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January 15, 2005

Smokers have higher COX-2 levels

Topics: Medicine

In a recent research article evidence is presented that cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR) are potential pharmacologic targets to prevent cancer. Key data implicating a causal relationship between COX-2, EGFR, and carcinogenesis and possible mechanisms of action were studied and evidence of crosstalk between COX-2 and EGFR in order to strengthen the rationale for combination chemoprevention were presented. The concept was determined to be sufficiently promising such that plans were discussed for a clinical trial that will evaluate the concept of combination chemoprevention targeting of COX-2 and EGFR. Now, in Medical News Today we read a report that smoke triggers the production of COX-2 and triggering of the EGFR cascade that leads to COX-2 production.

So we have in the two articles both the bad news for smokers that their smoking is triggering COX-2 production and the good news for smokers and the rest of us that have the good sense not to smoke that somewhere in the not-too-distant future chemoprevention may be possible by interfering with the EGFR cascade - because some of us will get cancer even if we don't smoke and never have(smokers just are at a much higher risk). I guess by knowing this if you are a smoker, whether you quit smoking or not depends on how lucky you think you are. Will chemopreventive drugs be developed in time to save you, assuming it's not already too late and carcinogenisis hasn't already occurred, or since the concept we discussed here hasn't even left the laboratory stage, will many years from now be too late. Let's just hope that you're lucky!

Medical News Today
Tobacco smoke triggers the production of COX-2, a cellular protein linked to the development and progression of cancer, according to research published in the January 15 issue of the journal Cancer Research.

Tobacco smoke also promoted rapid cellular production of two proteins that initiate an epidermal growth factor receptor (EGFR) driven cascade leading to the production of COX-2, the report stated.

The report by Andrew J. Dannenberg, M.D., director of cancer prevention, Weill Medical College of Cornell University, and colleagues, indicates that smokers produce as much as four times the amount of COX-2 in oral mucosal cells lining their mouths than their non-smoking counterparts.

After observing the increased amount of COX-2 in the oral mucosa of smokers, Dannenberg and his team of collaborating scientists exposed cells in culture to tobacco smoke to define the mechanism underlying smoke-induced elevation of COX-2.

The researchers determined that COX-2 levels were increased due to tobacco smoke induced activation of EGFR, a cell membrane protein also associated with various types of cancer. Tobacco smoke stimulated the oral mucosal cells to rapidly release two proteins that activate the EGFR, initiating a cascade resulting in COX-2 protein production.

"In an oral mucosal cell line, tobacco smoke clearly activated the epidermal growth factor receptor. Tobacco smoke caused increased EGFR phosphorylation leading to increased COX-2 production," Dannenberg reported.

"We were able to block the induction of COX-2 with either a small molecule that inhibited EGFR activity or an antibody that prevented ligands from binding to and activating the EGFR. These findings led us to question whether tobacco smoke initiated the process of increasing COX-2 production by first stimulating production of proteins that controlled activity of the EGF receptor," Dannenberg said.

Cells exposed to tobacco smoke increased production of two EGFR ligands, or proteins that bind to and activate the growth factor receptor. Tobacco smoke exposed oral mucosal cells produced more amphiregulin and TGF-alpha, both of which trigger EGFR function.

"Cellular release of both of these EGFR ligands occurred quickly after exposure to tobacco smoke," Dannenberg said. These findings appear to be directly relevant to people because increased levels of both proteins were also detected in oral biopsies from smokers.

"These results provide new insights into the mechanism by which tobacco smoke causes cancer. Mutations can only occur in proliferating cells and activation of EGFR signaling enhances cell proliferation," Dannenberg said.

"These results strengthen the rational for targeting not only COX-2, but also EGFR as approaches for reducing the risk of tobacco-related malignancies of the mouth and throat," Dannenberg said.

Read more...

Posted by Hyscience at January 15, 2005 1:31 PM

What? Does this mean that smoking might actually cause cancer??? I'm going to sue someone! hahaha

"Thanks" for the reminder that I'm a dumbass. (I'm reminded of it every time I light up already.) Gaahh.

Posted by: Beth at January 16, 2005 12:23 AM

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Posted by: Smooooker at February 7, 2005 4:24 PM

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Posted by: www.cigaretes.abc.pl at February 7, 2005 4:27 PM



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