Etoposide-induced DNA damage in a chromosomal breakpoint of gene is independent of expression.

In this work, we analyzed the association between gene expression and the accessibility of BCR3, one of gene breakpoint regions involved in the chromosomal translocation (8;21), a frequent translocation in treatment-related acute myeloid leukemia patients. To this end, we evaluate DNA damage generation induced by etoposide treatment of KG-1 and Colo320 cells. Our results show that treatment using clinical doses of etoposide for 24 h induces the generation of DNA double strand breaks in the BCR3 of gene in KG-1 cells, but not in Colo320 cells, even though both cell lines express gene.

Identification of a novel long non-coding RNA within RUNX1 intron 5.

Background: RUNX1 gene, a master regulator of the hematopoietic process, participates in pathological conditions as a partner for several genes in chromosomal translocations. One of the most frequent chromosomal translocations found in acute myeloid leukemia patients is the t(8;21), in which RUNX1 and ETO genes recombine. In RUNX1 gene, the DNA double-strand breaks that originate the t(8;21) are generated in the intron 5, specifically within three regions designated as BCR1, BCR2, and BCR3.