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Susceptibility to lung cancer

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From a Conference report: Highlights of the 6th Joint Conference of the American Association for Cancer Research and the Japanese Cancer Association held Jan 25-29,2004 in Waikoloa, Hawaii, as reprinted in Medscape General Medicine 6(1), 2004 , Kris Novak, PhD. Posted 03/03/2004.

Introduction ... " The Aim... was to bring together diverse groups of cancer researchers to share information..."

SUSCEPTIBILITY TO LUNG CANCER:Many of the presenters at the conference are undertaking a broad, multifaceted approach to dissecting cancer pathogenesis. For example, Dr Margaret Spitz of the MD Anderson Cancer Center, Houston, and colleagues have incorporated epidemiologic, genetic, and molecular research to investigate individual susceptibility to lung cancer. Since only a fraction of long term smokers develop lung cancer, researchers are using a variety of approaches to identify these high-risk subgroups for prevention strategies. A combination of factors, including genetics, smoking history, diet and other environmental exposures contribute to this risk.

In a recent study, Spitz's group evaluated the association between dietary folate intake and risk of lung cancer in a population of 470 histopathologically confirmed lung cancer cases, compared with 472 cancer-free individuals. Participants were matched for age, sex, and ethnicity. Spitz reported a significant inverse dose-response relationship between increasing dietary folate, and decreasing risk of lung cancer. A more pronounced inverse association between dietary folate intake and lung cancer risk was observed among subjects who drank alcohol, those who had smoked relatively more, those who did not take supplemental folate, and those who reported a family history of lung cancer. So there appears to be a possible protective role of dietary folate in lung carcinogenesis.

One of the ways in which tobacco causes carcinogenesis is by inducing DNA damage -- DNA strand breaks, crosslinking,oxidation, or formation of adducts. Normalcells repair this damage through DNA repair pathways, but defects in this repair process can cause a cell to become cancerous. People with defects in DNA repair mechanisms, such as those with xeroderma pigmentosum, are more susceptible to lung tumors and other types of cancer.

Spitz wanted to see if an individual's ability to repair damaged DNA was associated with lung cancer risk, so her group developed an assay to test the DNA repair capacity of an individual's cells.This assay tested the ability of cells to repair small circles of DNA called plasmids, which were damaged by the carcinogens benzo[a]pyrene -- a major constitutent of tobacco smoke. Her study involved more than 400 cases and 400 controls, and demonstrated that as an individual's DNA repair capacity increased, their probability of becoming a lung cancer patient decreased. Among lung cancer patients, those that had never smoked had the poorest DNA repair capacity, and long term smokers had the highest DNA repair capacity.

Of note, the women in the trial had lower DNA repair capacities than men. Furthermore, white individuals had more efficient DNA repair mechanisms than African American individuals, a result that may explain some of the differences seen in cancer mortality between these 2 groups. There was also a correlation between dietary folat intake and DNA repair capacity in the healthy population, indicating that folate modulates DNA repair ability.

Goes on to discuss DNA methylation and cancer prognosis, alternative ways to inactivate tumor suppressors, mechanisms of metastasis, tumor environment interactions (location within the body), and ends with a discussion of stomach cancer and Helicobacter pylori, with a tie in to the East Asian strains of H pylori, and a possible connection with the higher incidence of gastric carcioma observed in many East Asian countries.

Just for fun, since it keeps coming up in discussions about non-smokers...



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