PMID: 2118474Aug 1, 1990Paper

Chromosomes 17 and 22 involved in marker formation in neurofibrosarcoma in von Recklinghausen disease. A cytogenetic and in situ hybridization study

Human Genetics
H J DeckerA A Sandberg

Abstract

We describe the cytogenetic findings in a recurrent neurofibrosarcoma in a patient with nonfamilial von Recklinghausen disease. The composite karyotype was: 40,Y,-X,+dic r(X;20)(:Xp22.2----q26::20p13----q13:), -1, +der(1)t(1;3) (p21;p24),-3,-4,-5,+der(5) t(5;?)(q31;?),-9,-9,+der(9)t(3;9)(q21 or q13;p24 or p22), -11,+der(11)t(11;?)(q22.2;?), -17,+der(17)t(17; 22;?)(q21;q13.1;?), -20, -21, -22, -22, +der(22)t(17; 22;?)(q21;q13.1;?),t(2;10)(q37;q22). The derivative chromosomes were demonstrated at the 500 band level. Chromosomes 17 and 22 were shown to be involved in an unbalanced three-way translocation: t(17;22;?)(q21;q13.1;?). This event was confirmed by in situ hybridization, using two probes mapped to chromosome 17. Hill H is a probe derived from the novel oncogene TRE and is located at 17q12-22. The second probe, derived from the granulocyte colony-stimulating factor (G-CSF), is located at 17q11-q21. The rearrangement between chromosomes 17 and 22 showed breakpoints similar or close to the gene loci for neurofibromatosis 1 (NF-1) and NF-2. Based on our observations we recommend that genetic studies on NF-1 tumors include both gene sites (NF-1 and NF-2) rather than focus on one gene locus.

Citations

May 8, 2010·European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society·Jean-Paul SteibYann Philippe Charles
Oct 1, 1992·Cancer Genetics and Cytogenetics·H J DeckerB R Seizinger
Dec 1, 1993·Cancer Genetics and Cytogenetics·H Schmidt, F W Rath
Mar 1, 1993·Cancer Genetics and Cytogenetics·J A ReyA Pestaña
May 1, 1996·Cancer Genetics and Cytogenetics·U N RaoK Yaw
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