Research article Special Issues

The effect of cigarette smoking on lung cancer evolution

  • Received: 07 July 2019 Accepted: 08 August 2019 Published: 23 August 2019
  • The aim of this paper is to elucidate the risk of lung carcinogenesis from cigarette smoking among current and former smokers. To achieve this goal, we have set up a stochastic three-stage model to fit the data of Surveillance, Epidemiology, and End Results (SEER) program besides the data set of smoking derived from the Nurses' Health Study cohort of females (NHS) and the Health Professionals Follow up Study cohort of men (HPFS). The calculations are performed by considering both mutation and clonal expansion rates as parameters in each compartment. For current smokers, our findings show that cigarette smoking has more significant impact on the mutation rates of cells than the clonal expansion rates of premalignant cells among men and women. In particular, for male patients, cigarette smoking affects the mutation in normal cells and the transformation from premalignant cells to malignant ones in the optimal model. In addition, cigarette smoking induces only the initial mutation rates in normal cells among American women. For current and former smokers, cigarette smoking stimulates only the clonal expansion rate of the first premalignant cells in both sexes. However, we find that the impact of cigarette smoking is minimal in former smokers who have stopped smoking for over ten years among men and women in US.

    Citation: Ahmed Nagah, Asmaa Amer, Xinan Zhang. The effect of cigarette smoking on lung cancer evolution[J]. Mathematical Biosciences and Engineering, 2019, 16(6): 7771-7788. doi: 10.3934/mbe.2019390

    Related Papers:

  • The aim of this paper is to elucidate the risk of lung carcinogenesis from cigarette smoking among current and former smokers. To achieve this goal, we have set up a stochastic three-stage model to fit the data of Surveillance, Epidemiology, and End Results (SEER) program besides the data set of smoking derived from the Nurses' Health Study cohort of females (NHS) and the Health Professionals Follow up Study cohort of men (HPFS). The calculations are performed by considering both mutation and clonal expansion rates as parameters in each compartment. For current smokers, our findings show that cigarette smoking has more significant impact on the mutation rates of cells than the clonal expansion rates of premalignant cells among men and women. In particular, for male patients, cigarette smoking affects the mutation in normal cells and the transformation from premalignant cells to malignant ones in the optimal model. In addition, cigarette smoking induces only the initial mutation rates in normal cells among American women. For current and former smokers, cigarette smoking stimulates only the clonal expansion rate of the first premalignant cells in both sexes. However, we find that the impact of cigarette smoking is minimal in former smokers who have stopped smoking for over ten years among men and women in US.


