mateos, Maria-Victoria, San Miguel, Jesus F., Lahuerta, Juan-José, and Bladé, Joan

Abstract

Achieving and maintaining a high-quality response is the treatment goal for patients with newly diagnosed multiple myeloma (NDMM). The phase 3 PETHEMA/GEM2012 study, in 458 patients aged =65 years with NDMM, is evaluating bortezomib (subcutaneous) + lenalidomide + dexamethasone (VRD) for 6 cycles followed by autologous stem cell transplant (ASCT) conditioned with IV busulfan + melphalan vs melphalan and posttransplant consolidation with 2 cycles of VRD. We present grouped response analysis of induction, transplant, and consolidation. Responses deepened over time; in patients who initiated cycle 6 of induction (n = 426), the rates of a very good partial response or better were 55.6% by cycle 3, 63.8% by cycle 4, 68.3% by cycle 5, and 70.4% after induction. The complete response rate of 33.4% after induction in the intent-to-treat (ITT) population, which was similar in the 92 patients with high-risk cytogenetics (34.8%), also deepened with further treatment (44.1% after ASCT and 50.2% after consolidation). Rates of undetectable minimal residual disease (median 3 × 10-6 sensitivity) in the ITT population also increased from induction (28.8%) to transplant (42.1%) and consolidation (45.2%). The most common grade =3 treatment-emergent adverse events during induction were neutropenia (12.9%) and infection (9.2%). Grade =2 peripheral neuropathy (grouped term) during induction was 17.0%, with a low frequency of grade 3 (3.7%) and grade 4 (0.2%) events. VRD is an effective and well-tolerated regimen for induction in NDMM with deepening response throughout induction and over the course of treatment. This trial was registered at www.clinicaltrials.gov as #NCT01916252 and EudraCT as #2012-005683-10.

Published
2019
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22. Bortezomib, lenalidomide, and dexamethasone as induction therapy prior to autologous transplant in multiple myeloma

Author

Rosiñol, Laura, Oriol, Albert, Rios, Rafael, Sureda, Anna, Blanchard, María Jesús, Hernández, Miguel Teodoro, Martínez-Martínez, Rafael, Moraleda, Jose M., Jarque, Isidro, Bargay, Juan, Gironella, Mercedes, de Arriba, Felipe, Palomera, Luis, González-Montes, Yolanda, Martí, Josep M., Krsnik, Isabel, Arguiñano, Jose M., González, Maria Esther, González, Ana Pilar, Casado, Luis Felipe, López-Anglada, Lucia, Paiva, Bruno, Mateos, Maria-Victoria, San Miguel, Jesus F., Lahuerta, Juan-José, and Bladé, Joan

Abstract

Achieving and maintaining a high-quality response is the treatment goal for patients with newly diagnosed multiple myeloma (NDMM). The phase 3 PETHEMA/GEM2012 study, in 458 patients aged ≤65 years with NDMM, is evaluating bortezomib (subcutaneous) + lenalidomide + dexamethasone (VRD) for 6 cycles followed by autologous stem cell transplant (ASCT) conditioned with IV busulfan + melphalan vs melphalan and posttransplant consolidation with 2 cycles of VRD. We present grouped response analysis of induction, transplant, and consolidation. Responses deepened over time; in patients who initiated cycle 6 of induction (n = 426), the rates of a very good partial response or better were 55.6% by cycle 3, 63.8% by cycle 4, 68.3% by cycle 5, and 70.4% after induction. The complete response rate of 33.4% after induction in the intent-to-treat (ITT) population, which was similar in the 92 patients with high-risk cytogenetics (34.8%), also deepened with further treatment (44.1% after ASCT and 50.2% after consolidation). Rates of undetectable minimal residual disease (median 3 × 10−6sensitivity) in the ITT population also increased from induction (28.8%) to transplant (42.1%) and consolidation (45.2%). The most common grade ≥3 treatment-emergent adverse events during induction were neutropenia (12.9%) and infection (9.2%). Grade ≥2 peripheral neuropathy (grouped term) during induction was 17.0%, with a low frequency of grade 3 (3.7%) and grade 4 (0.2%) events. VRD is an effective and well-tolerated regimen for induction in NDMM with deepening response throughout induction and over the course of treatment. This trial was registered at www.clinicaltrials.govas #NCT01916252 and EudraCT as #2012-005683-10.

Published
2019
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23. A High Percentage of DNAM-1+ and Low Percentage of Tactile+ NK Cells at Diagnosis Correlate with Complete Response and Survival in AML: A Sub-Analysis of the Ven-a-Qui Pethema Trial

Author

Bergua Burgues, Juan Miguel, Tarazona, Raquel, Garcia Casado, Javier, Gordillo, Juan J, Casas Aviles, Ignacio, Rodriguez Veiga, Rebeca, Cano, Isabel, Vall-Llovera Calmet, Ferran, Garcia, Antonio, Gomez Espuch, Joaquin, Colorado, Mercedes, Esteve, Jordi, Verdugo Cabeza De Vaca, Victoria, Sanpol, Maria Antonia, Ramos, Fernando, Valero, Marta, Acuña-Cruz, Evelyn, Boluda, Blanca, Martinez-Lopez, Joaquin, Ayala, Rosa, Barragán, Eva, Martinez-Cuadron, David, and Montesinos, Pau

Abstract

Background:Natural killer (NK) immune status in Acute Myeloid Leukemia (AML) could influence therapeutic results and natural history of the disease.

