14 DAY TRIAL // A group of researchers from the University of California in Los Angeles (UCLA) says that studies conducted on the effects that the chemical steroid cholesterol has on the brain have revealed a potential role for it in the fight against highly-aggressive forms of brain cancer, such as glioblastomas.
Investigators have determined that blocking the uptake of large amounts of cholesterol by specialized receptors in the brain can have negative effects on the cancer's ability to grow and expand. These data could conceivably be organized into a new therapy against the disease.
Study researchers at the UCLA Jonsson Comprehensive Cancer Center (JCCC) say that glioblastomas are among the deadliest, fastest-acting brain malignancies ever discovered. Generally, patients succumb to their conditions in just three months.
This research focused on the actions of the mutated epidermal growth factor receptor (EGFR), one of the most commonly-activated oncogenes in the human body. Using a combination of research methods, the UCLA team managed to uncover a new mechanism through which EGFR acts.
Via this method, the factor can easily destroy regulatory mechanisms that are usually at work within cells, preventing them from mutating out of control, and triggering a death signal once the cell has outlived its purpose or usefulness.
When EGFR acts, these mechanisms are thrown into disarray or shutdown completely. This allows damaged cells to multiply out of control, producing clumps known as tumors. In glioblastomas, the factor goes out of its way to ensure the cancer cells are fed large amounts of cholesterol.
By disabling this capability, experts may succeed in delaying the growth of the dangerous tumors, at least while other treatment methods are tested, says Dr. Paul Mischel, the senior author of the study.
The expert also holds an appointment as a professor of pathology and laboratory medicine and of molecular and medical pharmacology at UCLA, and as a researcher at the JCCC. Details of the study appear in the September 15 issue of the medical journal Cancer Discovery,
“Our study found that the mutant EGFR hijacks this system, enabling cancer cells to import large amounts of cholesterol through the LDL receptor. This study identifies the LDL receptor as a key regulator of cancer cell growth and survival and as a potential drug target,” Mischel explains.
Usually, the LDL receptor does not allow the intake of too much cholesterol, but its regular function is undermined by EGFRvIII, a special form of the standard growth factor. By acting on LDL, experts could essentially become capable of starving tumors to death.