Display options
Share it on

Cancer Cell Int. 2018 Feb 20;18:26. doi: 10.1186/s12935-018-0523-1. eCollection 2018.

[No title available]

Cancer cell international

Doralina do Amaral Rabello, Vivian D'Afonseca da Silva Ferreira, Maria Gabriela Berzoti-Coelho, Sandra Mara Burin, Cíntia Leticia Magro, Maira da Costa Cacemiro, Belinda Pinto Simões, Felipe Saldanha-Araujo, Fabíola Attié de Castro, Fabio Pittella-Silva

Affiliations

  1. 1Laboratory of Molecular Pathology of Cancer, Faculty of Health Sciences and Medicine, University of Brasilia, Brasília, DF Brazil.
  2. 2Department of Clinical Analysis, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP Brazil.
  3. 3Department of Internal Medicine, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP Brazil.
  4. 4Laboratory of Molecular Pharmacology, Faculty of Health Sciences, University of Brasilia, Brasília, DF Brazil.

PMID: 29483845 PMCID: PMC5819641 DOI: 10.1186/s12935-018-0523-1

Abstract

BACKGROUND: Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm whose pathogenesis is linked to the Philadelphia chromosome presence that generates the

METHODS: Here we investigated the expression profile of both genes in CML patients in different stages of the disease, in patients showing different responses to therapy with IM and in non-neoplastic control samples. Imatinib sensitive and resistant CML cell lines were also used to investigate whether treatment with other tyrosine kinase inhibitors interfered in their expression.

RESULTS: In patients, both methyltransferases were either upregulated or with basal expression level during the chronic phase compared to controls. Interestingly,

CONCLUSION: Our results established a new association between

Keywords: Chronic myeloid leukemia; Epigenetic; Genetic alterations; Lysine methyltransferase; MLL2/KMT2D; MLL3/KMT2C

References

  1. Nucleic Acids Res. 2016 Jan 4;44(D1):D917-24 - PubMed
  2. Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2147-52 - PubMed
  3. Mol Cell. 2014 Mar 20;53(6):859-66 - PubMed
  4. Oncol Rep. 2015 Apr;33(4):2017-22 - PubMed
  5. Nat Rev Cancer. 2015 Jun;15(6):334-46 - PubMed
  6. Genes Dev. 2016 Feb 15;30(4):408-20 - PubMed
  7. J Clin Oncol. 2010 May 20;28(15):2529-37 - PubMed
  8. Semin Cell Dev Biol. 2010 Apr;21(2):209-20 - PubMed
  9. Oncogene. 2005 Apr 21;24(18):2929-43 - PubMed
  10. Cell. 2009 May 1;137(3):413-31 - PubMed
  11. Proc Natl Acad Sci U S A. 2012 Oct 23;109(43):17603-8 - PubMed
  12. Int J Oncol. 2013 Aug;43(2):653-60 - PubMed
  13. Nucleic Acids Res. 2000 Nov 15;28(22):4410-8 - PubMed
  14. PLoS One. 2014 Jul 31;9(7):e103915 - PubMed
  15. Science. 2012 May 11;336(6082):736-9 - PubMed
  16. Proc Natl Acad Sci U S A. 2009 May 26;106(21):8513-8 - PubMed
  17. Leukemia. 2011 Mar;25(3):557-60 - PubMed
  18. Nucleic Acids Res. 2001 May 1;29(9):e45 - PubMed
  19. Int J Cell Cloning. 1983 Jun;1(2):105-17 - PubMed
  20. J Hematol Oncol. 2009 Jul 14;2:28 - PubMed
  21. Genes Dev. 1995 Sep 1;9(17):2170-83 - PubMed
  22. Biochim Biophys Acta. 2010 Oct;1804(10):1974-87 - PubMed
  23. Cancer Cell. 2014 May 12;25(5):652-65 - PubMed
  24. Cancer Genet. 2015 May;208(5):178-91 - PubMed
  25. Oncotarget. 2016 Aug 30;7(35):57327-57350 - PubMed
  26. Cancer Sci. 2017 Apr;108(4):553-562 - PubMed
  27. Leukemia. 2003 Jul;17(7):1313-23 - PubMed
  28. Stem Cells. 2003;21(3):315-21 - PubMed

Publication Types