Myelodysplastic Syndrome Linked to Abnormal Stem Cells
THURSDAY, July 5 (HealthDay News) -- As researchers suspected, abnormal bone marrow stem cells trigger the development of myelodysplastic syndromes, serious blood diseases that affect the bone marrow and can progress to leukemia, according to a new study.
"Good Morning America" host Robin Roberts recently disclosed that she had developed myelodysplastic syndrome, or MDS, as a rare complication of her breast cancer treatment. The syndrome is diagnosed in about 10,000 to 15,000 people in the United States each year, mostly in men and in those over age 60.
The new findings, published in the July 2 online edition of Blood, could lead to improved treatments for myelodysplastic syndrome and cancers related to the syndrome, researchers from the Albert Einstein College of Medicine of Yeshiva University, in New York City, suggested in an Einstein news release.
"Researchers have suspected that [myelodysplastic syndrome] is a 'stem cell disease,' and now we finally have proof," said the study's co-senior author Amit Verma, an associate professor of medicine and of developmental and molecular biology at Einstein and attending physician in oncology at Montefiore Einstein Center for Cancer Care.
"Equally important, we found that even after [myelodysplastic syndrome] standard treatment, abnormal stem cells persist in the bone marrow. So, although the patient may be in remission, those stem cells don't die and the disease will inevitably return. Based on our findings, it's clear that we need to wipe out the abnormal stem cells in order to improve cure rates," Verma explained in the news release.
For the study, the researchers analyzed bone marrow stem cells and the progenitor cells, or cells formed by stem cells, of 16 patients with various types of myelodysplastic syndrome. They compared these cells to those of 17 people who did not have the syndrome.
The investigators found widespread genetic and epigenetic (related to environmental factors) variations in the stem and progenitor cells taken from myelodysplastic syndrome patients. The abnormalities were more obvious in those with more serious forms of the disease, the researchers noted.
"Our study offers new hope that [myelodysplastic syndromes] can be more effectively treated, with therapies that specifically target genes that are deregulated in early stem and progenitor cells," the study's co-senior author Dr. Ulrich Steidl, an assistant professor of cell biology and of medicine at Einstein, said in the news release. "In addition, our findings could help to detect minimal residual disease in patients in remission, allowing for more individualized treatment strategies that permanently eradicate the disease."
The U.S. National Library of Medicine has more about myelodysplastic syndromes.
SOURCE: Albert Einstein College of Medicine, news release, July 2, 2012