Published
2023
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24. Allele-Specific Expression of Leukemia Genes Is Associated with Pathogenicity in Poor Risk AML

Author

Zheng, Jiexin, Bewicke-Copley, Findlay, Vermeulen, Carlo, Casado, Pedro, Kaya, Fadimana, Demeulemeester, Jonas, Guscott, Molly, Krizsán, Szilvia, Benkwitz-Bedford, Sam, Miraki-Moud, Farideh, Matthews, Janet, Grantham, Marianne, Di Bella, Doriana, Gribben, John G., Cavenagh, James, Van Loo, Peter, McClelland, Sarah, Bödör, Csaba, Cazier, Jean-Baptiste, Taussig, David, Bonnet, Dominique, Cutillas, Pedro R, Wang, Jun, De Ridder, Jeroen, Fitzgibbon, Jude, and Rio-Machin, Ana

Abstract

Introduction:An imbalance in gene expression of the different alleles of a gene (allele-specific expression or ASE) is an intriguing genome-wide and dynamic phenomenon that could have an important role in tumorigenesis. Little is known about the causes and consequences of the differential cis-and trans-regulation on resultant ASE, aside from the impact of copy number alterations (CNAs) or imprinting. Acute myeloid leukemia (AML) is an aggressive clonal hematopoietic stem cell malignancy, with a low mutational burden in comparison with other cancers, where the impact of ASE may constitute a novel mechanism of pathogenesis.

Published
2023
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25. Efficacy and Safety of Fostamatinib for Immune Thrombocytopenia in Clinical Practice in Spain: Interim Results of Fostames, Our National Fostamatinib Registry

Author

Gonzalez-Lopez, Tomas Jose, Perez Segura, Gloria, Domingo, Abel, Lopez Ansoar, Elsa, Diaz Galvez, Francisco Javier, Jimenez Barcenas, Reyes, Martinez Carballeira, Daniel, De Miguel Llorente, Dunia, Perona Blazquez, Alvaro, Aguilar-Monserrate, Gerardo, Dávila-Valls, Julio, Gonzalez Gascon, Isabel, Cuesta, Amalia, Bengochea Casado, María Luisa, Hermida Fernandez, Gerardo Julio, Alonso Alonso, Jose Maria, Pozas Mañas, Miguel Angel, Torres-Tienza, Ana, Aguilar, Carlos, Fernandez-Jimenez, Dolores, Soto, Inmaculada, and Bernat, Silvia

Abstract

Background: Fostamatinib is a splenic tyrosine kinase (SYK) inhibitor that prevents antibody-mediated platelet destruction. This drug has demonstrated to be effective and safe in immune thrombocytopenia (ITP). However, clinical trials may not accurately reflect what happens in clinical practice. Here we evaluated the efficacy and safety of eltrombopag in ITP in a real-world setting.

Published
2023
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26. GEM2017FIT Trial: Induction Therapy with Bortezomib-Melphalan and Prednisone (VMP) Followed By Lenalidomide and Dexamethasone (Rd) Versus Carfilzomib, Lenalidomide and Dexamethasone (KRd) Plus/Minus Daratumumab (D), 18 Cycles, Followed By Consolidation and Maintenance Therapy with Lenalidomide and Daratumumab: Phase III, Multicenter, Randomized Trial for Elderly Fit Newly Diagnosed Multiple Myeloma (NDMM) Patients Aged between 65 and 80 Years

Author

Mateos, Maria-Victoria, Paiva, Bruno, Cedena Romero, Maria Teresa, Puig, Noemi, Sureda Balari, Anna Maria, Oriol, Albert, Ocio, Enrique M, Rosiñol, Laura, González-Montes, Yolanda, Bargay, Juan Jose, Gonzalez Garcia, Esther, Hernández Garcia, Miguel Teodoro, Ramirez, Angel, Suarez-Cabrera, Alexia, Blanchard, María-Jesús, Garzón, Sebastián, Casado Montero, Luis Felipe, Cabanas Perianes, Valentin, Pérez De Oteyza, Jaime, Gironella, Mercedes, Martinez-Lopez, Joaquin, -Teruel, Ana-Isabel, Delgado, Pilar, Prieto, Elena, Lahuerta Palacios, Juan Jose, Bladé, Joan, and San Miguel, Jesus

Abstract

Background: In transplant-ineligible patients (pts) with NDMM, VMP and Rd have been standards of care. The Spanish Myeloma Group examined induction with VMP followed by Rd, and results were particularly striking for “fit” pts aged 65-80 with a CR rate of 47% and an MRD negative rate (MRD(-)) of 20%. The median PFS was 34 months (m) and 4-years (yrs) OS rate was 70%.

