Giloblastoma is said to be a kind of central nervous system tumor that may form from glial tissue of the brain and spinal cord and encompasses cells that appears to look very dissimilar from normal cells. Glioblastoma is believed to generally take place in adults and apparently affects the brain more frequently as compared to the spinal cord. A drug already in clinical trials to treat an array of tumors seems to exhibit an amazing capability to halt the development of glioblastoma in both laboratory cells and in animals. At least this is what a research from Georgetown Lombardi Comprehensive Cancer Center and the University of California, San Francisco (UCSF) claims.
Their discoveries offers hope that the drug, PD-0332991, could present a new treatment alternative for glioblastoma, which is said to be the most general in addition to being the deadliest type of brain cancer. A clinical trial examining the therapy in patients with recurring brain cancer is said to be under development.
“We have had just amazing results in these preclinical studies. We are hopeful it will prove to be effective in brain cancer patients for which there is little effective therapy,” commented, Todd Waldman, MD, PhD, an associate professor of oncology at Lombardi.
C. David James, PhD, professor of neurological surgery at UCSF, added, “What is especially encouraging about this agent is that we found it can easily pass through the blood-brain barrier and access glioblastoma, and that there is already a simple test available for screening glioblastoma patients in advance to see whether or not they should be responsive to this therapy.”
The drug is presently being examined in clinical trials for otherwise untreatable teratomas, in addition to multiple myeloma and breast cancer. It is intended to close down the activity of molecules, cyclin-dependent kinases 4 and 6 (cdk4/6), that apparently impels cell division.
Waldman quoted, “In normal cells, these kinases are kept under exquisite control by a gene known as p16. But in glioblastoma, and other cancers, p16 is frequently deleted, and these two kinases are uncontrollably activated, which drives the cell to divide and form cancer.”
The agent, nevertheless, may not function if the cancer is said to be missing expression of a tumor suppressor protein called retinoblastoma (Rb) since Rb is required to manage development in these cells even if cdk4/6 are inhibited. A test to find out if RB is there is apparently already being used to scan patients for use of PD-0332991 in the continuing clinical trials.
A research team at Georgetown headed by Waldman, performed laboratory studies on roughly 21 different cell lines resultant from the tumors of patients suffering from glioblastoma. They supposedly examined PD-0332991 at several concentrations to observe if it could discontinue growth of the cancer cells, and discovered it to be effectual in all 16 cell lines with a running Rb gene, but it did not seem to function in 5 cell lines missing Rb.
James headed a team of researchers at UCSF that appears to have entrenched three diverse types of human glioblastoma straightaway into the brains of mice, and subsequently they treated them with PD-0332991. They primarily found that the agent may have efficiently attained intracranial tumors and that the cancer did not develop as long as the mice carried on with the drug. But it was also observed that they apparently swiftly died from the cancer when the agent was withdrawn.
Since PD-0332991 itself does not destroy cancer cells, the scientists then merged the agent with radiation and discovered that results seemed to be superior to use of PD-0332991 alone. They further effectively examined the agent in mice in which glioblastoma had returned following treatment with temozolomide, a chemotherapy that is said to be a standard-of-care for several patients.
The findings were published in Cancer Research.