Is lung cancer in non smokers completely different in non smokers?

This is one for anoraks only. Pierre Hainaut of the WHO/IARC and Gerd Pfeifer are experts in the aetiology (causation) of lung cancer via the mutation of the P53 gene. In smokers it is a G to T transversion while in non smokers it is a G to A transversion. The research was of particular interest to the WHO/IARC as this is the final proof, denied by tobacco companies that smoking causes lung cancer.  They conclude that it is the case. If the G to T Transversion is never seen in lung cancer then second hand smoke will never cause lung cancer in non smokers. Discuss.

http://carcin.oxfordjournals.org/content/22/3/367.full.pdf+html

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8 Responses to Is lung cancer in non smokers completely different in non smokers?

  1. Frank Davis says:

    Glad to see you have a blog!

  2. harleyrider1978 says:

    Dave,what about the HPV connection to that same gene,was it discussed at all or even bacterial genetic mutations of the 53 gene…………

  3. harleyrider1978 says:

    I believe CarolT has already wrote about this before and I have it on my other computer right now,however I cant access this dial up connection on it yet!

  4. harleyrider1978 says:

    JOINT STATEMENT ON THE RE-ASSESSMENT OF THE TOXICOLOGICAL TESTING OF TOBACCO PRODUCTS”
    7 October, the COT meeting on 26 October and the COC meeting on 18
    November 2004.

    http://cot.food.gov.uk/pdfs/cotstatementtobacco0409

    “5. The Committees commented that tobacco smoke was a highly complex chemical mixture and that the causative agents for smoke induced diseases (such as cardiovascular disease, cancer, effects on reproduction and on offspring) was unknown. The mechanisms by which tobacco induced adverse effects were not established. The best information related to tobacco smoke – induced lung cancer, but even in this instance a detailed mechanism was not available. The Committees therefore agreed that on the basis of current knowledge it would be very difficult to identify a toxicological testing strategy or a biomonitoring approach for use in volunteer studies with smokers where the end-points determined or biomarkers measured were predictive of the overall burden of tobacco-induced adverse disease.”

    In other words … our first hand smoke theory is so lame we can’t even design a bogus lab experiment to prove it. In fact … we don’t even know how tobacco does all of the magical things we claim it does.

    The greatest threat to the second hand theory is the weakness of the first hand theory

  5. Tony says:

    Hi Dave,

    Just found your blog and it looks good!

    As a self confessed anorak, I thought I’d take a look at the study you linked to.

    A few observations:

    They say (first page) that ‘More than 50% of all lung cancers show a mutation of the P53 gene’ and that ‘these mutations are more common in smokers’. Unfortunately, they don’t give a figure for this.

    Lets be generous and assume the figure is around 50% for non-smokers and nearer 100% for smokers.

    Fig 1. looks only at those cases where a P53 mutation is present. It shows 30% of smoker lung cancer cases have a G->T mutation. By contrast, only 10% of non-smoker lung cancer cases have a G->T mutation. This is a statistically significant result (above 99.9%) although the non-smoker figure is small enough that experimental error could alter it. No error bars are shown but I’ll assume the result is valid.

    So at most, a G->T mutation can account for only 30% of smoker lung cancer cases. However the figure is lower dependant on the proportion of non-mutated P53 cases. So probably somewhere between 20% and 25% (30% as opposed to expected 10% or 5% if only 50% of non-smokers have P53 mutation at all).

    The non-smoker figure of 10% is in line with other cancer cases. The trouble is that this is difficult to interpret without knowing exact figures for P53 mutations of all types.

    In conclusion, I agree that this is an interesting study and might give a clue as to what causes say 25% of smoker lung cancer cases. However I can’t see it shedding much light on passive smoking because the claimed SHS risk is so small it would be swallowed up in the uncertainties.

    Best regards to you and I look forward to more of your blog posts.

    P.S. I am aware that studies have shown that benzo(a)pyrene can cause P53 (G->T I think) mutations in sufficiently strong concentration. However the concentration of it in tobacco smoke is very much weaker even for active smokers.

  6. The anti-smokers commit flagrant scientific fraud by ignoring more than 50 studies which show that human papillomaviruses cause at least 1/4 of non-small cell lung cancers. Smokers and passive smokers are more likely to have been exposed to this virus for socioeconomic reasons. And the anti-smokers’ studies are all based on lifestyle questionnaires, so they’re cynically DESIGNED to blame tobacco for all those extra lung cancers that are really caused by HPV. And they commit the same type of fraud with every disease they blame on tobacco.
    http://www.smokershistory.com/hpvlungc.htm
    http://www.smokershistory.com/SGHDlies.html

    And, all their so-called “independent” reports were ring-led by the same guy, Jonathan M. Samet, including the Surgeon General Reports, the EPA report, the IARC report, and the ASHRAE report, and he’s now the chairman of the FDA Committee on Tobacco. He and his politically privileged clique exclude all the REAL scientists from their echo chamber. That’s how they make their reports “unanimous!”

    http://www.smokershistory.com/SGlies.html

    For the government to commit fraud to deprive us of our liberties is automatically a violation of our Constitutional rights to the equal protection of the laws, just as much as if it purposely threw innocent people in prison. And for the government to spread lies about phony smoking dangers is terrorism, no different from calling in phony bomb threats.

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