Washington: A team of researchers has identified a leukemia-specific stretch of DNA called an enhancer element that enables cancerous blood cells to proliferate in Acute Myeloid Leukemia (AML), a devastating cancer that is incurable in 70 percent of patients.
The findings by researchers at Cold Spring Harbor Laboratory (CSHL) offer a mechanistic insight into how a new class of promising drugs - one version of which is already in human clinical trials - appears to halt the growth of cancer cells so effectively.
The research led by CSHL Assistant Professor Chris Vakoc, centers on the way a cancer-promoting gene is controlled. When this oncogene, called Myc, is robustly expressed, it instructs cells to manufacture proteins that contribute to the uncontrolled growth that is cancer's hallmark.
Vakoc's team discovered an enhancer element that controls the Myc oncogene specifically in leukemia cells. Unlike many other DNA-based gene regulators, this string of DNA "letters" is nowhere near the Myc gene it regulates.
"The enhancer elements we discovered are 1.7 million DNA bases away from their target gene, Myc. But we were able to show that this long stretch of the genome is bent and looped in the cell nucleus in such a way that the remote enhancer segment literally touches the distant segment harboring the cancer gene," Vakoc said.
The researcher said that the study suggested that this regulatory conformation fuels the uncontrolled growth of cancer cells and may explain why the Myc gene is so uniquely sensitive to targeting with a new class of drugs being developed for leukemia.
The study is published in journal Genes and Development.
