Trisomy 19 as the Sole Chromosomal Abnormality in CML
International Journal of Genetics and Genomics
Volume 2, Issue 4, August 2014, Pages: 77-79
Received: Aug. 4, 2014; Accepted: Aug. 19, 2014; Published: Aug. 30, 2014
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Authors
Salil N. Vaniawala, Molecular Cytogenetic Unit, S. N. Gene Laboratory and Research Centre, President Plaza – A, Near RTO Circle, Surat, India
Pankaj K. Gadhia, Molecular Cytogenetic Unit, S. N. Gene Laboratory and Research Centre, President Plaza – A, Near RTO Circle, Surat, India
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Abstract
Presence of trisomy 19 in chronic myeloid leukemia (CML) normally considered as secondary abnormality but trisomy 19 rarely occur as sole abnormality. In the present study a total of 2312 Ph positive CML were screened from year2004 to 2014 and we found 2 cases of trisomy 19 as sole karyotype abnormalities. Both karyotype showed 47,XY,t(9;22)(q34;q11.2),+19,complements. It is not known that which gene(s) present on chromosome 19 plays important role in development of this condition.
Keywords
Trisomy 19, Sole Chromosome Abnormality, CML
To cite this article
Salil N. Vaniawala, Pankaj K. Gadhia, Trisomy 19 as the Sole Chromosomal Abnormality in CML, International Journal of Genetics and Genomics. Vol. 2, No. 4, 2014, pp. 77-79. doi: 10.11648/j.ijgg.20140204.15
References
[1]
R. La Sturza, N. Testoni, M. Lafage-Pochitaloff, D.Ruggeri, E. Ottaviani, G. Perla et al., “Complex variant Philadelphia translocation involving the Short arm of chromosome 6 in CML.” Hematologica, Vol. 87, pp. 143-47 2002.
[2]
T.G.Lugo, A.M. Pendergast, A. J. Muller, O.N. Witte, “Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. Science, Vol. 247, pp. 1079-82, 1990.
[3]
I.L.Soon, H.S.Cho, C.H.Lee, K. D. Kim, J. K.Ha, M.K. Kim, K.H. Lee, M.S.Hyun, “Two cases of Trisomy19 as a sole chromosomal abnormality in myeloid disorders”. Kor. J. Lab. Med, Vol. 28, pp. 174 – 178, 2008.
[4]
B. Johansson, T. Fioretos, F. Mitelman, “cytogenetic and molecular genetic evolution of chronic myeloid leukemia” Acta Hematol, Vol. 107(2), pp.76-94, 2002.
[5]
J. L. Diez-Martin, G.W. Dewald, R. V. Pierre, “Possible cytogenetic distinction between lymphoid and myeloid blast crisis in chronic granulocytic leukemia” Am. J. Hematol, Vol. 27, pp. 194-203, 1988.
[6]
International System for Human Cytogenetics Nomenclature (ISCN), S. Karger Pub. Inc. 2009, 2013.
[7]
S. Luatti, F.castagnetti, G.Marzocchi, C. Bladdazi, G. Gugliotta, I. Lacobucci et al., “Additional chromosomal abnormalities in Philadelphia-positive clone: adverse prognostic influence on frontline imatinib therapy: a GIMEMA working party on CML analysis”, Blood, Vol. 120(4), pp. 716-67, 2012.
[8]
M. Daskalkis, N. Mauritzson, B. Johansson, K. Bouabdallah, F. Onida, R. Kunzamann, H. Muller-Berndroff, A. Schmidt-Graff, M. Lubbert, “Trisomy 19 as the sole chromosomal abnormality in proliferative chronic myelomonocytic leukemia”. Leukemia Res. Vol. 30, pp. 1043-47, 2006.
[9]
R.W. Yen, P.M. Vertino, B.D. Nelkin, J.J. Yu, W. El-Deiry, A. Cumarswamy, “Isolation and characterization of c-DNA encoding human DNA methyl-transferase”, Nucleic acid Res. Vol. 20(9), pp. 2289-91, 1992.
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