Your browser doesn't support javascript.
loading
An unusual translocation, t(1;11)(q21;q23), in a case of chronic myeloid leukemia with a cryptic Philadelphia chromosome.
Gutiérrez, Leandro Germán; Noriega, María Fernanda; Laudicina, Alejandro; Quatrin, Mariana; Bengió, Raquel María; Larripa, Irene.
Afiliação
  • Gutiérrez LG; Laboratory of Hematological Genetics, Institute of Experimental Medicine, National Council of Scientific and Technical Research-National Academy of Medicine, C1425AUM Buenos Aires, Argentina.
  • Noriega MF; Genetics Division, Hematology Research Institute 'Mariano R. Castex', National Academy of Medicine, C1425AUM Buenos Aires, Argentina.
  • Laudicina A; Lexel SRL, Division In Vitro, C1135ABO Buenos Aires, Argentina.
  • Quatrin M; Laboratory of Genetics, 'Sor María Ludovica' Hospital, La Plata, B1904CSI Buenos Aires, Argentina.
  • Bengió RM; Clinical-Hematological Division, Hematology Research Institute 'Mariano R. Castex', National Academy of Medicine, C1425AUM Buenos Aires, Argentina.
  • Larripa I; Laboratory of Hematological Genetics, Institute of Experimental Medicine, National Council of Scientific and Technical Research-National Academy of Medicine, C1425AUM Buenos Aires, Argentina.
Oncol Lett ; 13(5): 3159-3162, 2017 May.
Article em En | MEDLINE | ID: mdl-28521421
Chronic myeloid leukemia (CML) is characterized by the translocation t(9;22)(q34;q11) [Philadelphia (Ph) chromosome). Although not frequently occurring, additional chromosome abnormalities (ACAs) can be detected at diagnosis and a number have been associated with an adverse cytogenetic and molecular outcome. The present study reports a case of CML presenting with the translocation t(1;11)(q21;q23) and a cryptic Ph chromosome. The presence of ACAs could generate greater genetic instability, promoting the emergence of further alterations. The present findings suggest that t(1;11)(q21;q23) can prevent a good response to tyrosine kinase inhibitor (TKI) therapy developing a primary resistance. In the present patient, at a recent follow-up, the T315I mutation was detected. This mutation confers full resistance to all available TKI, except ponatinib, which was not a therapeutic option due to comorbidities.
Palavras-chave
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Oncol Lett Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Argentina País de publicação: Grécia
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Oncol Lett Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Argentina País de publicação: Grécia