Published
2023
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27. Sustained Recovery of Uninvolved Heavy/Light Chain Pair Immunoparesis during Maintenance Discriminates Patients with Sustained Negative Minimal Residual Disease

Author

Lakhwani, Sunil, Rosiñol, Laura, Puig, Noemi, Pico Picos, Miguel Angel, Medina-González, Laura, Martinez Lopez, Joaquin, Paiva, Bruno, Cedena Romero, Maria Teresa, Oriol, Albert, Ríos, Rafael, Blanchard, María Jesús, Jarque, Isidro, Bargay, Joan, Moraleda, Jose Maria, Carrillo-Cruz, Estrella, Sureda Balari, Anna Maria, Krsnik, Isabel, Gonzalez Garcia, Esther, Casado Montero, Luis Felipe, Marti Tutusaus, Josep Maria, Encinas Rodriguez, Cristina, De Arriba, Felipe, Palomera, Luis, Sampol Mayol, Antonia, González-Montes, Yolanda, Motlló, Cristina, De la Cruz, Javier, Alonso Fernández, Rafael, Mateos, Maria-Victoria, Blade Creixenti, Joan, Lahuerta Palacios, Juan Jose, San Miguel, Jesus, and Hernández Garcia, Miguel Teodoro

Abstract

Introduction.Immunoparesis (IP) or the suppression of uninvolved immunoglobulins (Ig) is a very common finding in multiple myeloma (MM) patients at diagnosis that confers worse prognosis. In addition to classic total Ig, IP can be measured by the uninvolved heavy/light chain pair of the same immunoglobulin (uHLC). Previously, we have reported that recovery of uHLC IP in a single time point (at first year of maintenance) is an independent prognostic factor in newly diagnosed MM transplant eligible (NDMM-TE) patients with intensive treatment within a clinical trial, without significant prognostic value for recovery from classic IP in that setting. Moreover, recovery of uHLC IP affords complementary information to single time point minimal residual disease (MRD) for risk stratification. Although, negative sustained MRD is the most important evolutive favorable prognostic factor in MM, some patients relapse despite achieving negative sustained MRD.

Published
2023
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28. Outcomes of Chronic Myeloid Leukemia Patients after Therapeutic Failure to Asciminib, a Multicenter Observational Study

Author

Pérez-Lamas, Lucía, Segura Diaz, Adrian, Mora, Elvira, Hidalgo Soto, Marta, Paz Coll, Antonio, De Las Heras, Natalia, Cortes, Montse, Velez Tenza, Patricia, Sierra Pacho, Magdalena, Senin, María Alicia, Angona, Anna, Cervero, Carlos, De Paz Arias, Raquel, Salamanca Cuenca, Araceli, Santaliestra, Marta, López Marin, Javier, Casado Montero, Luis Felipe, and García Gutiérrez, Valentín

Abstract

Introduction:Asciminib has recently entered the market as a promising option for patients with chronic myeloid leukemia (CML) and therapeutic failure to ³ 2 tyrosine kinase inhibitors (TKIs). It presents a relevant rate of therapeutic success thanks to its different mechanism of action, being the first in its class to produce an allosteric inhibition on the myristoylated pocket of ABL. However, a percentage of patients fail this drug due to intolerance or resistance. This group constitutes a highly polytreated population with few therapeutic options. The aim of this analysis is to determine the most frequent treatment strategies in this setting, as well as to ascertain the prognosis in this difficult to treat group.

Published
2023
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29. Efficacy of Consolidation Therapy with Ponatinib 15mg on Treatment-Free Remission Rate in Patients with Chronic Myeloid Leukemia. Results of the Ponazero Trial

Author

Pérez-Lamas, Lucía, Hernandez Boluda, Juan Carlos, Casado Montero, Luis Felipe, Gómez Casares, Maria Teresa, Ayala, Rosa, Xicoy, Blanca, Ferrer Marin, Francisca, Orti, Guillermo, De Paz Arias, Raquel, Osorio Prendes, Santiago, Perez Lopez, Raul, Mora, Elvira, Ruiz Nuño, Concepción, Jimenez Velasco, Antonio, Boque, Concepcion, Sierra Pacho, Magdalena, Martinez Lopez, Joaquin, and Garcia Gutierrez, Valentin

Abstract

Introduction:Discontinuation of tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) has become part of routine clinical practice in recent years, thanks to growing evidence on their feasibility and safety. However, and despite adequate patient selection based on current recommendations, loss of response is observed in approximately 50% of patients. In this scenario, efforts are focused on finding strategies to increase the rate of successful discontinuations. Ponatinib has shown to induce deeper molecular responses compared with imatinib, but its risk of arterial occlusive events (AOE) limits its use in first line at its standard dose of 45mg. The risk of AOEs appears to be dose-related and following the results of the OPTIC study, dose reduction to 15mg in patients with good response is an increasingly popular strategy. Under these premises it has been postulated that a consolidation with ponatinib 15mg may increase the proportion of patients who could discontinue treatment successfully.

Published
2023
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30. The XPO1-FOXC1-HOX Functional Axis Opens New Therapeutic Avenues to Treat DEK-NUP214 AML Patients

Author

Kaya, Fadimana, Bewicke-Copley, Findlay, Casado Izquierdo, Pedro, Zheng, Jiexin, Miettinen, Juho Jalmari, Khan, Naeem, Krizsán, Szilvia, Saad, Joseph J, Lavallée, Vincent-Philippe, Nolin-Lapalme, Alexis, Hébert, Josée, Matthews, Janet, Grantham, Marianne, Di Bella, Doriana, Wennerberg, Krister, Parsons, Alun, Gribben, John G., Cavenagh, James D., Freeman, Sylvie D, Bödör, Csaba, Sauvageau, Guy, Heckman, Caroline A., Wang, Jun, Cazier, Jean-Baptiste, Taussig, David, Bonnet, Dominique, Cutillas, Pedro R, Rouault-Pierre, Kevin, Fitzgibbon, Jude, and Rio-Machin, Ana

Abstract

Introduction:t(6;9)(p23;q34.1)/DEK-NUP214 patients represent a discrete group of younger AML patients recognised as a separate disease entity in the World Health Organization classification of myeloid neoplasms. They typically display a dismal prognosis, higher relapse rate and a striking co-occurrence with FLT3-ITD mutations in > 70% of cases. DEK is a nuclear factor that has been attributed multifunctional roles, including gene regulation, while its fusion partner, NUP214, plays a pivotal role in nuclear export by interacting with transport receptors such as XPO1. However, the precise mechanism by which DEK-NUP214 drives leukaemia remains unclear.

