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12 results on '"Vela-Martín, Laura"'

3. Comprehensive characterization of a novel, oncogenic and targetable SEPTIN6::ABL2 fusion in T-ALL

Author

Lahera, Antonio, Vela-Martín, Laura, López-Nieva, Pilar, Salgado, Rocío N, Rodriguez Perales, Sandra, Raul, Torres-Ruiz, López-Lorenzo, José L, Cornago, Javier, Llamas, Pilar, Fernandez-Navarro, Pablo L, Sánchez-Domínguez, Rebeca, Segovia, José C, Sastre, Isabel, Cobos-Fernández, María Á, Menéndez, Pablo, Santos, Javier, Fernández-Piqueras, José, Villa-Morales, María, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Fundación Ramón Areces, Comunidad de Madrid (España), Asociación Española Contra el Cáncer, Instituto de Salud Carlos III, Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF), Instituto de Investigación Sanitaria de la Fundación Jiménez Díaz, Banco Santander, Fundación Asisa, and Harvard University (Estados Unidos)

Abstract

Sí

Published
2023

4. SOCS3 deregulation contributes to aberrant activation of the JAK/STAT pathway in precursor T-cell neoplasms

Author

Ministerio de Economía y Competitividad (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Fundación Ramón Areces, Comunidad de Madrid, Asociación Española Contra el Cáncer, Banco Santander, Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Lahera, Antonio, López-Nieva, Pilar, Alarcón, Hernán, Marín-Rubio, José L., Cobos-Fernández, M. A., Fernández-Navarro, Pablo, Fernández, Agustín F., Vela-Martín, Laura, Sastre, Isabel, Ruiz-García, Sara, Llamas, Pilar, López-Lorenzo, José L., Cornago, Javier, Santos, Javier, Fernández-Piqueras, José, Villa-Morales, María, Ministerio de Economía y Competitividad (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Fundación Ramón Areces, Comunidad de Madrid, Asociación Española Contra el Cáncer, Banco Santander, Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Lahera, Antonio, López-Nieva, Pilar, Alarcón, Hernán, Marín-Rubio, José L., Cobos-Fernández, M. A., Fernández-Navarro, Pablo, Fernández, Agustín F., Vela-Martín, Laura, Sastre, Isabel, Ruiz-García, Sara, Llamas, Pilar, López-Lorenzo, José L., Cornago, Javier, Santos, Javier, Fernández-Piqueras, José, and Villa-Morales, María

Abstract

Despite the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway being frequently altered in T-ALL/LBL, no specific therapy has been approved for T-ALL/LBL patients with constitutive signalling by JAK/STAT, so there is an urgent need to identify pathway members that may be potential therapeutic targets. In the present study, we searched for JAK/STAT pathway members potentially modulated through aberrant methylation and identified SOCS3 hypermethylation as a recurrent event in T-ALL/LBL. Additionally, we explored the implications of SOCS3 deregulation in T-ALL/LBL and demonstrated that SOCS3 counteracts the constitutive activation of the JAK/STAT pathway through different molecular mechanisms. Therefore, SOCS3 emerges as a potential therapeutic target in T-ALL/LBL.

Published
2023

5. Comprehensive characterization of a novel, oncogenic and targetable SEPTIN6::ABL2 fusion in T-ALL

Author

Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Fundación Ramón Areces, European Commission, Comunidad de Madrid, Asociación Española Contra el Cáncer, Instituto de Salud Carlos III, Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Banco Santander, Lahera, Antonio, Vela-Martín, Laura, López-Nieva, P., Salgado, Rocío N., Rodríguez-Perales, Sandra, Torres-Ruiz, Raúl, López-Lorenzo, Jose L, Cornago, Javier, Llamas, Pilar, Fernández-Navarro, Pablo, Sánchez-Domínguez, Rebeca, Segovia, Jose C., Sastre, Isabel, Cobos-Fernández, María, Menéndez, Pablo, Santos, Javier, Fernández-Piqueras, José, Villa-Morales, María, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Fundación Ramón Areces, European Commission, Comunidad de Madrid, Asociación Española Contra el Cáncer, Instituto de Salud Carlos III, Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Banco Santander, Lahera, Antonio, Vela-Martín, Laura, López-Nieva, P., Salgado, Rocío N., Rodríguez-Perales, Sandra, Torres-Ruiz, Raúl, López-Lorenzo, Jose L, Cornago, Javier, Llamas, Pilar, Fernández-Navarro, Pablo, Sánchez-Domínguez, Rebeca, Segovia, Jose C., Sastre, Isabel, Cobos-Fernández, María, Menéndez, Pablo, Santos, Javier, Fernández-Piqueras, José, and Villa-Morales, María

Abstract

descripción no proporcionada por scopus

Published
2023

7. SOCS3 deregulation contributes to aberrant activation of the JAK/STAT pathway in precursor T‐cell neoplasms

Author

Lahera, Antonio, primary, López‐Nieva, Pilar, additional, Alarcón, Hernán, additional, Marín‐Rubio, José L., additional, Cobos‐Fernández, María Á., additional, Fernández‐Navarro, Pablo, additional, Fernández, Agustín F., additional, Vela‐Martín, Laura, additional, Sastre, Isabel, additional, Ruiz‐García, Sara, additional, Llamas, Pilar, additional, López‐Lorenzo, José L., additional, Cornago, Javier, additional, Santos, Javier, additional, Fernández‐Piqueras, José, additional, and Villa‐Morales, María, additional

