Publicaciones en las que colabora con María José Larráyoz Ilundáin (19)

2024

  1. Epigenetic-based differentiation therapy for Acute Myeloid Leukemia

    Nature Communications, Vol. 15, Núm. 1

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