Nieuwe kansen bij bestrijding longkanker
Onderzoekers aan de Universiteit van Ohio hebben een nieuw proteïne ontdekt dat een grote rol lijkt te spelen bij het ontstaan van longkanker. Het eiwit verzwakt de werking van een gen dat kankercellen bestrijdt.
Er zijn al nieuwe medicijnen in de handel die de werking van dit eiwit kunnen tegengaan.
A newly-identified protein that can flag an important tumor suppressor gene for destruction may be a key player in the development of lung cancer.
Writing in the Nov. 17 issue of the Journal of the National Cancer Institute, scientists in the Ohio State University Comprehensive Cancer Center (OSUCCC) note that the protein, called Pirh2, when overexpressed, diminishes the activity of p53 – possibly the most powerful tumor suppressor in the entire genome. When it functions normally, p53 regulates several critical cellular processes, including cell growth and death, DNA repair and angiogenesis, the formation of new blood vessels. Studies show that p53 mutation is common, occurring in at least half of all cancer.
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Interestingly, additional analysis revealed that Pirh2 overexpression is not related to any mutations in p53 – only loss of function.
“In effect, we’ve discovered that Prih2 is an oncogene. It promotes cancer by undermining the tumor suppressor’s ability to do its job,” says Duan.
At the same time, these findings may offer scientists a possible new target for intervention.
Villalona points out that new drugs are already on the market that can inhibit the activity of the proteasome, and suggests that these drugs may be able to counter Pirh2’s oncogenic behavior by restoring p53 function. Additional studies would be needed to demonstrate that, however.
