Features Partner Sites Information LinkXpress
Sign In
Advertise with Us
Micromedic Technologies

Anti-Inflammatory Drugs May Treat Some Aggressive Tumors

By BiotechDaily International staff writers
Posted on 10 Jul 2014
Print article
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).
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.”

Related Links:

Washington University School of Medicine in St. Louis



Print article

Channels

Genomics/Proteomics

view channel
Image: Molecular model of E3 ubiquitin ligase (green), E2 ubiquitin enzyme (orange), \"activated ubiquitin\" (cyan), and \"allosteric ubiquitin\" (blue) (Photo courtesy of Dr. Bernhard Lechtenberg, Sanford Burnham Prebys Medical Discovery Institute).

Researchers Resolve Molecular Structure of Critical Ubiquitin-Binding Enzyme

The molecular structure of a protein complex critically involved in diverse cellular functions such as cell signaling, DNA repair, and mounting anti-inflammatory and immune responses has been elucidated... Read more

Business

view channel

Purchase Agreement to Boost Ebola Vaccine Development

A deal to help boost development of a vaccine to protect against Ebolavirus infection was finalized at the recent Davos Conference in Switzerland. Gavi (Geneva, Switzerland), the global alliance for vaccines and immunizations, announced that it would spend five million USD to purchase the Ebola vaccine under development... Read more
Copyright © 2000-2016 Globetech Media. All rights reserved.