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İnsan Kanserlerinin Etiyolojisinde Gen-Çevre Etkileşiminin Rolü

Yıl 2021, Cilt: 8 Sayı: 2, 30 - 37, 30.12.2021

Öz

Kanser, tüm dünyada ikinci önde gelen ölüm nedeni olarak sınıflandırılmaktadır. 2018'de meydana gelen her altı ölümden biri kanserden kaynaklanmıştır. Gen-çevre etkileşiminde en önemli odak noktası yerleşik kanser risk faktörlerinin metabolizmasında yer alan enzimleri kodlayan genlerdir. Bu genlerin, metabolizmayı değiştirebilen ve kanserojenlere maruziyeti artıran veya azaltan dolayısıyla kanser riskini etkileyen yaygın varyant formları vardır. Çeşitli epidemiyolojik ve deneysel çalışmalar, birçok insan hastalığının sadece belirli genetik ve çevresel faktörlerden değil, aynı zamanda gen-çevre etkileşimlerinden kaynaklandığını göstermiştir. Son yıllarda kanserin ne tamamen genetik ne de tamamen çevresel etmenlerden oluştuğu daha da açık bir şekilde ortaya konmuştur. Genetik polimorfizmlerin, insanların kansere ve diğer kronik hastalık durumlarına duyarlılığında kritik bir rol oynadığı geniş çapta bildirilmiş olmasına rağmen, birçok tek nükleotid polimorfizmine (SNP'ler), insanların çevresel stresörlere maruz kalmasından kaynaklanan somatik mutasyonlar neden olmaktadır. Bilimsel kanıtlar, birçok kanserin etiyolojisinin ve patogenizinin genetik ve çevre arasındaki ortak etkiden kaynaklandığını göstermektedir. Araştırmalar ayrıca çevresel faktörlerin spesifik allelik varyantlarla etkileşimlerinin hastalıklara karşı hassasiyeti oldukça değiştirdiğine dikkat çekmiştir. Bu derlemede, gen-çevre etkileşimlerinin doğasına genel bir bakış sağlamanın yanında bazı kanserlerin etkisine vurgu yaparak insan kanserlerindeki rollerini tartışıyoruz.

