A Hiroshima University team has identified the genetic defect that can cause leukemia and other blood-related diseases, raising the prospects for early detection and preventative treatment.
A pair of genes known as the Samd9L was pinpointed in the development of leukemia and other blood-related diseases by a research team headed by Hiroshima University professor Toshiya Inaba. The Samd9L pair are thought to regulate cell division and are among the 2,135 genes on the 7th chromosome.
Inaba’s study confirms earlier studies that had suggested that leukemia and MDS (myelodysplastic syndromes) were related to missing genes in the 7th chromosome of the human genome which comprises 46 chromosomes which together contain about 35,000 genes.
Inaba’s team used two types of mice. Half had their genes altered to have just one of the Samd9L pair and the other half to be missing both. Unlike healthy mice which have life spans averaging three years, 53% of mice with only one Samd9L gene and 60% of mice with neither gene lived no more than 25 months. Inaba believes that the mice with missing genes were unable to stop the growth of abnormal cells.
The Hiroshima team’s study is of special significance to their city. Hiroshima is one of the two Japanese cities — the only cities in history — to have suffered the US atomic bombing in mid-August of 1945 that hastened the end of World War II. Even 68 years after the bombing residents of Hiroshima and Nagasaki who had been exposed to high levels of radiation near the bombs’ hypocenters remain three times more likely than members of the Japanese population as a whole to develop eukemia and myelodysplastic syndromes (MDS) and other blood diseases.
“That’s because hematopoietic stem cells that are the source of blood get damaged by radiation, and the genes get lost due to various factors thereafter,” noted the Inaba team in their study published in the September 9 online edition of the US journal Cancer Cell.