Published
2023
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31. Multiomic Characterization of Myelodysplastic Neoplasms (MDS) with Micromegakaryocytes Highlights the Role of EZH2-RUNX1deregulation in Disease Physiopathology and Response to Targeted Therapies

Author

Fernandez-Serrano, Miranda, Mesa, Alba, Campillo-Marcos, Ignacio, Casado-Pelaez, Marta, Bhattacharya, Shubhra, Palomo, Laura, Walter, Wencke, Marin-Escudero, Pau, Mallo, Mar, Montoro, Julia, Sole, Francesc, Mereu, Elisabetta, Mata, Caterina, Corujo, David, Haferlach, Torsten, Buschbeck, Marcus, Esteller, Manel, Valcarcel, David, Saumell, Silvia, and Roue, Gael

Abstract

Micromegakaryocytes (micro-MKs), an unequivocal myeloid dysplastic feature in adults, are present in 15-20% of myelodysplastic neoplasms (MDS). We recently associated the detection of these small megakaryocytes with a mono- or bi-lobated nucleus in bone marrow (BM) smears of MDS patients with an unfavorable prognosis. The aim of the present study was to elucidate the molecular bases of micro-MK formation and its impact on MDS response to targeted therapies.

Published
2023
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32. Analysis of Immunological and Clinical Response to Vaccination Against Sars-COV-2 in Patients with Chronic Myeloid Leukemia

Author

ZURDO Castronuño, Alejandro, Solera Sainero, Miriam, Corona, Magdalena, Torres, Monserrat, Casado-Fernandez, Guiomar, Ramos-García, Fernando, Garcia-Pérez, Javier, Murciano-Antón, María Aranzazú, Blanchard, María Jesús, Marquet Palomanes, Juan, Martin Moro, Fernando, Pérez-Olmeida, Mayte, López Jiménez, Javier, Coiras, Maria Teresa, Rodriguez-Mora, Sara, and Garcia-Gutiérrez, Valentín

Published
2022
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33. Analysis of Immunological and Clinical Response to Vaccination Against Sars-COV-2 in Patients with Chronic Myeloid Leukemia

Author

ZURDO Castronuño, Alejandro, Solera Sainero, Miriam, Corona, Magdalena, Torres, Monserrat, Casado-Fernandez, Guiomar, Ramos-García, Fernando, Garcia-Pérez, Javier, Murciano-Antón, María Aranzazú, Blanchard, María Jesús, Marquet Palomanes, Juan, Martin Moro, Fernando, Pérez-Olmeida, Mayte, López Jiménez, Javier, Coiras, Maria Teresa, Rodriguez-Mora, Sara, and Garcia-Gutiérrez, Valentín

Published
2022
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35. Dynamic Response Assesment Combining Liquid Biopsy MRD and PET/CT in Follicular Lymphoma Patients Including CAR-T Cell Therapy

Author

Martín-Muñoz, Alejandro, Poza, María, Figaredo, Gloria, Dorado, Sara, Ruiz-Heredia, Yanira, Rodriguez, Margarita, Rufian, Laura, Rodriguez Izquierdo, Antonia, Parrilla-Navamuel, Laura, Wang, Chongwu, Toledo, Paula, Grande Garcia, Carlos, Baumann, Tycho, Calbacho, Maria, Rapado, Inmaculada, Gallardo, Miguel, Canales, Miguel, Sarandeses, Pilar, Mollejo, Manuela, Casado Montero, Luis Felipe, Ayala, Rosa, Martínez-López, Joaquín, Barrio, Santiago, and Jimenez-Ubieto, Ana

Published
2022
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37. Dynamic Response Assesment Combining Liquid Biopsy MRD and PET/CT in Follicular Lymphoma Patients Including CAR-T Cell Therapy

Author

Martín-Muñoz, Alejandro, Poza, María, Figaredo, Gloria, Dorado, Sara, Ruiz-Heredia, Yanira, Rodriguez, Margarita, Rufian, Laura, Rodriguez Izquierdo, Antonia, Parrilla-Navamuel, Laura, Wang, Chongwu, Toledo, Paula, Grande Garcia, Carlos, Baumann, Tycho, Calbacho, Maria, Rapado, Inmaculada, Gallardo, Miguel, Canales, Miguel, Sarandeses, Pilar, Mollejo, Manuela, Casado Montero, Luis Felipe, Ayala, Rosa, Martínez-López, Joaquín, Barrio, Santiago, and Jimenez-Ubieto, Ana

Published
2022
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38. Engraftment and in vivo proliferation advantage of gene-corrected mobilized CD34+cells from Fanconi anemia patients

Author

Río, Paula, Navarro, Susana, Guenechea, Guillermo, Sánchez-Domínguez, Rebeca, Lamana, Maria Luisa, Yañez, Rosa, Casado, Jose A., Mehta, Parinda A., Pujol, Maria Roser, Surrallés, Jordi, Charrier, Sabine, Galy, Anne, Segovia, José C., Díaz de Heredia, Cristina, Sevilla, Julián, and Bueren, Juan A.

