Tobacco industry continues to undercut research linking cigarettes and cancer
A study of once-confidential tobacco industry documents reveals that in the past few years several tobacco companies have continued to support research challenging the link between cancer and a potent carcinogen found in cigarette smoke. The companies continued this approach even after a landmark 1996 study demonstrated strong molecular evidence of the direct carcinogenic effect of the tobacco smoke constituent.
The new study from the Center for Tobacco Control Research and Education at UCSF, is being published in the British medical journal Lancet, EMBARGOED for 7:01 PM, EST, THURSDAY, JANUARY 13, 2005 (00:01 H Greenwich Mean Time).
The research sponsored by the tobacco industry challenges two key studies confirming that benzo[a]pyrene, a carcinogen in tobacco smoke, damages the tumor suppressor gene p53, permitting cancer to develop.
The Lancet paper can be downloaded at: EXPOSED: TOBACCO INDUSTRYS’ EFFORTS TO CAST DOUBT ON LINK BETWEEN SMOKING AND CANCER GENE
Below is a press release prepared by Lancet.
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EMBARGO: 0001 H (London time) Friday January 14 2005
To Coincide with Online Publication in Lancet
EARLY ONLINE PUBLICATION: Friday January 14 2005
EXPOSED: TOBACCO INDUSTRYS’ EFFORTS TO CAST DOUBT ON LINK BETWEEN SMOKING AND CANCER GENE
The strategies used by the tobacco industry to counteract research linking tobacco smoke to cancer-causing mutations in a gene called p53 are detailed in a study published online (Friday January 14, 2005) in THE LANCET.
Damage to the p53 gene leads to uncontrolled cell division. Mutations in this gene are found in over 50% of all human tumours, including 60% of lung cancers.
Benzo[a]pyrene, a potent carcinogen, was identified in cigarette smoke in 1952. In the 1990’s, studies demonstrated patterned changes in p53 after exposure to benzo[a]pyrene. A 1996 landmark study showed benzo[a]pyrene’s interaction with p53 mirrored mutations found in actual human lung tumours. This finding provided strong molecular evidence of the direct carcinogenic effect of a tobacco smoke constituent.
Stanton Glantz (University of California, San Francisco, USA) and colleagues examined 43 previously confidential tobacco industry documents relating to p53 and tobacco smoke. The researchers found that prior to 1996, several tobacco companies supported research projects investigating the mechanisms of p53 mutations. Following the 1996 landmark study, tobacco companies planned a number of research projects in response and supported studies which appeared to cast doubt on a link between p53 damage and benzo[a]pyrene in tobacco smoke.
In two instances research arguing against a connection was undertaken and published by individuals with links to tobacco companies. Both studies were published in a journal, whose editor-in-chief has an extensive and undisclosed history of working as a tobacco industry researcher and consultant.
Professor Glantz comments: “The tobacco companies claim that they are now working with the public health community to ‘support a single, consistent public health message on the role played by cigarette smoking in the development of the disease in smokers.’ But their multifaceted response to p53 research as recently as 2001, suggests that they have not changed their practices.”
Professor Glantz adds: “The extent and sophistication of the tobacco industry involvement in p53 research challenge authors, editors and users of scientific literature to be vigilant in demanding and maintaining rigorous standards for disclosing and evaluating potential conflicts of interest. Universities and other biomedical researchers should stop taking money from the tobacco industry in order to minimise the potential for any impairment of the integrity of the scientific process.” (Quote by e-mail; does not appear in published paper)
Contact: Professor Stanton A Glantz, Center for Tobacco Control Research and Education, Box 1390, University of California, 530 Parnassus Avenue San Francisco, CA 94143-0130, USA. T) +1 415 476 3893 [email protected]