Cleveland Clinic Researchers Identify Differences in Growth Mechanisms of Cancer Cells and Normal Cells
Study Shows That Future Cancer Treatments Could be Less Damaging, Toxic to Patients
Monday, Dec. 8, 2008, Cleveland:
Cleveland Clinic researchers today presented findings that suggest cancer could be treated in a novel way that is much less toxic.
The researchers found that they could alter an existing chemotherapy drug to stop the growth of cancer cells and encourage the growth of healthy cells. Current treatments kill both cancer cells and healthy cells, which leads to numerous side effects.
The results of the studies suggest that the mechanisms that cause cancer cells to divide and grow uncontrollably are often different from the mechanisms that drive the growth of healthy stem-cells. This difference can be exploited to selectively stop the growth of the cancer cells without stopping the growth of healthy stem-cells.
"Today, most cancer chemotherapy works the margins - the chemotherapy is marginally more poisonous to cancer cells than normal cells," said lead investigator Yogen Saunthararajah, MD, of Taussig Cancer Institute at Cleveland Clinic. "Therefore, treatment is difficult and risky for patients and can only be given for a few days at a time, with long periods without treatment during which the cancer can regrow."
"Using this alternative approach, which in the test-tube has opposite effects on cancer cells versus healthy stem-cells, perhaps therapy can be given regularly and for longer periods, to get the maximum benefits out of treatment. We are excited that we can modify the use of existing drugs to produce this effect, which will allow us to start clinical trials soon."
"We are excited that we can modify the use of existing drugs to [stop the growth of cancer cells and encourage the growth of healthy cells], which will allow us to start clinical trials soon."
The results were presented Monday at the annual meeting of the American Society of Hematology (ASH) in San Francisco.
The research team studied bone marrow samples of myelodysplastic syndrome (MDS) and leukemia patients as well as healthy blood stem-cells to discover that the enzyme known as DNMT1 plays opposite roles in the healthy stem-cells versus the cancerous cells. Therefore, inhibiting the function of this enzyme produced opposite effects on the healthy cells versus the cancerous cells. The drug used to inhibit this enzyme, decitabine, is already available for clinical use, allowing for clinical studies to be conducted in the next year to determine if using decitabine in this new method can reproduce the effects seen in the test-tube in patients.
The research team emphasized that this work needs to undergo the peer review process and publication and that clinical trials must be conducted to further test this approach in patients. This study is also scheduled to be highlighted as a "Best of ASH" presentation by the American Society of Hematology, the world’s largest professional association of blood specialists.
