Thomas Burris, chair of pharmacology and physiology at Saint Louis
University, has, for the first time, found a way to stop cancer cell
growth by targeting the Warburg Effect, a trait of cancer cell
metabolism that scientists have been eager to exploit. Metabolism, the ability to use energy, is a feature of all living
things. Cancer cells aggressively ramp up this process, allowing mutated
cells to grow unchecked at the expense of surrounding tissue.
“Targeting cancer metabolism has become a hot area over the past few years, though the idea is not new,” Burris said. Since the early 1900s, scientists have known that cancer cells prefer
to use glucose as fuel even if they have plenty of other resources
available. In fact, this is how doctors use PET (positron emission
tomography) scan images to spot tumors. PET scans highlight the glucose
that cancer cells have accumulated. This preference for using glucose as
fuel is called the Warburg effect, or glycolysis. In his paper, Burris reports that the Warburg effect is the metabolic
foundation of oncogenic (cancer gene) growth, tumor progression and
metastasis as well as tumor resistance to treatment. Burris and his colleagues created a class of compounds that affect a
receptor that regulates fat synthesis. The new compound, SR9243, which
started as an anti-cholesterol drug candidate, turns down fat synthesis
so that cells can’t produce their own fat. This also impacts the Warburg
pathway, turning cancer cells into more normal cells. SR9243 suppresses
abnormal glucose consumption and cuts off cancer cells’ energy supply.
When cancer cells don’t get the parts they need to reproduce through glucose or fat, they simply die.
Because the Warburg effect is not a feature of normal cells and
because most normal cells can acquire fat from outside, SR9243 only
kills cancer cells and remains non-toxic to healthy cells.
The drug also has a good safety profile; it is effective without causing weight loss, liver toxicity, or inflammation.
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