    加载中


    [1] D. M. Parkin, F. Bray, J. Ferlay, et al., Global cancer statistics, 2002 , CA Cancer J. Clin., 55 (2005), 74–108.
    [2] R. L. Siegel, K. D. Miller and A. Jemal, Cancer statistics, 2015, CA Cancer J. Clin., 65 (2015), 5–29.
    [3] M. Malvezzi, G. Carioli, P. Bertuccio, et al., European cancer mortality predictions for the year 2016 with focus on leukaemias, Ann. Oncol., 27 (2016), 725–731.
    [4] J. Ferlay, I. Soerjomataram, Dikshit, et al., Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012, Int. J. Cancer, 136 (2015), E359–E386.
    [5] J. Malhotra, M. Malvezzi, E. Negri, et al., Risk factors for lung cancer worldwide, Eur. Resp. J., 48 (2016), 889–902.
    [6] S. Sun, J. H. Schiller and A. F. Gazdar, Lung cancer in never smokersa different disease, Nat. Rev. Cancer, 7 (2007), 778–790.
    [7] A. Blair and L. B. Freeman, Lung cancer among nonsmokers, Epidemiology, 17 (2006), 601–613.
    [8] R. W. Field and B. L. Withers, Occupational and environmental causes of lung cancer, Clin. Chest Med., 33 (2012), 681–703.
    [9] C. S. D. Cruz, L. T. Tanoue and R. A. Matthay, Lung cancer: Epidemiology, etiology, and prevention, Clin. Chest Med., 32 (2011), 605–644.
    [10] S. Wu, S. Powers, W. Zhu, et al., Substantial contribution of extrinsic risk factors to cancer development, Nature, 529 (2016), 43–47.
    [11] G. Ray, D. E. Henson and A. M. Schwartz, Cigarette smoking as a cause of cancers other than lung cancer: An exploratory study using the Surveillance, Epidemiology, and End Results Program, Chest, 138 (2010), 491–499.
    [12] S. D. Coello, A. C. De Len, F. B. Ojeda, et al., High density lipoprotein cholesterol increases with living altitude, Int. J. Epidemiol., 29 (2000), 65–70.
    [13] V. L. Roger, M. E. Farkouh, S. A. Weston, et al., Sex differences in evaluation and outcome of unstable angina, JAMA, 283 (2000), 646–652.
    [14] M. Mori, M. Hara, I. Wada, et al., Prospective study of hepatitis B and C viral infections, cigarette smoking, alcohol consumption, and other factors associated with hepatocellular carcinoma risk in Japan, Am. J. Epidemiol., 151 (2000), 131–139.
    [15] K. Husgafvel-Pursiainen, P. Boffetta, A. Kannio, et al., p53 mutations and exposure to environ-mental tobacco smoke in a multicenter study on lung cancer, Cancer Res., 60 (2000), 2906–2911.
    [16] T. L. Holmen, E. Barrett-Connor, J. Holmen, et al., Health problems in teenage daily smokers versus nonsmokers, Norway, 1995–1997: The Nord-Trndelag Health Study, Am. J. Epidemiol., 151 (2000), 148–155.
    [17] G. Launoy, C. Milan, J. Faivre, et al., Tobacco type and risk of squamous cell cancer of the oesophagus in males: A French multicentre case-control study, Int. J. Epidemiol., 29 (2000), 36–42.
    [18] F. Barbone, M. Bovenzi, F. Cavallieri, et al., Cigarette smoking and histologic type of lung cancer in men, Chest, 112 (1997), 1474–1479.
    [19] L. M. Nelson, V. McGuire, W. T. Longstreth Jr, et al., Population-based case-control study of amyotrophic lateral sclerosis in western Washington State. I. Cigarette smoking and alcohol consumption, Am. J. Epidemiol., 151 (2000), 156–163.
    [20] K. Leffondr, M. Abrahamowicz, J. Siemiatycki, et al., Modeling smoking history: A comparison of different approaches, Am. J. Epidemiol., 156 (2002), 813–823.
    [21] R. Doll and R. Peto, Cigarette smoking and bronchial carcinoma: dose and time relationships among regular smokers and lifelong non-smokers, J. Epidemiol. Commun. Health, 32 (1978), 303–313.
    [22] W. D. Flanders, C. A. Lally, B. P. Zhu, et al., Lung cancer mortality in relation to age, duration of smoking, and daily cigarette consumption: results from Cancer Prevention Study II, Cancer Res., 63 (2003), 6556–6562.
    [23] C. O. Nordling, A new theory on the cancer-inducing mechanism, British J. Cancer, 7 (1953), 68–72.
    [24] P. Armitage and R. Doll, The age distribution of cancer and a multi-stage theory of carcinogenesis, British J. Cancer, 8 (1954), 1–12.
