Perhaps the only news cancer patients receive worse than their initial diagnosis is that the tumor trying to take their life is spreading.
Researchers at Johns Hopkins Kimmel Cancer Center have identified the mechanisms for both the beginning and spread of cancerous cells, giving hope that treatments being looked at in Alzheimer’s research could be developed to halt these processes.
Reports published in the journal Cancer Research describe experiments with mice and cell cultures that could lead to new treatments initially for childhood brain tumors and adult prostate cancers, and ultimately to a host of other types of cancer.
Barry Nelkin, Ph.D., professor of oncology at Hopkins, led a team of researchers who found an enzyme that appears to promote the deadly spread of prostate cancer. Blocking the enzyme CDK5 — a compound normally associated with the nervous system — could prevent metastasis, or spreading of cancer in high-risk patients.
It also appears to make cells that are trying to spread to other organs more vulnerable to chemotherapy.
“Cancer cells must be able to ‘crawl’ out of the primary tumor in order to spread,” Nelkin said. That motion is controlled by CDK5, which affects a cell’s inner structure, allowing it to change shape and move out to invade other tissues.
“It’s a very attractive target” for drug research, Nelkin said. Drug companies have long targeted enzyme CDK5 for treatment of Alzheimer’s, and compounds have been developed that could help stop the spread of lung, pancreatic, skin, thyroid and adrenal cancers.
