Giraldo, P. (P.)
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- Insertion (22;9)(q11;q34q21) in a patient with chronic myeloid leukemia characterized by fluorescence in situ hybridization(Elsevier, 2001) Gomez, E. (Emilio); Ferreira, C. (C.); Giraldo, P. (P.); Novo-Villaverde, F. J. (Francisco Javier); Lahortiga, I. (Idoya); García-Delgado, M. (Marina); Larrayoz, M.J. (María J.); Calasanz-Abinzano, M.J. (Maria Jose); Odero, M.D. (Maria Dolores); Martin-Subero, J.I. (Jose Ignacio)An unusual cytogenetic rearrangement, described as ins(22;9)(q11;q34q21), was detected in a 49-year-old male patient diagnosed with chronic myeloid leukemia (CML). Reverse transcriptase polymerase chain reaction (RT-PCR) revealed a b3a2 fusion transcript. In order to confirm the cytogenetic findings and fully characterize the inverted insertion, we performed fluorescence in situ hybridization (FISH) assays using locus-specific and whole chromosome painting probes. Our FISH analysis showed the presence of the BCR/ABL fusion gene, verified the insertion and determined that the breakpoint on chromosome 22 where the insertion took place was located proximal to the BCR gene and distal to the TUPLE1 gene on 22q11.
- Immune status of high-risk smoldering multiple myeloma patients and its therapeutic modulation under LenDex: a longitudinal analysis(American Society of Hematology, 2016) Perez-Simon, J.A. (José Antonio); Hernández-Martín, J. (J.); Bladé, J. (Joan); Vidriales, M.B. (María Belén); Mateos, M.V. (María Victoria); Arriba, F. (Felipe) de; Sanchez-Abarca, L.I. (Luis Ignacio); Esteves, G. (Graça); Hernandez, M.T. (Miguel Teodoro); Rosiñol, L. (Laura); Puig, N. (Noemí); Lahuerta, J.J. (Juan José); Giraldo, P. (P.); Teruel, A.I. (Ana Isabel); Paiva, B. (Bruno); Oriol, A. (Albert); Rubia, J. (Javier) de la; Corchete, L.A. (Luis A.); Prosper-Cardoso, F. (Felipe); Bargay, J. (Joan); Lopez-Corral, L. (Lucia); San-Miguel, J.F. (Jesús F.)Persistence of chemoresistant minimal residual disease (MRD) plasma cells (PCs) is associated with inferior survival in multiple myeloma (MM). Thus, characterization of the minor MRD subclone may represent a unique model to understand chemoresistance, but to our knowledge, the phenotypic and genetic features of the MRD subclone have never been investigated. Here, we compared the antigenic profile of MRD vs diagnostic clonal PCs in 40 elderly MM patients enrolled in the GEM2010MAS65 study and showed that the MRD subclone is enriched in cells overexpressing integrins (CD11a/CD11c/CD29/CD49d/CD49e), chemokine receptors (CXCR4), and adhesion molecules (CD44/CD54). Genetic profiling of MRD vs diagnostic PCs was performed in 12 patients; 3 of them showed identical copy number alterations (CNAs), in another 3 cases, MRD clonal PCs displayed all genetic alterations detected at diagnosis plus additional CNAs that emerged at the MRD stage, whereas in the remaining 6 patients, there were CNAs present at diagnosis that were undetectable in MRD clonal PCs, but also a selected number of genetic alterations that became apparent only at the MRD stage. The MRD subclone showed significant downregulation of genes related to protein processing in endoplasmic reticulum, as well as novel deregulated genes such as ALCAM that is prognostically relevant in MM and may identify chemoresistant PCs in vitro. Altogether, our results suggest that therapy-induced clonal selection could be already present at the MRD stage, where chemoresistant PCs show a singular phenotypic signature that may result from the persistence of clones with different genetic and gene expression profiles. This trial was registered at www.clinicaltrials.gov as #NCT01237249.
- NIN, a gene encoding a CEP110-like centrosomal protein, is fused to PDGFRB in a patient with a t(5;14)(q33;q24) and an imatinib-responsive myeloproliferative disorder(American Association for Cancer Research, 2004) Baxter, E.J. (E.J.); Cross, N.C.P. (Nicholas C.P.); Roman, J.P. (José P.); Giraldo, P. (P.); Novo-Villaverde, F. J. (Francisco Javier); Lahortiga, I. (Idoya); Vizmanos-Pérez, J.L. (José Luis); Larrayoz, M.J. (María J.); Calasanz-Abinzano, M.J. (Maria Jose); Odero, M.D. (Maria Dolores)We describe a new PDGFRB fusion associated with a t(5;14)(q33;q24) in a patient with a longstanding chronic myeloproliferative disorder with eosinophilia. After confirmation of PDGFRB involvement and definition of the chromosome 14 breakpoint by fluorescence in situ hybridization, candidate partner genes were selected on the basis of the presence of predicted oligomerization domains believed to be an essential feature of tyrosine kinase fusion proteins. We demonstrate that the t(5;14) fuses PDGFRB to NIN, a gene encoding a centrosomal protein with CEP110-like function. After treatment with imatinib, the patient achieved hematological and cytogenetical remission, but NIN-PDGFRB mRNA remained detectable by reverse transcription-PCR.