Abstract

Previous Fanconi anemia (FA) gene therapy studies have failed to demonstrate engraftment of gene-corrected hematopoietic stem and progenitor cells (HSPCs) from FA patients, either after autologous transplantation or infusion into immunodeficient mice. In this study, we demonstrate that a validated short transduction protocol of G-CSF plus plerixafor-mobilized CD34+cells from FA-A patients with a therapeutic FANCA-lentiviral vector corrects the phenotype of in vitro cultured hematopoietic progenitor cells. Transplantation of transduced FA CD34+cells into immunodeficient mice resulted in reproducible engraftment of myeloid, lymphoid, and CD34+cells. Importantly, a marked increase in the proportion of phenotypically corrected, patient-derived hematopoietic cells was observed after transplantation with respect to the infused CD34+graft, indicating the proliferative advantage of corrected FA-A hematopoietic repopulating cells. Our data demonstrate for the first time that optimized protocols of hematopoietic stem cell collection from FA patients, followed by the short and clinically validated transduction of these cells with a therapeutic lentiviral vector, results in the generation of phenotypically corrected HSPCs capable of repopulating and developing proliferation advantage in immunodeficient mice. Our results suggest that clinical approaches for FA gene therapy similar to those used in this study will facilitate hematopoietic repopulation in FA patients with gene corrected HSPCs, opening new prospects for gene therapy of FA patients.

Published
2017
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39. Engraftment and in vivo proliferation advantage of gene-corrected mobilized CD34+ cells from Fanconi anemia patients

Author

Río, Paula, Navarro, Susana, Guenechea, Guillermo, Sánchez-Domínguez, Rebeca, Lamana, Maria Luisa, Yañez, Rosa, Casado, Jose A., Mehta, Parinda A., Pujol, Maria Roser, Surrallés, Jordi, Charrier, Sabine, Galy, Anne, Segovia, José C., Díaz de Heredia, Cristina, Sevilla, Julián, and Bueren, Juan A.

Abstract

Previous Fanconi anemia (FA) gene therapy studies have failed to demonstrate engraftment of gene-corrected hematopoietic stem and progenitor cells (HSPCs) from FA patients, either after autologous transplantation or infusion into immunodeficient mice. In this study, we demonstrate that a validated short transduction protocol of G-CSF plus plerixafor-mobilized CD34+ cells from FA-A patients with a therapeutic FANCA-lentiviral vector corrects the phenotype of in vitro cultured hematopoietic progenitor cells. Transplantation of transduced FA CD34+ cells into immunodeficient mice resulted in reproducible engraftment of myeloid, lymphoid, and CD34+ cells. Importantly, a marked increase in the proportion of phenotypically corrected, patient-derived hematopoietic cells was observed after transplantation with respect to the infused CD34+ graft, indicating the proliferative advantage of corrected FA-A hematopoietic repopulating cells. Our data demonstrate for the first time that optimized protocols of hematopoietic stem cell collection from FA patients, followed by the short and clinically validated transduction of these cells with a therapeutic lentiviral vector, results in the generation of phenotypically corrected HSPCs capable of repopulating and developing proliferation advantage in immunodeficient mice. Our results suggest that clinical approaches for FA gene therapy similar to those used in this study will facilitate hematopoietic repopulation in FA patients with gene corrected HSPCs, opening new prospects for gene therapy of FA patients.

Published
2017
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40. Lenalidomide and dexamethasone maintenance with or without ixazomib, tailored by residual disease status in myeloma

Author

Rosiñol, Laura, Oriol, Albert, Ríos, Rafael, Blanchard, María Jesús, Jarque, Isidro, Bargay, Joan, Hernández, Miguel Teodoro, Cabañas, Valentín, Carrillo-Cruz, Estrella, Sureda, Anna, Martínez-López, Joaquín, Krsnik, Isabel, González, Maria Esther, Casado, Luis Felipe, Martí, Josep María, Encinas, Cristina, de Arriba, Felipe, Palomera, Luis, Sampol, Antonia, González-Montes, Yolanda, Cabezudo, Elena, Paiva, Bruno, Puig, Noemí, Cedena, María Teresa, de la Cruz, Javier, Mateos, María-Victoria, San Miguel, Jesús, Lahuerta, Juan José, and Bladé, Joan

Abstract

•Postransplant maintenance with lenalidomide and dexamethasone resulted in a 6-year PFS of 61.3%, with no benefit of adding ixazomib.•Discontinuation of maintenance in patients with negative MRD (2 × 10−6) at 2 years was associated with a low progression rate.

Published
2023
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41. Down-regulated expression of hsa-miR-181c in Fanconi anemia patients: implications in TNFα regulation and proliferation of hematopoietic progenitor cells

Author

Río, Paula, Agirre, Xabier, Garate, Leire, Baños, Rocío, Álvarez, Lara, San José-Enériz, Edurne, Badell, Isabel, Casado, José A., Garín, Marina, Prósper, Felipe, and Bueren, Juan A.

