Early-life family structure and cancer risk.

Early-Life Family Structure and Microbially Induced Cancer Risk

Martin J. Blaser1,2,3, Abraham Nomura4, James Lee4, Grant N. Stemmerman4,5, Guillermo I. Perez-Perez1

1 Department of Medicine, New York University School of Medicine, New York, New York, United States of America, 2 Department of Microbiology, New York University School of Medicine, New York, New York, United States of America, 3 Veterans Administration Medical Center, New York, New York, United States of America, 4 Kuakini Medical Center and University of Hawaii, Honolulu, Hawaii, United States of America, 5 University of Cincinnati, Cincinnati, Ohio, United States of America

Cancer is generally a disease of old age with mortality rates increasing with each succeeding decade of life. However, for many forms of cancer, the relevant risks are conferred by exposure to environmental agents decades earlier. Long latencies between exposure to a carcinogen and clinical expression of malignancy occur with asbestos and mesothelioma, cigarette smoking and lung cancer, and hepatitis B virus and hepatoma. Adenocarcinoma of the stomach, one of the most common causes of cancer death in the world, clearly follows this pattern.

Carriage of the gram-negative gastric bacterium, Helicobacter pylori, increases the risk for development of gastric adenocarcinoma. H. pylori is predominantly acquired in childhood, most commonly after the first year of life; perinatal transmission is uncommon. Family size and birth order affect transmission; later-born children from large sibships are at greatest risk for acquiring the organism. Such observations suggest that sibling-to-sibling transmission is critical, and the progressive disappearance of H. pylori seen with socioeconomic development is consistent with falling family sizes. For hepatitis B virus, birth order influences risk of disease, and for measles, viral acquisition from a family member increases disease severity. Studies of migrants have shown that early life is the window for the critical environmental exposure that heightens gastric cancer risk; the most important environmental risk factor for gastric cancer is acquisition of H. pylori. Since early-life family structure affects microbial transmission, we hypothesized that it would influence risk of H. pylori-associated gastric cancer. Consistent with this notion has been the repeated observation that gastric cancer risk is related to the number of siblings during childhood.

H. pylori strains can be characterized by the presence or absence of the cag island, a 35–40-kb chromosomal region containing type IV secretion system genes that encode proteins that inject the CagA protein into the host epithelium]. The cagA status of the H. pylori cells colonizing a host can be determined by the presence of serum IgG antibodies to the CagA protein. Compared with cagA- strains, carriage of cagA+ H. pylori strains is associated with increased risk of both premalignant lesions and gastric cancer.

(Reprinted under Creative Commons Attribution License from http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1...)

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