Publications dans lesquelles il/elle collabore avec María José Larráyoz Ilundáin (18)

2023

  1. Preclinical models for prediction of immunotherapy outcomes and immune evasion mechanisms in genetically heterogeneous multiple myeloma

    Nature Medicine, Vol. 29, Núm. 3, pp. 632-645

2021

  1. Endogenous retroelement activation by epigenetic therapy reverses the warburg effect and elicits mitochondrial-mediated cancer cell death

    Cancer Discovery, Vol. 11, Núm. 5, pp. 1268-1285

2019

  1. Epigenomic profiling of myelofibrosis reveals widespread DNA methylation changes in enhancer elements and ZFP36L1 as a potential tumor suppressor gene that is epigenetically regulated

    Haematologica, Vol. 104, Núm. 8, pp. 1572-1579

2015

  1. Correlation of myelodysplastic syndromes with i(17)(q10) and TP53 and SETBP1 mutations

    British Journal of Haematology

2013

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

    Haematologica, Vol. 98, Núm. 9, pp. 1414-1420

2012

  1. Mutation patterns of 16 genes in primary and secondary acute myeloid leukemia (AML) with normal cytogenetics

    PLoS ONE, Vol. 7, Núm. 8

2005

  1. Coexistence of different clonal populations harboring the b3a2 (p210) and e1a2 (p190) BCR-ABL1 fusion transcripts in chronic myelogenous leukemia resistant to imatinib

    Cancer Genetics and Cytogenetics, Vol. 160, Núm. 1, pp. 22-26

  2. Erratum: NUP98 is fused to HOXA9 in a variant complex t(7;11;13;17) in a patient with AML-M2 (Cancer Genetics and Cytogenetics (2005) 157 (151-6))

    Cancer Genetics and Cytogenetics

  3. NUP98 is fused to HOXA9 in a variant complex t(7;11;13;17) in a patient with AML-M2

    Cancer Genetics and Cytogenetics, Vol. 157, Núm. 2, pp. 151-156

  4. p53 Aberrations do not predict individual to response to fludarabine in patients with B-cell chronic lymphocytic leukaemia in advanced stages Rai III/IV

    British Journal of Haematology, Vol. 129, Núm. 1, pp. 53-59

2004

  1. Cryptic ins(2;11) with clonal evolution showing amplification of 11q23-q25 either on hsr(11) or on dmin, in a patient with AML-M2 [4]

    Leukemia

  2. Molecular characterization of a t(1;3)(p36;q21) in a patient with MDS. MEL1 is widely expressed in normal tissues, including bone marrow, and it is not overexpressed in the t(1;3) cells

    Oncogene, Vol. 23, Núm. 1, pp. 311-316

  3. Molecular heterogeneity in AML/MDS patients with 3q21q26 rearrangements

    Genes Chromosomes and Cancer, Vol. 40, Núm. 3, pp. 179-189

2003

  1. Lack of Bcr-Abl point mutations in chronic myeloid leukemia patients in chronic phase before imatinib treatment is not predictive of response

    Haematologica, Vol. 88, Núm. 12, pp. 1425-1426

  2. Methylation of CpG dinucleotides and/or CCWGG motifs at the promoter of TP53 correlates with decreased gene expression in a subset of acute lymphoblastic leukemia patients

    Oncogene, Vol. 22, Núm. 7, pp. 1070-1072

  3. 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)

    Cancer Research, Vol. 63, Núm. 12, pp. 3079-3083

  4. TP53 Is Frequently Altered by Methylation, Mutation, and/or Deletion in Acute Lymphoblastic Leukaemia

    Molecular Carcinogenesis, Vol. 38, Núm. 4, pp. 201-208

2002

  1. Exon concatenation to increase the efficiency of mutation screening by DGGE

    BioTechniques, Vol. 32, Núm. 5, pp. 1064-1070