Kaynakça

  • World Health Organization. World Cancer Report 2014; Steward, B.W., Wild, C.P., Eds.; International Agency for Research on Cancer: Lyon, France, 2014.
  • Vogelstein B, Kinzler KW. The Genetic Basis of Human Cancer. 2nd ed: New York, NY; 2002.
  • Brennan P. Gene-environment interaction and aetiology of cancer: what does it mean and how can we measure it? Carcinogenesis. 2002; 23(3): 381-7.
  • Murcray CE, Lewinger JP, Gauderman WJ. Gene-environment interaction in genome-wide association studies. Am J Epidemiol. 2009;169(2): 219–226.
  • Parsa N. Environmental Factors Inducing Human Cancers. Iran. J. Public Health. 2012; 41: 1–9.
  • Simonds NI, Ghazarian AA, Pimentel CB, Schully SD, Ellison GL, Gillanders EM, et al. Review of the Gene-Environment Interaction Literature in Cancer: What do we know? Genet Epidemiol. 2017; 40: 356–365.
  • Hutter CM, Mechanic LE, Chatterjee N, Kraft P, Gillanders EM. Geneenvironment interactions in cancer epidemiology: a National Cancer Institute Think Tank report. Genet Epidemiol. 2013; 37(7): 643–657.
  • Department of Health and Human Services. Analysis of genomewide gene-environment (GxE) interactions (R21). 2013; PAR-13-382. Erişim adresi: http://grants.nih.gov/grants/guide/pa-files/PAR-13-382.html
  • National Cancer Institute. Genetic associations and mechanisms in oncology (GAME-ON): A post-genome wide association initiative; 2012. Erişim adresi: http://epi.grants.cancer.gov/gameon/.
  • Thomas DC. Methods for investigating gene-environment interactions in candidate pathway and genome-wide association studies. Annu. Rev. Public Health. 2010; 31: 21–36.
  • Vekasalo PK, Kaprio J, Koskenvuo M, Pukkala E. Genetic predisposition, environment and cancer incidence: A nation wide twin study in Findland, 1976–1995. Int. J. Cancer. 1999; 83: 743–749.
  • Liu G, Mukherjee B, Lee S, Lee A, Wu AH, Bandera EV, et al. Practice of Epidemiology Robust Tests for Additive Gene-Environment Interaction in Case-Control Studies Using Gene-Environment Independence. Hum. Mol. Genet. 2018; 187: 366–377.
  • Smith PG, Day NE. The Design of Case-Control Studies: The Influence of Confounding and Interaction Effects. Int. J. Epidemiol. 1984; 13: 356–365.
  • Smith GD, Hemani G. Mendelian randomization: Genetic anchors for causal inference in epidemiological studies. Int. J. Epidemiol. 2014; 23: R89–R98.
  • Lissowska J, Gaudet MM, Brinton LA, Chanock SJ, Peplonska B, Welch, R, et al. Genetic polymorphisms in the one-carbon metabolism pathway and breast cancer risk: A population-based case–Control study and meta-analyses. Int. J. Cancer. 2007; 120: 2696–2703.
  • Gong Z, Yao S, Zirpoli G, Cheng TYD, Roberts M, Khoury T, et al. Genetic variants in one-carbon metabolism genes and breast cancer risk in European American and African American women. Int. J. Cancer. 2015; 137: 666–677.
  • Jones PA, Baylin SB. The Epigenomics of Cancer. Cell. 2007; 128: 683–692.
  • Issa JP. Aging and epigenetic drift: A vicious cycle. J. Clin. Investig. 2014; 124: 24-29
  • Klutstein M, Nejman D, Greenfield R, Cedar H. DNA Methylation in Cancer and Aging. Cancer Res. 2016; 76: 3446–3450.
  • Yin Z, Cui Z, Guan P, Li X, Wu W, Ren Y, et al. Interaction between Polymorphisms in Pre-MiRNA Genes and Cooking Oil Fume Exposure on the Risk of Lung Cancer in Chinese Non-Smoking Female Population. Oncotargets Ther. 2016; (9) :395–401.
  • Zhang Z, Li H, Li J, Lv X, Yang Z, Gao M, et al. Polymorphisms in the PVT1 Gene and Susceptibility to the Lung Cancer in a Chinese Northeast Population: A Case-control Study. J. Cancer. 2020; 11: 468–478.
  • Song N, Lee J, Cho S, Kim J, Oh JH, Song N. Evaluation of gene-environment interactions for colorectal cancer susceptibility loci using case-only and case-control designs. BMC Cancer. 2019; 19: 1231.
  • Neslund-Dudas C, Levin AM, Beebe-Dimmer L, Bock CH, Nock NL, Rundle A, et al. Gene–environment interactions between JAZF1 and occupational and household lead exposure in prostate cancer among African American men. Cancer Causes Control. 2014; 25: 869–879.
  • Strange RC, Fryer AA. The glutathione S-transferases: influence of polymorphism on cancer susceptibility. IARC Sci. Publ. 1999; 148: 231–249.
  • Seker H, Butkiewicz D, Bowman ED, Rusin M, Hedayati M, Grossman L, et al. Functional significance of xpd polymorphic variants: attenuated apoptosis in human lymphoblastoid cells with the xpd 312 asp/as genotype. Cancer Res. 2001; 61: 7430–7434.
  • Wu X, Hudmon KS, Detry MA, Chamberlain RM, Spitz MR. D2 dopamine receptor gene polymorphisms among African- Americans and Mexican-Americans: a lung cancer case-control study. Cancer Epidemiol. Biomarkers Prev. 2000; 9(10): 1021–1026.
  • Mucci LA, Wedren S, Tamimi RM, Trichopoulos D, Adami HO. The role of gene-environment interaction in the aetiology of human cancer: examples from cancers of the large bowel, lung and breast. J Intern Med. 2001; 249(6): 477-93. doi: 10.1046/j.1365-2796.2001.00839.x. PMID: 11422654.
  • Vineis P, Bartsch H, Caporaso N et al. Genetically based N-acetyltransferase metabolic polymorphism and low-level environmental exposure to carcinogens. Nature 1994; 369: 154±6.
  • Elfaki I, Mir R, Almutairi FM, Duhier FMA. Cytochrome P450: polymorphisms and roles in cancer, diabetes and atherosclerosis. Asian Pacific journal of cancer prevention: APJCP. 2018; 19(8): 2057.
  • He X, Feng S. Role of metabolic enzymes P450 (CYP) on activating procarcinogen and their polymorphisms on the risk of cancers. Curr Drug Metab. 2015; 16: 850-63.
  • Feigelson HS, Shames LS, Pike MC, Coetzee GA, Stanczyk FZ, Henderson BE. Cytochrome P450c17a is associated withserum estrogen and progesterone concentrations. Cancer Res.1998; 58: 585±7.
  • Elfaki I, Almutairi MF, Mir R, Khan R, Abu-Duhier FM. Cytochrome P450 CYP1B1*2 gene and its Association with T2D in Tabuk Population, Northwestern Region of Saudi Arabia. Asian J Pharm Clin Res. 2018; 11: 55-9.
  • Nebert DW, Vasiliou V. Analysis of the glutathione S-transferase (GST) gene family. Hum Genomics. 2004; 1(6): 460.
  • Reszka E, Wasowicz W, Gromadzinska J. Genetic polymorphism of xenobiotic metabolising enzymes, diet and cancer susceptibility. Br J Nutr. 2006; 96(4): 609-19.
  • van Poppel G, de Vogel N, van Balderen PJ, Kok FJ. Increased cytogenetic damage in smokers deficient in glutathione S-transferase isozyme mu. Carcinogenesis. 1992; 13: 303±5.
  • Gauderman WJ, Mukherjee B, Aschard H, Hsu L, Lewinger JP, Patel CJ, et al. Update on the State of the Science for Analytical Methods for Gene-Environment Interactions. Am. J. Epidemiol. 2017; 186: 762–770.
  • Hutter CM, Mechanic LE, Chatterjee N, Kraft P, Gillanders EM, Tank NG-ET, et al. Gene-environment interactions in cancer epidemiology: A National Cancer Institute Think Tank report. Genet. Epidemiol. 2014; 37: 643–657.
  • Patel CJ, Ioannidis JPA. Placing epidemiological results in the context of multiplicity and typical correlations of exposures. J. Epidemiol. Community Health. 2014; 68: 1096–1100.
  • Hsu L, Jiao S, Dai JY, Hutter C, Peters U, Kooperberg, C. Powerful cocktail Interaction, methods for detecting genome-wide gene-environment. Genet. Epidemiol. 2012; 36: 183–194.
  • Dai JY, Kooperberg C, Leblanc M, Prentice RL. Two-stage testing procedures with independent filtering for genome-wide gene-environment interaction. Biometrika. 2012; 99: 929–944.

