Brain cancer gene culprit detected

Posted Dec 21, 2016 by Tim Sandle
Research into a type of brain cancer has identified a gene that plays a role in helping a tumor to survive radiation treatment and even to expand.
Brain In A Dish
A 3-D model brain organoid with different brain regions. All cells show up blue  neu...
Brain In A Dish A 3-D model brain organoid with different brain regions. All cells show up blue, neural stem cells are red and neurons are green.
Dr Lancaster Cambridge University
The type of brain cancer studied is glioblastoma and the suspect gene is called NAMPT. The gene forms part of a pathway associated with energy production and cellular aging.
Glioblastoma (or ‘glioblastoma multiforme’) is the most common and most aggressive cancer that begins within the brain. Typically treatment involves surgery after which chemotherapy and radiation therapies are used. The tumors arise from astrocytes — the star-shaped cells that make up the “glue-like,” or supportive tissue of the brain, which results in the cancer sometimes being called the “octopus tumor.”
The chances of survival are low and often the tumor is inoperable, resulting in 70 percent of patients diagnosed with this brain cancer rarely surviving for more than two years. This has led to researchers to try to work out why the cancer is so difficult to treat.
The research, conducted at Washington University, has revealed that glioblastoma cells have an overexpression of the NAMPT gene (which is part of the nicotinamide adenine dinucleotide (NAD+) pathway). The purpose of this pathway is to produce energy for the cells and it thought the tumor is aided by an increase in energy production.
The research group, led by Professor Albert Kim, think that a way forwards will be to target the NAD+ pathway with the aim of disrupting the ability of the cancer cells to renew. Such targeting may also make the cells more vulnerable to radiation treatment. Professor Kim told Laboratory Roots: “in a patient, that could mean that if you suppress the pathway, the same dose of radiation may be more effective at destroying the tumor."
These proposals are borne out in cellular studies; however, the theory has yet to be tested on using an animal model. The trick here will be to devise an NAD+ strategy that is specific for cancer cells.
The research is published in the journal PNAS, with the paper headed “An NAD+-dependent transcriptional program governs self-renewal and radiation resistance in glioblastoma.”