Researchers say a rare and unique tumor cell appears to help a form of blood cancer mutate and spread
THURSDAY, May 15, 2014 (HealthDay News) -- Although the very concept of cancer stem cells has been controversial, new research provides proof that these distinct types of cells exist in humans.
Using genetic tracking, researchers found that a gene mutation tied to cancer's development can be traced back to cancer stem cells. These cells are at the root of cancer and responsible for supporting the growth and progression of the disease, the scientists report.
Cancer stem cells are able to replenish themselves and produce other types of cancer cells, just as healthy cells produce other normal cells, the study's British and European authors explained.
"It's like having dandelions in your lawn. You can pull out as many as you want, but if you don't get the roots they'll come back," study first author Dr. Petter Woll, of the MRC Weatherall Institute for Molecular Medicine at the University of Oxford, said in a university news release.
The researchers, led by a team of scientists at Oxford and the Karolinska Institute in Sweden, said their findings could have significant implications for cancer treatment. They explained that by targeting cancer stem cells, doctors could not only get rid of a patient's cancer but also prevent any remaining cancer cells from sustaining the disease.
The study, published May 15 in Cancer Cell, involved 15 patients diagnosed with myelodysplastic syndromes (MDS), a type of cancer that often develops into acute myeloid leukemia, a form of blood cancer.
The researchers examined the cancer cells in the patients' bone marrow. Four of the patients were also monitored over time. One patient was followed for two years. Two patients were followed for 30 months and another patient was monitored for 10 years.
According to the researchers, in prior studies citing the existence of cancer stem cells, the lab tests that were used to identify these cells were considered by many to be unreliable.
However, "In our studies we avoided the problem of unreliable lab tests by tracking the origin and development of cancer-driving mutations in MDS patients," explained study leader Sten Eirik Jacobsen, of Oxford's MRC Molecular Haematology Unit and the Weatherall Institute for Molecular Medicine.
According to the research, a distinct group of MDS cells had all the characteristics of cancer stem cells, and only these particular cancer cells appeared able to cause tumor spread.
The researchers added that this subset of MDS stem cells was rare, but they could replenish other MDS cancer cells. They were also the root of all genetic mutations that caused the disease to progress.
"This is conclusive evidence for the existence of cancer stem cells in myelodysplastic syndromes," Woll concluded. "We have identified a subset of cancer cells, shown that these rare cells are invariably the cells in which the cancer originates, and also are the only cancer-propagating cells in the patients. It is a vitally important step because it suggests that if you want to cure patients, you would need to target and remove these cells at the root of the cancer -- but that would be sufficient, that would do it."
Although the findings do not offer up any new cancer treatment, the study authors believe they may help scientists develop more efficient treatments that specifically target cancer stem cells.
They stressed, however, that this particular study identified only MDS stem cells -- other forms of cancer likely have a unique set of stem cells that work differently, the team said.
"We need to understand more about what makes these cancer stem cells unique, what makes them different to all the other cancer cells," Woll said. "If we can find biological pathways that are specifically dysregulated in cancer stem cells, we might be able to target them with new drugs."
The U.S. National Institutes of Health provides more information on stem cells (http://stemcells.nih.gov/info/basics/Pages/Default.aspx ).
SOURCE: Oxford University, news release, May 15, 2014.