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Human tumor-associated antigen prame overexpression is associated with chronic myeloid leukemia progression

D D Carvalho R Proto-Siqueira; J M G Leroy; W O Pereira; A E Bueno-da-Silva; J F Jacysyn; M A Zanichelli; D Camanho; M D Collassanti; N Hamerschlak; M A Zago; F A Castro; João Gustavo Pessini Amarante-Mendes; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)

Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006

São Paulo 2006

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  • Título:
    Human tumor-associated antigen prame overexpression is associated with chronic myeloid leukemia progression
  • Autor: D D Carvalho
  • R Proto-Siqueira; J M G Leroy; W O Pereira; A E Bueno-da-Silva; J F Jacysyn; M A Zanichelli; D Camanho; M D Collassanti; N Hamerschlak; M A Zago; F A Castro; João Gustavo Pessini Amarante-Mendes; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)
  • Assuntos: IMUNOLOGIA
  • É parte de: Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006
  • Notas: Disponível em CD-ROM
  • Descrição: Introduction and Aims: Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by clonal expansion of neoplastic hematopoietic stem cell, the neogene Bcr-Abl is a hallmark of CML. PRAME (Preferentially Expressed Antigen in Melanoma) was first described as an antigen in human melanoma, which triggers autologous cytotoxic T cell-mediated immune responses. The correlation between the bcr-abl and prame expression has previously been suggested but this association is still unclear. Our goals were to determine the possible correlation among prame expression, Bcr-Abl levels, CML progression, and response to imatinib (Gleevec ® ). Methods and Results: prame expression was evaluated in many cell lines, such as HL-60, HL-60.BcrAbl, HeLa, HeLa.BcrAbl, Jurkat, Jurkat.BcrAbl, K562, KBM5, KBM7, KCL22, LAMA-84, SKW.64, SKW.BcrAbl, THP1, and THP1.BcrAbl (with or without imatinib) and 22 CML patients in different phases and in cytogenetic remission post-imatinib by real-time RT-PCR. We found a correlation between bcr-abl and prame in HL-60 X HL-60.BcrAbl in which prame expression was 48-times higher in HL-60.Bcr-Abl. Moreover, we did not detect any association between imatinib treatment and prame expression, which support that this is independent of the Bcr-Abl tyrosine kinase activity. On the other hand, a higher prame expression was related to disease progression. This gene expression was 8-times and 29-times higher in
    accelerated and blastic phase than in chronic phase, respectively. Prame levels were lower in post-imatinib cytogenetic remission patients when comparing to refractory patients. Conclusion: Tyrosine kinase-independent prame expression and its correlation with disease progression suggest that PRAME might be involved in Bcr-Abl mediated leukemogenesis. Besides, prame was recently described as a dominant repressor of retinoic acid receptor (RAR). Signaling through RAR induce growth arrest, differentiation, and apoptosis in many cell types. Taken these data together, new treatments can be developed, aiming to inhibit the function or expression of prame, for the most delayed phase, in imatinib-refractory patients.
  • Editor: São Paulo
  • Data de criação/publicação: 2006
  • Formato: res. TU.025.
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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