nd re-growth by inhibiting HIF-1," said Moeller.
Conversely, when the scientists blocked HIF-1 before radiation, there was no overall inhibition of tumor growth. The tumor's center became "necrotic" or populated with dead cells, but the perimeter of the tumor continued to grow.
In fact, blocking HIF-1 before radiation was detrimental to radiation's effects: it prevented cancer cells from engaging in the very behaviors that radiation targets for destruction, said Dewhirst.
"HIF-1 assists cancer cells in dying by a process of self-directed suicide called 'apoptosis,'" said Dewhirst. "If HIF-1 is inhibited prior to radiation, it will make the cell less sensitive to apoptosis and will thereby make the tumor cells more resistant to radiation."
Moreover, because radiation itself boosts HIF-1 levels, blocking HIF-1 at the height of its activity ?after radiation has occurred -- is the most logical sequence of therapy, said Dewhirst.
HIF-1 has become the focus of numerous anti-cancer therapies worldwide, said Dewhirst. Yet its impact on cancer cells is so diverse ?it regulates more than 70 genes -- that simply blocking its activity without regard to its myriad effects has yielded conflicting results. Some of HIF-1's effects promote cancer, while others inhibit cancer, so it is critical to block the protein at a juncture where it promotes cancer growth.
The environment inside the tumor ?and the timing of a given treatment -- can make all the difference in a tumor's response to that therapy, said Moeller.
"Just as putting on a coat and gloves in the middle of summer would yield no benefit and could actually cause harm, blocking HIF-1 at the wrong time and place produces no benefit," said Moeller. "But blocking HIF-1 in the right environment can dramatically inhibit the growth of new blood vessels that feed the tumor."
A multitude of factors influence how HIF-1 behaves in a cancer cell. Cells that are low in oxygen
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Source:DukeHealth
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