The Role of Gene-Environment Interactions in the Etiology of Human Cancers

Yıl 2021, Cilt: 8 Sayı: 2, 30 - 37, 30.12.2021

Öz

Cancer is the second biggest cause of mortality on the world. In 2018, cancer claimed the lives of one out of every six people. Genes encoding enzymes involved in the metabolism of known cancer risk factors are one of the most significant areas of study in gene-environment interaction. These genes have frequent variant forms that can change metabolism and increase or decrease exposure to carcinogens, affecting risk of cancer. According to many observational and clinical research, a large number of human illnesses are caused not only by certain hereditary and environmental variables, as well as by gene-environment interactions. In recent years, it has become revealed more clearly that cancer is neither entirely genetic nor entirely composed of environmental factors. Altough genetic polymorphisms have been widely reported to play a crucial role in the sensivity of humans to cancer and different diseases states, somatic mutations produced by human exposure to environmental factors are responsible for several single nucleotide polymorphisms (SNPs). Studies in this field shows that the etiology and pathogenesis of many cancers arise through a complex interaction mechanism of genetic and environmental factors. According to scientific studies, the combination of environmental variables with particular allelic variations has a substantial impact on disease risk. In this article, presented a summary of the dynamics of gene-environment interactions and explained how they work in human malignancies, with a focus on the influence of specific tumors.

