© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 16, 1355-1357,
August 16, 2000
© 2000 Oxford University Press
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Chromosome 19 Translocation, Overexpression of Notch3, and Human Lung Cancer
Affiliations of authors: T. P. Dang, T. Sepetavec, K. R. Hande, D. P. Carbone, Division of Hematology and Oncology, Experimental Therapeutics Program, Vanderbilt-Ingram Cancer Center, Nashville, TN; A. F. Gazdar, A. K. Virmani, J. D. Minna, Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas; J. R. Roberts, Division of General Thoracic Surgery, Vanderbilt-Ingram Cancer Center, Nashville.
Correspondence to: David P. Carbone, M.D., Ph.D., Division of Hematology and Oncology, Experimental Therapeutics Program, Vanderbilt-Ingram Cancer Center, 648 Medical Research Bldg. II, Nashville, TN 37232-6838 (e-mail: d.carbone@vanderbilt.edu).
Somatically acquired chromosome translocations are the major mechanism for gene activation in hematologic malignancies, but they have not been described previously in the more common epithelial tumors, such as lung cancers. Furthermore, lung carcinomas often exhibit complex karyotypes, and this complexity has been assumed to imply a lack of specificity. Indeed, chromosomal deletions associated with mutations in tumor suppressor genes, or gene amplifications of dominant oncogenes, are well-known genetic abnormalities in these tumors (1).
Here we describe the identification and mapping of a novel balanced t(15;19) somatically acquired translocation arising in an aggressive, metastatic lung carcinoma. A review of the literature shows three case reports (2–4) of t(15;19) translocations in undifferentiated epithelial intrathoracic tumors, diagnosed as thymic and/or lung in origin on the basis of the site of the disease and immunohistochemical findings. We have mapped the breakpoint to the 5` region of the
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