Inhibition of the translocated c-myc in Burkitt's lymphoma by a PNA complementary to the E mu enhancer
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Updated: Aug 30, 2026

Inducible and Reversible Dominant-negative (DN) Protein Inhibition
Published on: January 7, 2019
Giovanna Cutrona1, Elisabetta M Carpaneto, Anna Ponzanelli
1Division of Medical Oncology C, National Cancer Research Institute, Istituto Superiore di Sanità, Largo R. Benzi 10, 16132 Genoa, Italy. giovanna.cutrona@istge.it
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 E mu enhancer of the immunoglobulin heavy chain locus (IgH). In Burkitt's Lymphoma cells, a peptide nucleic acid complementary for a specific unique E mu intronic sequence selectively blocked the expression of the c-myc oncogene under E mu 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.
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 E mu enhancer of the immunoglobulin heavy chain locus (IgH). In Burkitt's Lymphoma cells, a peptide nucleic acid complementary for a specific unique E mu intronic sequence selectively blocked the expression of the c-myc oncogene under E mu 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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