Kaynakça

  • World Health Organization. World Cancer Report 2014; Steward, B.W., Wild, C.P., Eds.; International Agency for Research on Cancer: Lyon, France, 2014.
  • Vogelstein B, Kinzler KW. The Genetic Basis of Human Cancer. 2nd ed: New York, NY; 2002.
  • Brennan P. Gene-environment interaction and aetiology of cancer: what does it mean and how can we measure it? Carcinogenesis. 2002; 23(3): 381-7.
  • Murcray CE, Lewinger JP, Gauderman WJ. Gene-environment interaction in genome-wide association studies. Am J Epidemiol. 2009;169(2): 219–226.
  • Parsa N. Environmental Factors Inducing Human Cancers. Iran. J. Public Health. 2012; 41: 1–9.
  • Simonds NI, Ghazarian AA, Pimentel CB, Schully SD, Ellison GL, Gillanders EM, et al. Review of the Gene-Environment Interaction Literature in Cancer: What do we know? Genet Epidemiol. 2017; 40: 356–365.
  • Hutter CM, Mechanic LE, Chatterjee N, Kraft P, Gillanders EM. Geneenvironment interactions in cancer epidemiology: a National Cancer Institute Think Tank report. Genet Epidemiol. 2013; 37(7): 643–657.
  • Department of Health and Human Services. Analysis of genomewide gene-environment (GxE) interactions (R21). 2013; PAR-13-382. Erişim adresi: http://grants.nih.gov/grants/guide/pa-files/PAR-13-382.html
  • National Cancer Institute. Genetic associations and mechanisms in oncology (GAME-ON): A post-genome wide association initiative; 2012. Erişim adresi: http://epi.grants.cancer.gov/gameon/.
  • Thomas DC. Methods for investigating gene-environment interactions in candidate pathway and genome-wide association studies. Annu. Rev. Public Health. 2010; 31: 21–36.
  • Vekasalo PK, Kaprio J, Koskenvuo M, Pukkala E. Genetic predisposition, environment and cancer incidence: A nation wide twin study in Findland, 1976–1995. Int. J. Cancer. 1999; 83: 743–749.
  • Liu G, Mukherjee B, Lee S, Lee A, Wu AH, Bandera EV, et al. Practice of Epidemiology Robust Tests for Additive Gene-Environment Interaction in Case-Control Studies Using Gene-Environment Independence. Hum. Mol. Genet. 2018; 187: 366–377.
  • Smith PG, Day NE. The Design of Case-Control Studies: The Influence of Confounding and Interaction Effects. Int. J. Epidemiol. 1984; 13: 356–365.
  • Smith GD, Hemani G. Mendelian randomization: Genetic anchors for causal inference in epidemiological studies. Int. J. Epidemiol. 2014; 23: R89–R98.
  • Lissowska J, Gaudet MM, Brinton LA, Chanock SJ, Peplonska B, Welch, R, et al. Genetic polymorphisms in the one-carbon metabolism pathway and breast cancer risk: A population-based case–Control study and meta-analyses. Int. J. Cancer. 2007; 120: 2696–2703.
  • Gong Z, Yao S, Zirpoli G, Cheng TYD, Roberts M, Khoury T, et al. Genetic variants in one-carbon metabolism genes and breast cancer risk in European American and African American women. Int. J. Cancer. 2015; 137: 666–677.
  • Jones PA, Baylin SB. The Epigenomics of Cancer. Cell. 2007; 128: 683–692.
  • Issa JP. Aging and epigenetic drift: A vicious cycle. J. Clin. Investig. 2014; 124: 24-29
  • Klutstein M, Nejman D, Greenfield R, Cedar H. DNA Methylation in Cancer and Aging. Cancer Res. 2016; 76: 3446–3450.
  • Yin Z, Cui Z, Guan P, Li X, Wu W, Ren Y, et al. Interaction between Polymorphisms in Pre-MiRNA Genes and Cooking Oil Fume Exposure on the Risk of Lung Cancer in Chinese Non-Smoking Female Population. Oncotargets Ther. 2016; (9) :395–401.
  • Zhang Z, Li H, Li J, Lv X, Yang Z, Gao M, et al. Polymorphisms in the PVT1 Gene and Susceptibility to the Lung Cancer in a Chinese Northeast Population: A Case-control Study. J. Cancer. 2020; 11: 468–478.
  • Song N, Lee J, Cho S, Kim J, Oh JH, Song N. Evaluation of gene-environment interactions for colorectal cancer susceptibility loci using case-only and case-control designs. BMC Cancer. 2019; 19: 1231.
  • Neslund-Dudas C, Levin AM, Beebe-Dimmer L, Bock CH, Nock NL, Rundle A, et al. Gene–environment interactions between JAZF1 and occupational and household lead exposure in prostate cancer among African American men. Cancer Causes Control. 2014; 25: 869–879.