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-miR-181c, 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 TNFα 3′-untranslated region confirmed in silico predictions suggesting an interaction between hsa-miR-181c and TNFα mRNA. These observations were consistent with the down-regulated expression of TNFα mediated by hsa-miR-181c in cells from healthy donors and cells from FA patients. Because of the relevance of TNFα 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.

Published
2012
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42. Down-regulated expression of hsa-miR-181cin Fanconi anemia patients: implications in TNFα regulation and proliferation of hematopoietic progenitor cells

Author

Río, Paula, Agirre, Xabier, Garate, Leire, Baños, Rocío, Álvarez, Lara, San José-Enériz, Edurne, Badell, Isabel, Casado, José A., Garín, Marina, Prósper, Felipe, and Bueren, Juan A.

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-miR-181c, 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 TNFα 3′-untranslated region confirmed in silico predictions suggesting an interaction between hsa-miR-181cand TNFα mRNA. These observations were consistent with the down-regulated expression of TNFα mediated by hsa-miR-181cin cells from healthy donors and cells from FA patients. Because of the relevance of TNFα in the hematopoietic defects of FA patients, in the present study, we transfected BM cells from FA patients with hsa-miR-181cto evaluate the impact of this miRNA on their clonogenic potential. hsa-miR-181cmarkedly 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.

Published
2012
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43. Origin, functional role, and clinical impact of Fanconi anemia FANCAmutations

Author

Castella, Maria, Pujol, Roser, Callén, Elsa, Trujillo, Juan P., Casado, José A., Gille, Hans, Lach, Francis P., Auerbach, Arleen D., Schindler, Detlev, Benítez, Javier, Porto, Beatriz, Ferro, Teresa, Muñoz, Arturo, Sevilla, Julián, Madero, Luis, Cela, Elena, Beléndez, Cristina, de Heredia, Cristina Díaz, Olivé, Teresa, de Toledo, José Sánchez, Badell, Isabel, Torrent, Montserrat, Estella, Jesús, Dasí, Ángeles, Rodríguez-Villa, Antonia, Gómez, Pedro, Barbot, José, Tapia, María, Molinés, Antonio, Figuera, Ángela, Bueren, Juan A., and Surrallés, Jordi

Abstract

Fanconi anemia is characterized by congenital abnormalities, bone marrow failure, and cancer predisposition. To investigate the origin, functional role, and clinical impact of FANCAmutations, we determined a FANCAmutational spectrum with 130 pathogenic alleles. Some of these mutations were further characterized for their distribution in populations, mode of emergence, or functional consequences at cellular and clinical level. The world most frequent FANCAmutation is not the result of a mutational “hot-spot” but results from worldwide dissemination of an ancestral Indo-European mutation. We provide molecular evidence that total absence of FANCA in humans does not reduce embryonic viability, as the observed frequency of mutation carriers in the Gypsy population equals the expected by Hardy-Weinberg equilibrium. We also prove that long distance Alu-Alu recombination can cause Fanconi anemia by originating large interstitial deletions involving FANCAand 2 adjacent genes. Finally, we show that all missense mutations studied lead to an altered FANCA protein that is unable to relocate to the nucleus and activate the FA/BRCA pathway. This may explain the observed lack of correlation between type of FANCAmutation and cellular phenotype or clinical severity in terms of age of onset of hematologic disease or number of malformations.

Published
2011
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44. Origin, functional role, and clinical impact of Fanconi anemia FANCA mutations

Author

Castella, Maria, Pujol, Roser, Callén, Elsa, Trujillo, Juan P., Casado, José A., Gille, Hans, Lach, Francis P., Auerbach, Arleen D., Schindler, Detlev, Benítez, Javier, Porto, Beatriz, Ferro, Teresa, Muñoz, Arturo, Sevilla, Julián, Madero, Luis, Cela, Elena, Beléndez, Cristina, de Heredia, Cristina Díaz, Olivé, Teresa, de Toledo, José Sánchez, Badell, Isabel, Torrent, Montserrat, Estella, Jesús, Dasí, Ángeles, Rodríguez-Villa, Antonia, Gómez, Pedro, Barbot, José, Tapia, María, Molinés, Antonio, Figuera, Ángela, Bueren, Juan A., and Surrallés, Jordi

Abstract

Fanconi anemia is characterized by congenital abnormalities, bone marrow failure, and cancer predisposition. To investigate the origin, functional role, and clinical impact of FANCA mutations, we determined a FANCA mutational spectrum with 130 pathogenic alleles. Some of these mutations were further characterized for their distribution in populations, mode of emergence, or functional consequences at cellular and clinical level. The world most frequent FANCA mutation is not the result of a mutational “hot-spot” but results from worldwide dissemination of an ancestral Indo-European mutation. We provide molecular evidence that total absence of FANCA in humans does not reduce embryonic viability, as the observed frequency of mutation carriers in the Gypsy population equals the expected by Hardy-Weinberg equilibrium. We also prove that long distance Alu-Alu recombination can cause Fanconi anemia by originating large interstitial deletions involving FANCA and 2 adjacent genes. Finally, we show that all missense mutations studied lead to an altered FANCA protein that is unable to relocate to the nucleus and activate the FA/BRCA pathway. This may explain the observed lack of correlation between type of FANCA mutation and cellular phenotype or clinical severity in terms of age of onset of hematologic disease or number of malformations.

