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5 December 2013 11:26 am ,
Vol. 342 ,
An animal rights group known as the Nonhuman Rights Project filed lawsuits in three New York courts this week in an...
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
Thousands of scientists in the Russian Academy of Sciences (RAS) are about to lose their jobs as a result of the...
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
Snake venoms are remarkably complex mixtures that can stun or kill prey within minutes. But more and more researchers...
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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Cracking Gut Bugs' Cancer-Causing Strategy
13 December 2001 (All day)
Most disease-causing bacteria were tracked down long ago, but for decades one microbe got away with murder. Discovered in 1982, Helicobacter pylori triggers ulcers and cancer that kill 7 million people each year, and scientists have learned much about the bug's ulcer-causing abilities. Now a new study clarifies H. pylori's more deadly talent, showing exactly how it forces stomach cells to deform and migrate--an early step in turning cancerous.
People infected with H. pylori are two to six times as likely as uninfected people to develop either stomach cancer or lymphoma. When H. pylori infects the stomach lining, stomach cells may elongate until they resemble hummingbird beaks. The microbe is known to inject a protein called CagA into the stomach cells, where it is tagged with phosphate groups. Because adding or removing phosphate from proteins can scramble cell signals and help induce cancer, scientists wondered if this was H. pylori's strategy.
To find out, molecular oncologist Masanori Hatakeyama of Hokkaido University in Sapporo, Japan, and his colleagues first made an educated guess about which human protein CagA interacts with inside stomach cells. They picked hepatocyte growth factor (HGF), because stomach cells treated with it look exactly like CagA-treated cells. The HGF receptor alters a signaling protein called SHP-2, and the group wondered whether CagA does too.
The scientists found that antibodies to CagA fish out SHP-2 from stomach cell extracts, and vice versa, indicating that the two proteins team up. What's more, cells infected with a mutated version of CagA that didn't bind SHP-2 helped CagA elongate the cells. They proved the point by showing that SHP-2 clips phosphates from additional signaling proteins, but only when it's bound to CagA. Together, these results mean that CagA plugs into the normal cellular signaling system, Hatakeyama says, leading the cell astray and putting it at risk of becoming cancerous.
Cellular microbiologist Brett Finlay calls the work "a major step forward" in explaining how H. pylori tweaks normal cell signaling pathways, nudging stomach cells one step closer to malignancy. Other experts emphasize that many of the molecular links between H. pylori and cancer remain to be discovered--but H. pylori investigators are closing in on their quarry.
Facts on H. pylori infection from the CDC
More background on H. pylori, sponsored by the drug company AstraZenica
Information on H. pylori and ulcers from the National Institutes of Health
The benefits of H. pylori