  • Strange RC, Fryer AA. The glutathione S-transferases: influence of polymorphism on cancer susceptibility. IARC Sci. Publ. 1999; 148: 231–249.
  • Seker H, Butkiewicz D, Bowman ED, Rusin M, Hedayati M, Grossman L, et al. Functional significance of xpd polymorphic variants: attenuated apoptosis in human lymphoblastoid cells with the xpd 312 asp/as genotype. Cancer Res. 2001; 61: 7430–7434.
  • Wu X, Hudmon KS, Detry MA, Chamberlain RM, Spitz MR. D2 dopamine receptor gene polymorphisms among African- Americans and Mexican-Americans: a lung cancer case-control study. Cancer Epidemiol. Biomarkers Prev. 2000; 9(10): 1021–1026.
  • Mucci LA, Wedren S, Tamimi RM, Trichopoulos D, Adami HO. The role of gene-environment interaction in the aetiology of human cancer: examples from cancers of the large bowel, lung and breast. J Intern Med. 2001; 249(6): 477-93. doi: 10.1046/j.1365-2796.2001.00839.x. PMID: 11422654.
  • Vineis P, Bartsch H, Caporaso N et al. Genetically based N-acetyltransferase metabolic polymorphism and low-level environmental exposure to carcinogens. Nature 1994; 369: 154±6.
  • Elfaki I, Mir R, Almutairi FM, Duhier FMA. Cytochrome P450: polymorphisms and roles in cancer, diabetes and atherosclerosis. Asian Pacific journal of cancer prevention: APJCP. 2018; 19(8): 2057.
  • He X, Feng S. Role of metabolic enzymes P450 (CYP) on activating procarcinogen and their polymorphisms on the risk of cancers. Curr Drug Metab. 2015; 16: 850-63.
  • Feigelson HS, Shames LS, Pike MC, Coetzee GA, Stanczyk FZ, Henderson BE. Cytochrome P450c17a is associated withserum estrogen and progesterone concentrations. Cancer Res.1998; 58: 585±7.
  • Elfaki I, Almutairi MF, Mir R, Khan R, Abu-Duhier FM. Cytochrome P450 CYP1B1*2 gene and its Association with T2D in Tabuk Population, Northwestern Region of Saudi Arabia. Asian J Pharm Clin Res. 2018; 11: 55-9.
  • Nebert DW, Vasiliou V. Analysis of the glutathione S-transferase (GST) gene family. Hum Genomics. 2004; 1(6): 460.
  • Reszka E, Wasowicz W, Gromadzinska J. Genetic polymorphism of xenobiotic metabolising enzymes, diet and cancer susceptibility. Br J Nutr. 2006; 96(4): 609-19.
  • van Poppel G, de Vogel N, van Balderen PJ, Kok FJ. Increased cytogenetic damage in smokers deficient in glutathione S-transferase isozyme mu. Carcinogenesis. 1992; 13: 303±5.
  • Gauderman WJ, Mukherjee B, Aschard H, Hsu L, Lewinger JP, Patel CJ, et al. Update on the State of the Science for Analytical Methods for Gene-Environment Interactions. Am. J. Epidemiol. 2017; 186: 762–770.
  • Hutter CM, Mechanic LE, Chatterjee N, Kraft P, Gillanders EM, Tank NG-ET, et al. Gene-environment interactions in cancer epidemiology: A National Cancer Institute Think Tank report. Genet. Epidemiol. 2014; 37: 643–657.
  • Patel CJ, Ioannidis JPA. Placing epidemiological results in the context of multiplicity and typical correlations of exposures. J. Epidemiol. Community Health. 2014; 68: 1096–1100.
  • Hsu L, Jiao S, Dai JY, Hutter C, Peters U, Kooperberg, C. Powerful cocktail Interaction, methods for detecting genome-wide gene-environment. Genet. Epidemiol. 2012; 36: 183–194.
  • Dai JY, Kooperberg C, Leblanc M, Prentice RL. Two-stage testing procedures with independent filtering for genome-wide gene-environment interaction. Biometrika. 2012; 99: 929–944.
Toplam 40 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Kurumları Yönetimi
Bölüm Derleme Bölümü
Yazarlar

Mehmet Emin Arayıcı 0000-0002-0492-5129

Yasemin Başbınar 0000-0001-9439-2217

Hülya Ellidokuz 0000-0001-8503-061X

Yayımlanma Tarihi 30 Aralık 2021
Gönderilme Tarihi 3 Eylül 2021
Yayımlandığı Sayı Yıl 2021 Cilt: 8 Sayı: 2

Kaynak Göster

APA Arayıcı, M. E., Başbınar, Y., & Ellidokuz, H. (2021). İnsan Kanserlerinin Etiyolojisinde Gen-Çevre Etkileşiminin Rolü. ERÜ Sağlık Bilimleri Fakültesi Dergisi, 8(2), 30-37.