Mantle cell lymphoma harboring Burkitt's-like translocations presents differential expression of aurora kinase genes compared with others 8q abnormalities

Autor(es)

de Oliveira, Fabio Morato ^[1] ; Nunes Rodrigues-Alves, Ana Paula ^[1] ; Lucena-Araujo, Antonio Roberto ^[1] ; Silva, Ferdinando de Paula ^[1] ; da Silva, Fernanda Borges ^[1] ; Falcao, Roberto Passetto ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: MEDICAL ONCOLOGY; v. 31, n. 5 MAY 2014.
• Citações Web of Science: 0

Resumo

We compared the levels of AURKA and AURKB in 24 (mantle cell lymphoma) MCL patients harboring 8q abnormalities and its relationship with MYCC gene status. Two distinct subgroups were observed, in terms of MYCC expression. Except for the patients with Burkitt'slike translocation, none of the patients harboring 8q abnormalities, including balanced translocations or duplications of MYCC band, identified both by G-banding and SKY, showed differential expression levels of MYCC. These previous findings also reflected in the differential expression of AURKA and AURKB genes. We found that AURKA and AURKB mRNA were expressed at significantly higher levels in MCL patients harboring Burkitt'slike translocation, when compared to patients with 8q rearrangements. The high expression of aurora kinase genes is reported to be associated with some parameters of clinical oncologic aggressiveness, such as high histological grade, invasion and increased rates of metastasis in several types of cancers. It is possible that in MCL patients expressing abnormal levels of MYCC together with a high expression of AURKA might offer some resistant to the conventional therapy purposes. Thus, aurora kinase inhibitors may also be considered for this specific subgroup on MCL, whose aggressive clinical course resembles high-grade lymphoma. (AU)

• Processo FAPESP: 11/01647-2 - Avaliação da instabilidade genômica, por meio da organização tridimensional nuclear de telômeros, na sindrome mielodisplásica (SMD)
• Beneficiário: Fábio Morato de Oliveira
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores