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Biologia i chemia nowotworu płuca

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Warianty tytułu
EN
Biology and chemistry of lung cancer
Języki publikacji
PL
Abstrakty
EN
Lung cancer is the most common fatal cancer disease in the world. A characteristic feature of lung cancer is genetic diversity. In the overwhelming majority of cases, smoking is the most important etiopathogenic factor. Lung cancer is a cancer with a very bad prognosis regarding long-term survival. The risk of lung cancer depends primarily on active or passive exposure to the carcinogenic components of tobacco smoke. According to available data, the development of lung cancer in addition to active and passive smoking is directly affected by environmental pollution such as smog and fumes, ionizing radiation, mycotoxins and long-term exposure to asbestos (occupational exposure). Research on the pharmacoprevention of lung cancer began over 30 years ago. The first nutrient that the researchers said could inhibit the development of lung cancer was beta carotene. Unfortunately, long-term regular supplementation with high doses of antioxidant in the form of beta-carotene brought the opposite effect. An increase in the incidence of lung cancer was found in people who received beta carotene in the form of a synthetic food supplement. The other component tested was N-acetylcysteine. It is a sulfur compound and a powerful antioxidant that supports the synthesis of glutathione and cysteine, with destructive effects on carcinogenic substances. N-acetyl-cysteine, used in the form of NAC adduct and epigallocatechin-3-gallate, showed efficacy in inhibiting the development of lung cancer only in animal models. In the pharmacoprevention of lung cancer, the use of vitamin E was also tested in the form of tocotrienol and tocopherol. The following work also shows the existence of a high concentration correlation which belongs to the steroid hormone, mainly estrogen, in the blood and the development of lung cancer in women. An increased risk of lung cancer has been observed in women undergoing long-term hormone replacement therapy. The results show that 2-methoxyestradiol, the endogenous metabolite of 17ß-estradiol, shows positive results that inhibit the growth of lung cancer cell lines. The aim of the work was to present the correlation between tobacco abuse and passive smoking and lung cancer, pharmacoprevention of lung cancer and the association of elevated estrogen concentration in women with an increased risk of lung cancer.
Rocznik
Strony
505--522
Opis fizyczny
Bibliogr. 34 poz., schem.
Twórcy
  • Katedra i Zakład Chemii Medycznej, Gdański Uniwersytet Medyczny
  • Klinika Onkologii i Radioterapii Gdańskiego Uniwersytetu Medycznego
  • Katedra i Zakład Chemii Medycznej, Gdański Uniwersytet Medyczny
autor
  • Katedra i Zakład Chemii Medycznej, Gdański Uniwersytet Medyczny
  • Katedra i Zakład Chemii Medycznej, Gdański Uniwersytet Medyczny
Bibliografia
  • [1] H.H. Hansen, Lung cancer: European commission: series for general practitioners. Springer- Verlag, Berlin, 1990.
  • [2] H. Lemjabbar-Alaoui, O. UI Hassan, Y. Yang, P. Buchanan, Lung cancer: Biology and treatment options. Biochim. Biophys. Acta, 2015, 2, 189.
  • [3] D.F. Church, W.A. Pryor, Free-radical chemistry of cigarette smoke and its toxicological implications. Environ. Health Perspect., 1985, 64, 111.
  • [4] D.M. Parkin, F. Bray, J. Ferlay, Global cancer statistics, 2002. CA Cancer J. Clin., 2005, 55(2), 74.
  • [5] R.A. Schnoll, E. Martinez, K. L. Tatum, D. M. Weber, N. Kuzla, M. Glass, J.A.A. Ridge, C. Langer, C. Miyamoto, E. P. Wileyto, F. Leone, A bupropion smoking cessation clinical trial for cancer patients. Cancer Causes Control, 2010, 21(6), 811.
  • [6] J.K. Cataldo, S. Dubey, J.J. Prochaska, Smoking cessation: An integral part of lung cancer treatment. Oncology, 2010, 78(5-6), 289.
  • [7] S.S. Hecht, Tobacco carcinogens, their biomarkers and tobacco-induced cancer. Nat. Rev. Cancer, 2003, 3(10), 733.
  • [8] C.H. Chan, C.F. Hsiao, G.C. Chang, Interactive effect of cigarette smoking with human 8- oxoguanine DNA N-glycosylase 1 (hOGG1) polymorphisms on the risk of lung cancer: a case-control study in Taiwan. Am. J. Epidemiol., 2009, 170, 695.
  • [9] J.M. Samet, E. Avila-Tong, P. Boffetta, Lung cancer in never smokers: clinical epidemiology and environmental risk factors. Clin. Can. Res., 2009, 15, 5626.
  • [10] C.M. Tammemagi, C. Neslund-Dudas, M. Simoff, Smoking and lung cancer survival: the role of comorbidity and treatment. Chest, 2004, 125, 27.
  • [11] R. Goralczyk, Beta-carotene and lung cancer in smokers: review of hypotheses and status of research. Nutr. Cancer, 2009, 61(6), 767.
  • [12] D. Albanes, O.P. Heinonen, P.R. Taylor, a-tocopherol and ß-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance. J. Natl. Cancer Inst., 1996, 88(21), 1560.
  • [13] Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group, The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N. Engl. J. Med., 1994, 330(15),1029.
  • [14] G.E. Goodman, M.D. Thornquist, J. Balmes, The beta-carotene and retinol efficacy trial: incidence of lung cancer and cardiovascular disease mortality during 6-year follow-up after stopping ß-carotene and retinol supplements. J. Natl. Cancer Inst. 2004, 96(23),1743.
  • [15] W. MacNee, M.M.E. Bridgeman, M. Marsden, The effects of N-acetylcysteine and glutathione on smoke induced changes in lung phagocytes and epithelial cells. Am. J. Med. 1991, 91(3), 60.
  • [16] S. De Flora, M. Astengo, D. Serra, Inhibition of urethan-induced lung tumors in mice by dietary N-acetylcysteine. Cancer Lett. 1986, 32(3), 235.
  • [17] J.D. Lambert, C.S. Yang, Cancer chemopreventive activity and bioavailability of tea and tea polyphenols. Mutat. Res. 2003, 523-524, 201-208.
  • [18] J.V. Higdon, B. Frei, Tea catechins and polyphenols: health effects, metabolism, and antioxidant functions. Crit. Rev. Food Sci. Nutr. 2003, 43(1), 89.
  • [19] S. Sang, M.J. Lee, Z. Hou, C.T. Ho, C.S. Yang. Stability of tea polyphenol (-)-epigallocatechin-3-gallate and formation of dimers and epimers under common experimental conditions. J. Agric. Food Chem. 2005; 53(24), 9478.
  • [20] J.D. Lambert, S. Shengmin, S.Y. Chung, N-Acetylcysteine enhances the lung cancer inhibitory effect of epigallocatechin-3-gallate and forms a new adduct, Free Radic. Biol. Med., 2008, 44(6), 1069.
  • [21] M.B. Schabath, Wu X, R. Vassilopoulou-Sellin, A.A. Vaporciyan, M.R. Spitz, Hormone replacement therapy and lung cancer risk: a case-control analysis. Clin. Cancer Res. 2004, 1, 113.
  • [22] N. Ramnath, R.J. Menezes, G. Loewen, Hormone replacement therapy as a risk factor for non-small cell lung cancer: results of a case-control study. Oncology. 2007, 10, 305.
  • [23] B.J. Deroo, K.S. Korach, Estrogen receptors and human disease. J. Clin. Invest, 2006, 116(3), 561.
  • [24] H.O. Adami, I. Persson, R. Hoover, C. Schairer, L. Bergkvist, Risk of cancer in women receiving hormone replacement therapy. Int. J. Cancer. 1989; 44(5), 833.
  • [25] E. Taioli, E.L. Wynder, Endocrine factors and adenocarcinoma of the lung in women, J. Natl Cancer Inst. 1994, 86(11), 869.
  • [26] T. Mukhopadhyay, J.A. Roth, Induction of apoptosis in human lung cancer cells after wild-type p53 activation by methoxyestradiol. Oncogene, 1997, 14(3), 379.
  • [27] T. M. LaVallee, X. H. Zhan, C. J. Herbstritt, E. C. Kough, S. J. Green, V. S. Pribluda, 2-Methoxyestradiol inhibits proliferation and induces apoptosis independently of estrogen receptors a and ß. Cancer Reaserch, 62, 2002, 3691.
  • [28] www.cancer.gov/publications/dictionaries/cancer-drug/def/Z-m^o^esfradiol [dostęp: 2019-04-11]
  • [29] G. Schumacher, 2-Methoxyestradiol als neue Substanz zur Behandlung solider Tumore, Medizinischen Fakultät Charité der Humboldt-Universität zu Berlin, 2004.
  • [30] J. Jihyeung S. C. Picinich, Z. Yang, Y. Zhao, N. Suh, A.N. Kong S.C. Yang, Cancer-preventive activities of tocopherols and tocotrienols. Carcinogenesis, 2010, 31(4), 533.
  • [31] Q. Jiang, S. Christen, M.K. Shigenaga, B.N. Ames, γ-tocopherol, the major form of vitamin E in the US diet, deserves more attention. Am. J. Clin. Nutr. 2001, 74(6), 714.
  • [32] Alpha-Tocopherol Beta-Carotene Cancer Prevention Study Group. The effect of vitamin E and beta-carotene on the incidence of lung cancer and other cancers in male smokers. N. Engl. J. Med. 1994, 52(7), 1029.
  • [33] F.E. Speizer, G.A. Colditz, D.J. Hunter, B. Rosner, C. Hennekens, Prospective study of smoking, antioxidant intake, and lung cancer in middle-aged women (USA). Cancer Causes Control, 1999, 10(5), 475.
  • [34] G. Wang, B. Yu, Y. Wu, Controlled preparation and antitumor efficacy of vitamin E TPGS- functionalized PLGA nanoparticles for delivery of paclitaxel. Int. J. Pharm., 2013, 446(1-2), 24.
Uwagi
Opracowanie rekordu w ramach umowy 509/P-DUN/2018 ze środków MNiSW przeznaczonych na działalność upowszechniającą naukę (2019).
Typ dokumentu
Bibliografia
Identyfikator YADDA
bwmeta1.element.baztech-dba8fd2d-4bee-46e4-9209-f5d236c62842
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