(RxWiki News) For a lot of medical conditions the relationship between genetics and disease is fuzzy, but for people born with errors in a certain gene known as Von-Hippel Lindau (VHL), the link to kidney cancer clear. New research reveals more information about the complex relationship between genes and cancer.
Researchers recently published a study on how the VHL gene is associated with not only cancers of the kidney, but in blood vessel growth and in how cells feed themselves. The mystery behind the Von-Hippel Lindau gene and the disease of the same name seems to be solved.
"Ask your oncologist about genome sequencing."
Damage to the gene that codes for the microRNA miR-204 appears to prevent a cellular process known as autophagy that allows cells to take large amounts of nutrients from the blood. MicroRNA such as miR-204 are part of the regulation process where genetic material is turned into a product, protein.
Researchers found that the mutation affected the ability of cancers to redirect blood flow, and take nutrients and oxygen from the blood. A surprising finding was that mutation also affected chemotherapy, and drugs were prevented from entering the tumor due to the same cellular malfunction.
The VHL gene is also involved in blood vessel growth, which enhances the ability of the tumor to feed itself and grow. This relationship between blood vessels and the kidney cancer is also shown in Von Hippel Lindau, as symptoms include problems with arterial growth as well as cancer.
In order to find the purpose of the VHL gene, researchers looked at human kidney cancer cells, and observed the tumor cells when placed in mice. Further studies took place on mice where the gene had been removed from their DNA entirely.
"VHL has emerged as a master controller of access to intracellular nutrients through autophagy and to extracellular nutrients through formation of blood vessels. Our work shows that there are different autophagic programs—pro-and anti-oncogenic. Drugs that inhibit the final stages of autophagy non-specifically, such as derivatives of chloroquine, may not be as beneficial as hoped," explains Czyzyk-Krzeska, a professor of cancer and cell biology at the UC College of Medicine and researcher with the UC Cancer Institute.
"Current drugs for metastatic kidney cancer target angiogenesis—blocking the formation of blood vessels that feed the tumor—but they typically only increase survival by a matter of months," says Dr. Czyzyk-Krzeska. "We hope this new body of evidence can help pave a new path to more effective treatment options for this disease."
Research was published in the journal Cancer Cell on April 17.
The study was sponsored by grants from the National Cancer Institute, U.S. Department of Veterans Affairs and U.S. Department of Defense.