Published
2023
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8. A Dual Role for FADD in Human Precursor T-Cell Neoplasms

Author

Marín-Rubio, José Luis, primary, Vela-Martín, Laura, additional, Gudgeon, Jack, additional, Pérez-Gómez, Eduardo, additional, Sidgwick, Frances R., additional, Trost, Matthias, additional, Cunningham, Debbie L., additional, Santos, Javier, additional, Fernández-Piqueras, José, additional, and Villa-Morales, María, additional

Published
2022
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10. FADD in cancer: Mechanisms of altered expression and function, and clinical implications

Author

Ministerio de Economía y Competitividad (España), Fundación Ramón Areces, Comunidad de Madrid, Asociación Española Contra el Cáncer, Instituto de Salud Carlos III, Universidad Autónoma de Madrid, Martín-Rubio, José L., Vela-Martín, Laura, Fernández-Piqueras, José, Villa-Morales, María, Ministerio de Economía y Competitividad (España), Fundación Ramón Areces, Comunidad de Madrid, Asociación Española Contra el Cáncer, Instituto de Salud Carlos III, Universidad Autónoma de Madrid, Martín-Rubio, José L., Vela-Martín, Laura, Fernández-Piqueras, José, and Villa-Morales, María

Abstract

FADD was initially described as an adaptor molecule for death receptor-mediated apoptosis, but subsequently it has been implicated in nonapoptotic cellular processes such as proliferation and cell cycle control. During the last decade, FADD has been shown to play a pivotal role in most of the signalosome complexes, such as the necroptosome and the inflammasome. Interestingly, various mechanisms involved in regulating FADD functions have been identified, essentially posttranslational modifications and secretion. All these aspects have been thoroughly addressed in previous reviews. However, FADD implication in cancer is complex, due to pleiotropic effects. It has been reported either as anti- or protumorigenic, depending on the cell type. Regulation of FADD expression in cancer is a complex issue since both overexpression and downregulation have been reported, but the mechanisms underlying such alterations have not been fully unveiled. Posttranslational modifications also constitute a relevant mechanism controlling FADD levels and functions in tumor cells. In this review, we aim to provide detailed, updated information on alterations leading to changes in FADD expression and function in cancer. The participation of FADD in various biological processes is recapitulated, with a mention of interesting novel functions recently proposed for FADD, such as regulation of gene expression and control of metabolic pathways. Finally, we gather all the available evidence regarding the clinical implications of FADD alterations in cancer, especially as it has been proposed as a potential biomarker with prognostic value.

Published
2019

11. The JAK3 Q988P mutation reveals oncogenic potential and resistance to ruxolitinib.

Author

Lahera A, Vela-Martín L, Fernández-Navarro P, Llamas P, López-Lorenzo JL, Cornago J, Santos J, Fernández-Piqueras J, and Villa-Morales M

Subjects
Humans, Signal Transduction, STAT Transcription Factors genetics, STAT Transcription Factors metabolism, STAT Transcription Factors pharmacology, Mutation, Recurrence, Janus Kinase 3 genetics, Janus Kinases genetics, Janus Kinases metabolism, Janus Kinases pharmacology, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma genetics
Abstract

T-cell acute lymphoblastic leukemia (T-ALL) arises from the malignant transformation of T-cell progenitors at various differentiation stages. Given that patients who relapse have a dismal prognosis, there is an urgent need to identify the molecular alterations that are present in such patients and promote leukemogenesis to implement personalized therapies with higher efficacy and fewer adverse effects. In the present manuscript, we identified the JAK3 Q988P mutation in a T-ALL patient who did not achieve a durable response after the conventional treatment and whose tumor cells at relapse presented constitutive activation of the JAK/STAT pathway. Although JAK3 Q988P has been previously identified in T-ALL patients from different studies, the functional consequences exerted by this mutation remain unexplored. Through the combination of different hematopoietic cellular models, we functionally characterize JAK3 Q988P as an oncogenic mutation that contributes to leukemogenesis. Notably, JAK3 Q988P not only promotes constitutive activation of the JAK/STAT pathway in the absence of cytokines and growth factors, as is the case for other JAK3 mutations that have been functionally characterized as oncogenic, but also functions independently of JAK1 and IL2RG, resulting in high oncogenic potential as well as resistance to ruxolitinib. Our results indicate that ruxolitinib may not be efficient for future patients bearing the JAK3 Q988P mutation who instead may obtain greater benefits from treatments involving other pharmacological inhibitors such as tofacitinib., (© 2023 The Authors. Molecular Carcinogenesis published by Wiley Periodicals LLC.)

Published
2024
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12. Comprehensive characterization of a novel, oncogenic and targetable SEPTIN6::ABL2 fusion in T-ALL.

Author

Lahera A, Vela-Martín L, López-Nieva P, Salgado RN, Rodríguez-Perales S, Torres-Ruiz R, López-Lorenzo JL, Cornago J, Llamas P, Fernández-Navarro P, Sánchez-Domínguez R, Segovia JC, Sastre I, Cobos-Fernández MÁ, Menéndez P, Santos J, Fernández-Piqueras J, and Villa-Morales M

Subjects
Humans, DNA-Binding Proteins, Protein-Tyrosine Kinases, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Leukemia-Lymphoma, Adult T-Cell
Published
2023
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