Ormazábal, C. (Cristina)
- Publications
- item.page.relationships.isContributorAdvisorOfPublication
- item.page.relationships.isContributorOfPublication
25 results
Search Results
Now showing 1 - 10 of 25
- Estudio mediante dHPLC del perfil mutacional de los genes SYK y ZAP70 en pacientes con Síndromes Mieloproliferativos Crónicos BCR-ABL negativos(Editorial Doyma, 2007-10-25) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
- FISH and mutational screening of the ABL, SYK and JAK tirosine kinase family genes in BCR-ABL1 negative and V617FJAK2 negative chronic myeloproliferative neoplasms (CMPNs)(Ferrata-Storti Foundation, 2009-06-04) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
- ¿Existen más mutaciones en JAK2 en pacientes con Síndromes Mieloproliferativos Crónicos BCR-ABL negativos?(Editorial Doyma, 2007-10-25) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
- Receptor of Activated Protein C Promotes Metastasis and Correlates with Clinical Outcome in Lung Adenocarcinoma(American Thoracic Society, 2012) Pajares, M.J. (María José); Ormazábal, C. (Cristina); Agorreta, J. (Jackeline); Hermida, J. (José); Martinez-Canarias, S. (Susana); Luis-Ravelo, D. (Diego); Perurena, N. (Naiara); Rivas, J. (Javier) de las; Montuenga-Badia, L.M. (Luis M.); Molina, E. (Eva); Valencia, K. (Karmele); Wistuba, I.I. (Ignacio I.); Anton, I. (Iker); Lecanda, F. (Fernando); Segura, V. (Víctor); Zandueta, C. (Carolina)RATIONALE: Efficient metastasis requires survival and adaptation of tumor cells to stringent conditions imposed by the extracellular milieu. Identification of critical survival signaling pathways in tumor cells might unveil novel targets relevant in disease progression. OBJECTIVES: To investigate the contribution of activated protein C (APC) and its receptor (EPCR) in animal models of lung cancer metastasis and in patients with lung adenocarcinoma. METHODS: Signaling pathway triggered by APC/EPCR and its relevance in apoptosis was studied in vitro. Functional significance was assessed by silencing and blocking antibodies in several in vivo models of lung cancer metastasis. We examined EPCR levels using a microarray dataset of 107 patients. Immunohistochemical analysis was performed in an independent cohort of 295 patients with lung adenocarcinoma. MEASUREMENTS AND MAIN RESULTS: The effects of APC binding to EPCR rapidly triggered Akt and ERK signaling pathways, leading to attenuated in vitro apoptosis. In vivo, silencing of EPCR expression or blocking APC/EPCR interaction reduced homing resulting in impaired prometastatic activity. Moreover, overexpression of EPCR induced an increase metastatic activity to target organs. Analysis of clinical samples showed a robust association between high EPCR levels and poor prognosis particularly in stage I patients. CONCLUSIONS: EPCR and its ligand APC promote cell survival that contributes to tumor cell endurance to stress favoring prometastatic activity of lung adenocarcinoma (ADC). EPCR/APC is a novel target of relevance in the clinical outcome of early-stage lung cancer.
- Análisis de la expresión diferencial de distintos transcritos de PDGFRA en neoplasias hematológicas con eosinofilia(Editorial Doyma, 2009-11-12) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
- Absence of rearrangements or activating mutations in the RTK III and IV family genes in BCR-ABL1 negative and V617FJAK2 negative chronic myeloproliferative neoplasms (CMPNs)(Ferrata-Storti Foundation, 2009-06-04) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
- FISH screening of Receptor- and Cytoplasmatic Tyrosine Kinase genes in BCR-ABL1 negative and JAK2V617F negative chronic myeloproliferative neoplasms (CMPNs)(Springer, 2009-07-04) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)
- A new potential oncogenic mutation in the FERM domain of JAK2 in BCR-ABL1 negative and V617F negative chronic myeloproliferative neoplasms (CMPNs) revealed by a comprehensive screening of 17 tyrosine kinase coding genes(Elsevier Inc., 2010-05-01) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Aranaz-Oroz, P. (Paula); Calasanz-Abinzano, M.J. (Maria Jose)BCR/ABL1-negative chronic myeloproliferative neoplasms (CMPNs) are a heterogeneous group of clonal hematological malignancies. Over recent years, some genetic events in tyrosine kinase (TK) genes have been described as causal events of these diseases. To identify new genetic aberrations underlying these diseases, we used denaturing high performance liquid chromatography and fluorescence in situ hybridization (FISH) to analyze 17 genes from two receptor-TK families (III and IV) and from three cytoplasmic-TK families (Syk, Abl, and Jak) on samples from 44 BCR/ABL1-negative and JAK2(V617F)-negative CMPN patients with different clinical phenotypes. Although screening by FISH did not reveal novel chromosomal aberrations, several sequence changes were detected. None of them were frequent events, but we identified a new potential activating mutation in the FERM domain of JAK2(R340Q). None of the germline JAK2(V617F) single-nucleotide polymorphisms detected differed in distribution between patients and control subjects. In summary, data presented here show that these genes are not frequently mutated or rearranged in CMPNs, suggesting that molecular events causing these disorders must be located in other genes.
- JAK2 V617F mutation in classic chronic myeloproliferative diseases: a report on a series of 349 patients(Nature Publishing Group, 2006-03-01) Ormazábal, C. (Cristina); Cross, N.C.P. (Nicholas C.P.); Vizmanos-Pérez, J.L. (José Luis); Larrayoz, M.J. (María J.); Calasanz-Abinzano, M.J. (Maria Jose)
- Incidencia de la mutación V617F de JAK2 en una serie de 1076 pacientes con neoplasias hematológicas de origen mieloide(Editorial Doyma, 2007-10-25) Ormazábal, C. (Cristina); Hurtado, C. (Cristina); Novo-Villaverde, F. J. (Francisco Javier); Vizmanos-Pérez, J.L. (José Luis); García-Delgado, M. (Marina); Erquiaga, I. (Ignacio); Calasanz-Abinzano, M.J. (Maria Jose)
- «
- 1 (current)
- 2
- 3
- »