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Inhibition of the Translocated c-myc in Burkitt’s Lymphoma by a PNA Complementary to the Eµ Enhancer¹

Division of Medical Oncology C [G. C., A. P., S. R., M. F.] and Laboratory of Epigenetics [L. C. B., E. M. C.], National Cancer Research Institute, IST, Genoa; Department of Oncology, Biology and Genetics, University of Genoa 16132 Genoa [G. C., M. F.]; TIB MolBiol s.r.l., 16132 Genoa [M. U.]; Center of Excellence for Biomedical Research, 16132 Genoa [E. M., S. S., U. B.]; and Division of Pathology, Sant’Andrea Hospital, 19100 La Spezia [S. R.], Italy

In Burkitt’s Lymphoma there is an up-regulation of the c-myc oncogene caused by its translocation from chromosome 8 to chromosome 14, often close to the Eµ enhancer of the immunoglobulin heavy chain locus (IgH). In Burkitt’s Lymphoma cells, a peptide nucleic acid complementary for a specific unique Eµintronic sequence selectively blocked the expression of the c-myc oncogene under Eµ control but not of other c-myc alleles. This Peptide Nucleic Acid also inhibited IgM expression in B cells. The finding that PNAs specific for a regulatory noncoding sequence can block gene expression has important conceptual and practical implications.

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