- Combined vaccination with idiotype-pulsed allogeneic dendritic cells and soluble protein idiotype for multiple myeloma patients relapsing after reduced-intensity conditioning allogeneic stem cell transplantation.(Informa Healthcare, 2006) Perez-Simon, J.A. (José Antonio); Orfao, A. (Alberto); Lopez-Diaz-de-Cerio, A. (Ascensión); Garcia-Montero, A. (A.); Rodriguez-Caballero, A. (Arancha); Almeida, J. (J.); Inoges, S. (Susana); Giraldo, P. (P.); Bendandi, M. (Maurizio); Zabalegui, N. (Natalia); San-Miguel, J.F. (Jesús F.); Rodriguez-Calvillo, M. (Mercedes)BACKGROUND AND OBJECTIVE: To combine the use of idiotype-pulsed allogeneic dendritic cells (alloDC) and soluble protein Id conjugated with KLH (Id-KLH) in a vaccine strategy for multiple myeloma (MM). DESIGN AND METHODS: Four MM patients received the combined vaccine after having experienced disease relapse/progression following reduced intensity conditioning (RIC) allogeneic stem cell transplantation (alloSCT) and failure to rescue therapy with donor lymphocyte infusion or chemotherapy (CHT). RESULTS: Vaccination was well tolerated and induced an anti-KLH antibody response in all 4 patients as well as substantial cell proliferation. In contrast, no case showed similar effects against either tumor-specific Id or irrelevant isotype control immunoglobulins (Ig). In turn, vaccination was associated with modulation of biological responses linked to both inflammatory and T-cell activation, with secretion of effector Th1 cytokines. In particular, an important increase in the spontaneous ex vivo secretion of TNFalpha, IL-6 and IFNgamma as well as IL-2 and IL-10 was frequently observed prior to the fourth vaccination. Moreover, in vitro stimulation with Id-KLH and Id-KLH plus alloDC, but not with alloDC alone was associated with an enhanced number of TNF-alpha+ T-cells and an increased secretion of IFNgamma and IL-2 before the third and fourth vaccination. From a clinical standpoint, 2 patients had a transient response and 1 has stable disease after stopping vaccination, while 3 of them ultimately progressed. INTERPRETATION AND CONCLUSIONS: The results show for the first time that the use of Id-pulsed alloDC following RIC alloSCT is safe and feasible. However, crucial strategy improvements are warranted to possibly achieve clinical benefit.
- p53 Aberrations do not predict individual response to fludarabine in patients with B-cell chronic lymphocytic leukaemia in advanced stages Rai III/IV(Blackwell Publishing, 2005) Valgañon, M. (Mikel); Rubio-Martinez, A. (Araceli); Rubio-Felix, D. (Daniel); Giraldo, P. (P.); Larrayoz, M.J. (María J.); Calasanz-Abinzano, M.J. (Maria Jose); Odero, M.D. (Maria Dolores); Aguirre-Ena, X. (Xabier)Abnormalities of p53 have been associated with short survival and non-response to therapy in chronic lymphocytic leukaemia (CLL). We have evaluated the rate of response to fludarabine as first-line therapy in 54 patients with advanced stage CLL, analysing the cytogenetic profile, aberrations in p53, including the methylation status of its promoter, and the immunoglobulin heavy-chain variable-region (IGVH) mutation status. According to the advanced stage of the disease in this series, 75% of patients presented genetic aberrations associated with poor prognosis: del(17p) and/or del(11q), and no-mutated IGVH genes. Ten patients (18.5%) had methylation in the promoter region of p53. Eighty-three per cent of patients treated achieved a response, with a high rate of complete remission (47.6%). Although we found a significant correlation between failures and the presence of p53 aberrations (P = 0.0065), either with methylation (P = 0.018) or deletion (P = 0.015), 64% of the patients with aberrations in this gene responded to treatment (11/17), suggesting that fludarabine induces high remission rates, even in these patients. This is the first time that the significance of p53 promoter methylation status is described in this pathology, and our data support that this epigenetic phenomenon could be involved in the pathogenesis and clinical evolution of CLL.