Analysis of lung cancer incidence in the Nurses' Heath and the Health Professionals' Follow-Up Studies using a multistage carcinogenesis model

Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109-1024, USA.
Cancer Causes and Control (Impact Factor: 2.74). 05/2008; 19(3):317-28. DOI: 10.1007/s10552-007-9094-5
Source: PubMed

ABSTRACT We analyzed lung cancer incidence among non-smokers, continuing smokers, and ex-smokers in the Nurses Health Study (NHS) and the Health Professionals Follow-Up Study (HPFS) using the two-stage clonal expansion (TSCE) model. Age-specific lung cancer incidence rates among non-smokers are identical in the two cohorts. Within the framework of the model, the main effect of cigarette smoke is on the promotion of partially altered cells on the pathway to cancer. Smoking-related promotion is somewhat higher among women, whereas smoking-related malignant conversion is somewhat lower. In both cohorts the relative risk for a given daily level of smoking is strongly modified by duration. Among smokers, the incidence in NHS relative to that in HPFS depends both on smoking intensity and duration. The age-adjusted risk is somewhat larger in NHS, but not significantly so. After smokers quit, the risk decreases over a period of many years and the temporal pattern of the decline is similar to that reported in other recent studies. Among ex-smokers, the incidence in NHS relative to that in HPFS depends both on previous levels of smoking and on time since quitting. The age-adjusted risk among ex-smokers is somewhat higher in NHS, possibly due to differences in the age-distribution between the two cohorts.

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Available from: Rafael Meza, Apr 04, 2015
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    • "Every 2 years the participants respond to questionnaires on disease risk factors including smoking. We employed the tabled age-specific lung cancer incidence rates stratified by smoking status for Caucasians as published in Meza et al. 2008 (10). These rates are used in this analysis for fitting the TSCE model for women. "
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    ABSTRACT: Lung cancer is the leading cancer killer for both men and women worldwide. Over 80% of lung cancers are attributed to smoking. In this analysis, the authors propose to use a two-stage clonal expansion (TSCE) model to predict an individual's lung cancer risk based on gender and smoking history. The TSCE model is traditionally fitted to prospective cohort data. Here, the authors describe a new method that allows for the reconstruction of cohort data from the combination of risk factor data obtained from a case-control study, and tabled incidence/mortality rate data, and discuss alternative approaches. The method is applied to fit a TSCE model based on smoking. The fitted model is validated against independent data from the control arm of a lung cancer chemoprevention trial, CARET, where it accurately predicted the number of lung cancer deaths observed.
    International Journal of Cancer 10/2011; 129(8):1907-13. DOI:10.1002/ijc.25834 · 5.09 Impact Factor
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    • "Knoke JD et al. [17], in a study with results later confirmed by other studies [18], concluded that the duration of smoking for a patience is more important to take into account in terms of risk for developing Warthin tumor than the number of smoked cigarettes. Meza R et al. [19] assess in their study the likelihood for appearance of Warthin tumor both for smokers and for people who have stopped smoking. They concluded that after the cessation of smoking Warthin tumor risk decreases over a period of 15–25 years. "
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    ABSTRACT: Warthin tumor is the second most common benign tumors of the parotid gland, after pleomorphic adenoma. Our study was performed on 21 cases with Warthin tumor diagnosed between 2005-2010, which were analyzed clinically, histologically and immunohistochemically, using anti-CD20 and anti-CD45RO antibodies. The analysis of age distribution within the investigated cases indicated that Warthin tumor incidence is increasing in the seventh decade of life, most patients being male (M/F 5/2). Histopathological, the analysis report of stroma÷parenchyma in 14 cases revealed a balanced distribution of the two components, in four cases, the epithelial component was predominant and in three cases, the stromal component was predominant. Immunohistochemical study for the two specific lymphocyte proliferation markers indicated positivity for both epithelial component and stroma. Cell layout of CD45RO and CD20cy at the level of lymphoid stroma had a similar pattern with normal or reactive lymph nodes.
    Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie 01/2011; 52(4):1319-23. · 0.66 Impact Factor
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    • " pathogenetic differences , appear to share such similarity in the analytic features of their respective age-specific incidence is noteworthy. Both cancers exhibit an exponential phase that can be attributed to uniform promotion, that is, the constant slow clonal expansion of initiated (premalignant) clones. There appears to be no hint in the data Meza et al. PNAS October 21, 2008 vol. 105 no. 42 16287 that multiple expansive stages, with disparate growth rates, are involved. Strikingly, the expansion rate parameters, α − β, are very similar for these two cancers (in the range of 0.14–0.18 per year for the three-stage model, and 0.14–0.19 per year for the four-stage model; see SI Appendix, Tables 1 and 2). Becaus"
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    ABSTRACT: The observation that the age-specific incidence curve of many carcinomas is approximately linear on a double logarithmic plot has led to much speculation regarding the number and nature of the critical events involved in carcinogenesis. By a consideration of colorectal and pancreatic cancers in the Surveillance Epidemiology and End Results (SEER) registry we show that the log-log model provides a poor description of the data, and that a much better description is provided by a multistage model that predicts two basic phases in the age-specific incidence curves, a first exponential phase until the age of approximately 60 followed by a linear phase after that age. These two phases in the incidence curve reflect two phases in the process of carcinogenesis. Paradoxically, the early-exponential phase reflects events between the formation (initiation) of premalignant clones in a tissue and the clinical detection of a malignant tumor, whereas the linear phase reflects events leading to initiated cells that give rise to premalignant lesions because of abrogated growth/differentiation control. This model is consistent with Knudson's idea that renewal tissue, such as the colon, is converted into growing tissue before malignant transformation. The linear phase of the age-specific incidence curve represents this conversion, which is the result of recessive inactivation of a gatekeeper gene, such as the APC gene in the colon and the CDKN2A gene in the pancreas.
    Proceedings of the National Academy of Sciences 11/2008; 105(42):16284-9. DOI:10.1073/pnas.0801151105 · 9.67 Impact Factor
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