Anti-Inflammatory Drugs May Treat Some Aggressive Tumors
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By LabMedica International staff writers Posted on 10 Jul 2014 |
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Image: A mouse mammary gland missing the tumor-suppressor p53 shows expression of ARF (green), now known for a backup role in protecting cells from becoming cancerous. If both p53 and ARF are mutated, the tumors that form are aggressive and may benefit from treatment with anti-inflammatory drugs called JAK inhibitors, currently prescribed for rheumatoid arthritis (Photo courtesy of Raleigh Kladney).
New research raises the possibility that some cancer patients with aggressive tumors may benefit from a class of anti-inflammatory drugs used to treat rheumatoid arthritis.
By studying triple-negative breast cancer, researchers from Washington University School of Medicine in St. Louis (MO, USA) found that some aggressive tumors rely on an antiviral pathway that seems to fuel the inflammation process, widely recognized for roles in rheumatoid arthritis, cancer, and other inflammatory diseases.
The investigators reported their findings in the June 26, 2014, issue of the journal Cell Reports. Until now, even though ARF was known to be expressed in some tumors with mutated p53, ARF largely was thought to be nonfunctional in this scenario. But the investigators showed that in the absence of p53, ARF actually protects against even more aggressive tumor formation.
“It’s probably inaccurate to say that ARF completely replaces p53, which is a robust tumor suppressor with multiple ways of working,” said senior author Jason D. Weber, PhD, an associate professor of medicine. “But it appears the cell has set up a sort of backup system with ARF. It’s not surprising that these are the two most highly mutated tumor suppressors in cancer. Because they’re backing one another up, the most aggressive tumors form when you lose both.”
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Washington University School of Medicine in St. Louis
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By studying triple-negative breast cancer, researchers from Washington University School of Medicine in St. Louis (MO, USA) found that some aggressive tumors rely on an antiviral pathway that seems to fuel the inflammation process, widely recognized for roles in rheumatoid arthritis, cancer, and other inflammatory diseases.
The investigators reported their findings in the June 26, 2014, issue of the journal Cell Reports. Until now, even though ARF was known to be expressed in some tumors with mutated p53, ARF largely was thought to be nonfunctional in this scenario. But the investigators showed that in the absence of p53, ARF actually protects against even more aggressive tumor formation.
“It’s probably inaccurate to say that ARF completely replaces p53, which is a robust tumor suppressor with multiple ways of working,” said senior author Jason D. Weber, PhD, an associate professor of medicine. “But it appears the cell has set up a sort of backup system with ARF. It’s not surprising that these are the two most highly mutated tumor suppressors in cancer. Because they’re backing one another up, the most aggressive tumors form when you lose both.”
Related Links:
Washington University School of Medicine in St. Louis
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