Published
2011
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45. Safety and Efficacy Profile of Asciminib As Treatment in Chronic Myeloid Leukemia Patients after Several Tyrosine-Kinase Inhibitors Failure

Author

Luna, Alejandro, Estrada, Natalia, Boque, Concepcion, Xicoy, Blanca, Giraldo, Pilar, Angona, Anna, Alvarez-Larrán, Alberto, Sanchez-Guijo, Fermin, Ramírez, María José, Alonso-Domínguez, Juan M., Mora, Elvira, Vélez, Patricia, Rosell, Ana, Araujo, Mercedes Colorado, Cuevas, Beatriz, Sagüés, Miguel, Cortes, Montserrat, Perez Encinas, Manuel, Casado Montero, Luis Felipe, Moreno Vega, Melania, Serrano, Luis, Gomez, Valle, Garcia-Hernandez, Carmen, Lakhwani Lakhwani, Sunil, Paz Coll, Antonio, de Paz, Raquel, Suarez-Varela, Sara, Fernandez-Ruiz, Andrés, Perez Lopez, Raul, Ortiz-Fernández, Almudena, Jiménez-Velasco, Antonio, and Garcia-Gutiérrez, Valentín

Abstract

Garcia-Gutiérrez: Novartis: Consultancy, Other: Travel, Accommodation, Expenses, Research Funding; Bristol-Myers Squibb: Consultancy, Other: Travel, Accommodation, Expenses, Research Funding; Pfizer: Consultancy, Other: Travel, Accommodation, Expenses, Research Funding; Incyte: Consultancy, Other: Travel, Accommodation, Expenses, Research Funding.

Published
2020
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46. Validation of the Response Speed Rule to Predict the Efficacy of a Therapeutic Regimen in Myeloma

Author

De La Puerta Rueda, Jose Enrique, Gómez Pérez, Clara, Velado Rodriguez, Concepción, Carrascosa Vallejo, Tomas, Sancho Garaizabal, Begoña, Ereño Ealo, Maria José, Pastor Ausin, Elixabete, Uriarte, Isabel, Vicente Olabarria, Iñigo, Cabrera Zubizarreta, Alberto, Ontañón Garcés, José María, Saralegui Prieto, Ibone, Olivares Salaverri, Matxalen, Barredo Santamaría, Inmaculada, Sáiz López, Alberto, Arana Berganza, Paula, Maruri Machado, Natalia, Pérez Garay, Raquel, Urrechaga Igartua, Eloisa, Etxeguren Urkixo, Ianire, Letamendi Madariaga, Garazi, Martínez Bilbao, Cristina, Amarika Ibarrondo, Itxaso, Casado Diez, Amaia, González Vallejo, Inés, Cortes Fernández, Cristina, Gainza González, Eukene, Ojanguren Bergaz, Jesus, Ibarrondo Chamorro, Paloma, Aranbarri Chamorro, Ane, Goikolea Ugarte, Javier, Bustos Martínez, Miriam, Sierra Zabala, Amaia, Aguirre Larracoechea, Urko, and Alonso Varela, Marta

Abstract

BACKGROUND

Published
2020
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47. Integration of Deep Multi-Omics Profiling Veals New Insights into the Biology of Poor-Risk Acute Myeloid Leukemia

Author

Rio-Machin, Ana, Casado-Izquierdo, Pedro, Miettinen, Juho, Bewicke-Copley, Findlay, Khan, Naeem, Demeulemeester, Jonas, Krizsán, Szilvia, Zheng, Jiexin, Middleton, Christopher, Yin, Wencheng, Grey, William, Miraki-Moud, Farideh, Matthews, Janet, Grantham, Marianne, Rouault-Pierre, Kevin, Wennerberg, Krister, Parsons, Alun, Armes, Hannah, Close, Karina EM, Di Bella, Doriana, Cavenagh, James, Freeman, Sylvie D, Van Loo, Peter, Bödör, Csaba, Porkka, Kimmo, Heckman, Caroline A, Wang, Jun, Taussig, David, Bonnet, Dominique, Cazier, Jean-Baptiste, Cutillas, Pedro, and Fitzgibbon, Jude

Abstract

Background:

Published
2020
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48. Integration of Deep Multi-Omics Profiling Veals New Insights into the Biology of Poor-Risk Acute Myeloid Leukemia

Author

Rio-Machin, Ana, Casado-Izquierdo, Pedro, Miettinen, Juho, Bewicke-Copley, Findlay, Khan, Naeem, Demeulemeester, Jonas, Krizsán, Szilvia, Zheng, Jiexin, Middleton, Christopher, Yin, Wencheng, Grey, William, Miraki-Moud, Farideh, Matthews, Janet, Grantham, Marianne, Rouault-Pierre, Kevin, Wennerberg, Krister, Parsons, Alun, Armes, Hannah, Close, Karina EM, Di Bella, Doriana, Cavenagh, James, Freeman, Sylvie D, Van Loo, Peter, Bödör, Csaba, Porkka, Kimmo, Heckman, Caroline A, Wang, Jun, Taussig, David, Bonnet, Dominique, Cazier, Jean-Baptiste, Cutillas, Pedro, and Fitzgibbon, Jude

Abstract

Wennerberg: Novartis: Research Funding; Pfizer: Honoraria. Heckman:Celgene: Research Funding; Novartis: Research Funding; Oncopeptides: Research Funding; Orion Pharma: Research Funding; Innovative Mediicines Initiative project Harmony: Research Funding.