    [25] I. Tomlinson and W. Bodmer, Selection, the mutation rate and cancer: ensuring that the tail does not wag the dog, Nat. Med., 5 (1999), 11–12.
    [26] K. Anderson, C. Lutz, F. W. Van Delft, et al., Genetic variegation of clonal architecture and propagating cells in leukaemia, Nature, 469 (2011), 356–361.
    [27] M. Gerlinger, S. Horswell, J. Larkin, et al., Genomic architecture and evolution of clear cell renal cell carcinomas defined by multiregion sequencing, Nat. Genet., 46 (2014), 225–233.
    [28] M. R. Stratton, P. J. Campbell and P. A. Futreal, The cancer genome, Nature, 458 (2009), 719–724.
    [29] L. D. Wood, D. W. Parsons, S. Jones, et al., The genomic landscapes of human breast and colorectal cancers, Science, 318 (2007), 1108–1113.
    [30] H. M. Byrne, Dissecting cancer through mathematics: from the cell to the animal model, Nat. Rev. Cancer, 10 (2010), 221–230.
    [31] S. H. Moolgavkar, A. Dewanji and G. Luebeck, Cigarette smoking and lung cancer: reanalysis of the British doctor's data, J. Nat. Cancer Inst., 81 (1989), 415–420.
    [32] A. S. Whittemore, Effect of cigarette smoking in epidemiological studies of lung cancer, Statist. Med., 7 (1988), 223–238.
    [33] M. Gaffney and B. Altshuler, Examination of the Role of Cigarette Smoke in Lung Carcinogenesis Using Multistage Models, J. Nat. Cancer Inst., 80 (1988), 925–931.
    [34] S. H. Moolgavkar and A. G. Knudson, Mutation and cancer: A model for human carcinogenesis, J. Nat. Cancer Inst., 66 (1981), 1037–1052.
    [35] R. Meza, W. D. Hazelton, G. A. Colditz, et al., Analysis of lung cancer incidence in the nurses health and the health professionals follow-up studies using a multistage carcinogenesis model, Cancer Causes Control, 19 (2008), 317–328.
    [36] Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database: Incidence-SEER 13 Regs Research Data, Nov 2012 Sub (1992-2010) $<$Katrina/Rita Population Adjustment$>$, National Cancer Institute, DCCPS, Surveillance Research Program, Surveillance Systems Branch, released April 2013, based on the November 2012 submission.
    [37] D. R. Lewis, D. P. Check, N. E. Caporaso, et al., US lung cancer trends by histologic type, Cancer, 120 (2014), 2883–2892.
    [38] C. Bain, D. Feskanich, F. E. Speizer, et al., Lung cancer rates in men and women with comparable histories of smoking, J. Nat. Cancer Inst., 96 (2004), 826–834.
    [39] D. Hanahan and R. A. Weinberg, Hallmarks of cancer: The next generation, Cell, 144 (2011), 646–674.
    [40] T. E. Harris, The theory of branching processes, Prentice-Hall Applied Mathematics Series, Englewood CLiffs, NJ, 2002.
    [41] C. Tomasetti, L. Marchionni, M. A. Nowak, et al., Only three driver gene mutations are required for the development of lung and colorectal cancers, Proceed. Nat. Aca. Sci., 112 (2015), 118–123.
    [42] L. Li, T. Tian and X. Zhang, The impact of radiation on the development of lung cancer, J. Theor. Biol., 428 (2017), 147–152.
    [43] L. A. Loeb, K. R. Loeb and J. P. Anderson, Multiple mutations and cancer, Proceed. Nat. Aca. Sci., 100 (2003), 776–781.
    [44] L. A. Loeb, Mutator phenotype may be required for multistage carcinogenesis, Cancer Res., 51 (1991), 3075–3079.45. H. Schllnberger, N. Beerenwinkel, R. Hoogenveen, et al., Cell selection as driving force in lung and colon carcinogenesis, Cancer Res., 70 (2010), 6797–6803.
    [45] 46. W. F. Heidenreich, E. G. Luebeck and S. H. Moolgavkar, Some properties of the hazard function of the twomutation clonal expansion model, Risk Anal., 17 (1997), 391–399.
    [46] 47. R. Meza, J. Jeon, S. H. Moolgavkar, et al., Age-specific incidence of cancer: Phases, transitions, and biological implications, Proceed. Nat. Aca. Sci., 105 (2008), 16284–16289.
  • Reader Comments
  • © 2019 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(4182) PDF downloads(635) Cited by(2)

Article outline

Figures and Tables

Figures(3)  /  Tables(10)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog