Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/42183
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dc.contributor.authorGutierrez-Angulo, M.
dc.contributor.authorGonzalez-Garcia, J.R.
dc.contributor.authorMeza-Espinoza, J.P.
dc.contributor.authorPicos-Cardenas, V.J.
dc.contributor.authorEsparza-Flores, M.A.
dc.contributor.authorLopez-Guido, B.
dc.contributor.authorRivera, H.
dc.date.accessioned2015-09-15T18:11:36Z-
dc.date.available2015-09-15T18:11:36Z-
dc.date.issued2004
dc.identifier.urihttp://www.scopus.com/inward/record.url?eid=2-s2.0-22244488704&partnerID=40&md5=60d09261ca0032adbed975ceeba722ab
dc.identifier.urihttp://hdl.handle.net/20.500.12104/42183-
dc.description.abstractA semi-quantitative expression analysis of both AML1-a and AML1-total was performed by RT-PCR in 19 children with acute lymphoblastic leukemia (ALL) at diagnosis. AML1-a expression was assessed in 16 bone marrow (BM) and 13 peripheral blood (PB) samples whereas AML1-total was assessed in 17 BM and 16 PB samples. These analyses were also carried out in 15 PB samples of healthy controls. In addition, 18/19 patients were karyotyped: 11 had an unmodified constitutional karyotype (CK) and seven exhibited acquired chromosomal abnormalities (ACA). The expression of AML1-a was significantly increased in BM and PB when compared with the controls (p < 0.013 and p < 0.035, respectively). A significant increase was found in the expression of AML1-a in BM of the ACA group compared with the CK group (p < 0.0009). The expression of AML1-a in BM and PB showed a significant increase in the ACA group compared with controls (p < 0.00001 and p < 0.012, respectively); in contrast, the CK group did not differ from the controls. These observations may mean that the increase of AML1-a favours the progression of leukemia. Copyright � 2005 John Wiley & Sons, Ltd.
dc.relation.isreferencedbyScopus
dc.relation.isreferencedbyWOS
dc.titleIncreased expression of AML1-a and acquired chromosomal abnormalities in childhood acute lymphoblastic leukemia
dc.typeReview
dc.identifier.doi10.1002/hon.734
dc.relation.ispartofjournalHematological Oncology
dc.relation.ispartofvolume22
dc.relation.ispartofissue3
dc.relation.ispartofpage85
dc.relation.ispartofpage90
dc.subject.keywordAcquired chromosomal abnormalities; Aml1-A isoform; Gene expression
dc.contributor.affiliationGuti�rrez-Angulo, M., Divisi�n de Gen�tica, Centro de Investigaci�n Biom�dica de Occidente, IMSS, Tepatitl�n, Jalisco, Mexico, Universidad de Guadalajara, Centro Universitario de Los Altos, Tepatitl�n, Jalisco, Mexico; Gonz�lez-Garc�a, J.R., Divisi�n de Gen�tica, Centro de Investigaci�n Biom�dica de Occidente, IMSS, Tepatitl�n, Jalisco, Mexico; Meza-Espinoza, J.P., Divisi�n de Gen�tica, Centro de Investigaci�n Biom�dica de Occidente, IMSS, Tepatitl�n, Jalisco, Mexico; Picos-C�rdenas, V.J., Divisi�n de Gen�tica, Centro de Investigaci�n Biom�dica de Occidente, IMSS, Tepatitl�n, Jalisco, Mexico; Esparza-Flores, M.A., Departamento de Hematolog�a, Hospital de Pediatr�a, IMSS, Tepatitl�n, Jalisco, Mexico; L�pez-Guido, B., Departamento de Hematolog�a, Hospital de Pediatr�a, IMSS, Tepatitl�n, Jalisco, Mexico; Rivera, H., Divisi�n de Gen�tica, Centro de Investigaci�n Biom�dica de Occidente, IMSS, Tepatitl�n, Jalisco, Mexico, Centro de Investigaci�n Biom�dica de Occidente, IMSS, Ap-postal 1-3838, Tepatitl�n, Jal., Mexico
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