Published
2020
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49. Randomized Phase 2 Study of Weekly Carfilzomib 70 Mg/m2 and Dexamethasone Plus/Minus Cyclophosphamide in Relapsed and/or Refractory Multiple Myeloma (RRMM) Patients (GEM-KyCyDex)

Author

Mateos, Maria-Victoria, Ocio, Enrique M., Sureda Balari, Anna, Oriol, Albert, Garcia, Esther González, Moreno, Maria José, Granell, Miquel, Escalante, Fernando, Gonzalez De La Calle, Veronica, Rosinol Dachs, Laura, Carrillo-Cruz, Estrella, Martínez-López, Joaquín, Dourdil Sahun, Maria Victoria, Gonzalez, Marta Sonia, Perez De Oteyza, Jaime, De Arriba, Felipe, Hernández, Miguel T, García Mateo, Aránzazu, Gonzalez, Ana Pilar, Rios, Rafael, Cabrera, Carmen, Bargay, Juan Jose, Rodriguez-Otero, Paula, Casado, Felipe, Casanova, Maria, Blanchard, María Jesús, Blade Creixenti, Joan, Lahuerta, Juan Jose, and San-Miguel, Jesus F.

Abstract

Mateos: Abbvie/Genentech: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Pfizer: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Regeneron: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Janssen-Cilag: Consultancy, Honoraria; PharmaMar-Zeltia: Consultancy; Sanofi: Honoraria, Membership on an entity's Board of Directors or advisory committees; Oncopeptides: Honoraria, Membership on an entity's Board of Directors or advisory committees; Roche: Honoraria, Membership on an entity's Board of Directors or advisory committees; Seattle Genetics: Honoraria, Membership on an entity's Board of Directors or advisory committees; GlaxoSmithKline: Consultancy; Takeda: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Amgen: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Janssen: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Adaptive Biotechnologies: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees. Ocio:Janssen: Consultancy, Honoraria, Speakers Bureau; Celgene: Consultancy, Honoraria; Asofarma: Honoraria; Sanofi: Consultancy, Honoraria; Amgen: Consultancy, Honoraria; Takeda: Honoraria; GSK: Consultancy; MDS: Honoraria; Secura-Bio: Consultancy; Oncopeptides: Consultancy. Sureda Balari:Novartis: Consultancy, Honoraria; Janssen: Consultancy, Honoraria; Roche: Honoraria; Takeda: Consultancy, Honoraria, Speakers Bureau; Sanofi: Consultancy, Honoraria; Merck Sharpe and Dohme: Consultancy, Honoraria, Speakers Bureau; Celgene/Bristol-Myers Squibb: Consultancy, Honoraria; BMS: Speakers Bureau; Incyte: Consultancy; Celgene: Consultancy, Honoraria; Gilead/Kite: Consultancy, Honoraria. Oriol:Celgene/Bristol-Myers Squibb: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Amgen: Consultancy, Speakers Bureau; Janssen: Consultancy; Sanofi: Consultancy, Membership on an entity's Board of Directors or advisory committees; GlaxoSmithKline: Membership on an entity's Board of Directors or advisory committees. Rosinol Dachs:Janssen: Honoraria; Celgene: Honoraria; Amgen: Honoraria; Takeda: Honoraria; Sanofi: Honoraria. Blade Creixenti:Takeda: Membership on an entity's Board of Directors or advisory committees; Oncopeptides: Membership on an entity's Board of Directors or advisory committees; Janssen: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Amgen: Membership on an entity's Board of Directors or advisory committees. San-Miguel:Amgen, BMS, Celgene, Janssen, MSD, Novartis, Takeda, Sanofi, Roche, Abbvie, GlaxoSmithKline and Karyopharm: Consultancy, Membership on an entity's Board of Directors or advisory committees.

Published
2020
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50. Validation of the Response Speed Rule to Predict the Efficacy of a Therapeutic Regimen in Myeloma

Author

De La Puerta Rueda, Jose Enrique, Gómez Pérez, Clara, Velado Rodriguez, Concepción, Carrascosa Vallejo, Tomas, Sancho Garaizabal, Begoña, Ereño Ealo, Maria José, Pastor Ausin, Elixabete, Uriarte, Isabel, Vicente Olabarria, Iñigo, Cabrera Zubizarreta, Alberto, Ontañón Garcés, José María, Saralegui Prieto, Ibone, Olivares Salaverri, Matxalen, Barredo Santamaría, Inmaculada, Sáiz López, Alberto, Arana Berganza, Paula, Maruri Machado, Natalia, Pérez Garay, Raquel, Urrechaga Igartua, Eloisa, Etxeguren Urkixo, Ianire, Letamendi Madariaga, Garazi, Martínez Bilbao, Cristina, Amarika Ibarrondo, Itxaso, Casado Diez, Amaia, González Vallejo, Inés, Cortes Fernández, Cristina, Gainza González, Eukene, Ojanguren Bergaz, Jesus, Ibarrondo Chamorro, Paloma, Aranbarri Chamorro, Ane, Goikolea Ugarte, Javier, Bustos Martínez, Miriam, Sierra Zabala, Amaia, Aguirre Larracoechea, Urko, and Alonso Varela, Marta

Abstract

No relevant conflicts of interest to declare.

Published
2020
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