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A second nonrandom translocation, der(16)t(1;16)(q21;q13), in Ewing sarcoma and peripheral neuroectodermal tumor
E C Douglass1, S T Rowe, M Valentine
1Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, TN 38101.
Cytogenetics and Cell Genetics
|January 1, 1990
Summary
A second nonrandom translocation, der(16)t(1;16)(q21;q13), was identified in Ewing sarcoma and peripheral neuroectodermal tumors (PNET). This finding, alongside the common t(11;22) translocation, aids in understanding tumor pathogenesis.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Ewing sarcoma and peripheral neuroectodermal tumors (PNET) frequently exhibit the t(11;22)(q23;q11) translocation.
- Identifying additional genetic alterations is crucial for understanding the pathogenesis of these rare cancers.
Purpose of the Study:
- To report a novel nonrandom translocation, der(16)t(1;16)(q21;q13), in Ewing sarcoma and PNET.
- To investigate the co-occurrence of this new translocation with the established t(11;22) translocation.
Main Methods:
- Karyotyping of tumor samples from patients with Ewing sarcoma and PNET.
- Comparative C-banding analysis of tumor and peripheral lymphocyte karyotypes.
Main Results:
- The der(16)t(1;16)(q21;q13) translocation was detected in 2 of 20 Ewing sarcoma cases and 2 of 7 PNET cases.
- All cases with the der(16)t(1;16) translocation also possessed the t(11;22) translocation.
- Likely breakpoints for the der(16)t(1;16) translocation were identified as 1q21 and 16q13.
Conclusions:
- The der(16)t(1;16)(q21;q13) translocation is a recurrent genetic abnormality in a subset of Ewing sarcoma and PNET.
- The presence of this translocation in cell lines will facilitate molecular studies into Ewing sarcoma and PNET pathogenesis.