Título:	Residual expression of SMYD2 and SMYD3 is associated with the acquisition of complex karyotype in chronic lymphocytic leukemia
Autor(es):	Santos, Wilson Oliveira Ramos, Doralina do Amaral Rabello Araujo, Antônio Roberto Lucena Oliveira, Fábio Morato de Rêgo, Eduardo Magalhães Pittella-Silva, Fabio Araujo, Felipe Saldanha de
Afiliação do autor:	Universidade de Brasília, Faculdade de Ciências da Saúde, Laboratório de Patologia Molecular do Câncer Universidade de São Paulo, Faculdade de Medicina, Ribeiro Preto
Assunto:	Leucemia linfoide crônica (LLC) Citogenética Cariótipo
Data de publicação:	2016
Editora:	Springer
Referência:	OLIVEIRA-SANTOS, Wilson et al. Residual expression of SMYD2 and SMYD3 is associated with the acquisition of complex karyotype in chronic lymphocytic leukemia. Tumor Biology, [S.l.], v. 37, p. 9473–9481, 2016. DOI: https://doi.org/10.1007/s13277-016-4846-z.
Abstract:	SET and MYND domain containing 2 (SMYD2) and the SET and MYND domain containing 3 (SMYD3) are the most studied and well-characterized members of SMYD family. It has been demonstrated that their altered expression is associated with the progression of several solid tumors. Nevertheless, whether these methyltransferases exert any impact in chronic lymphocytic leukemia (CLL) remains unknown. Here, we investigated the gene expression profile of SMYD2 and SMYD3 in 59 samples of CLL and 10 normal B cells. The obtained results were associated with white blood cells (WBC) and platelet counts, ZAP-70 protein expression, and cytogenetic analysis. We found that SMYD2 and SMYD3 are overexpressed in CLL patients and, interestingly, patients with residual expression of both genes presented a high WBC count and complex karyotype. Furthermore, a strong correlation between SMYD2 and SMYD3 gene expression was unveiled. Our data demonstrate the association of a residual expression of SMYD2 and SMYD3 with CLL progression indicators and suggests both genes are regulated by a common transcriptional control in this type of cancer. These results may provide the basis for the development of new therapeutic strategies to prevent CLL progression.
DOI:	https://doi.org/10.1007/s13277-016-4846-z
Versão da editora:	https://link.springer.com/article/10.1007/s13277-016-4846-z
Aparece nas coleções:	Artigos publicados em periódicos e afins

Os itens no repositório estão protegidos por copyright, com todos os direitos reservados, salvo quando é indicado o contrário.