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American Journal of Medicine Studies

ISSN (Print): 2333-8881

ISSN (Online): 2333-889X

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Cystic Lymphangioma of the Adrenal Gland: A Case Report and a Review of the Literature

1Department of endocrinology, Hedi Chaker Hospital, Sfax, Tunisia

2Department of radiology, Habib Bourguiba Hospital, Sfax, Tunisia

American Journal of Medicine Studies. 2015, 3(1), 1-3
doi: 10.12691/ajms-3-1-1
Copyright © 2015 Science and Education Publishing

Cite this paper:
Faten hadjkacem, Mouna Ammar, Ayman Maalej, Mouna Elleuch, Nessrine Cheikrouhou, Mouna Mnif, Nabila Rekike, Fatma Mnif, Nadia Charfi, Mohamed Abid. Cystic Lymphangioma of the Adrenal Gland: A Case Report and a Review of the Literature. American Journal of Medicine Studies. 2015; 3(1):1-3. doi: 10.12691/ajms-3-1-1.

Correspondence to: Mouna  Elleuch, Department of endocrinology, Hedi Chaker Hospital, Sfax, Tunisia. Email:


Adrenal lymphangiomas, also known as cystic adrenal lymphangiomas are benign vascular lesions, most often found incidentally during abdominal imaging studies, abdominal surgery or at autopsy. We present a case of a 45-year-old female who was evaluated for recurrent abdominal pain. Imaging studies revealed a large cystic lesion in the right adrenal region considered as a hydatid cyst. Right adrenalectomy was performed. Histopathologic examination demonstrates that the definite diagnosis is cystic lymphangioma of the right adrenal gland.



[1]  C. L. Ellis, P. Banerjee, E. Carney, R. Sharma, and G. J. Netto. Adrenal lymphangioma: clinicopathologic and immunohistochemical characteristics of a rare lesion. Human Pathology( 2011);( 42): 1013-1018.
[2]  Khoda J, Hertzanu Y, Sebbag G, Lantsberg L, Barky Y. Adrenal cysts: diagnosis and therapeutic approach. Int Surg. (1993); (78): 239-242.
[3]  J.M. Longo, S.Z. Jafri, andK. B. Bis, “Adrenal lymphangioma: a case report,”. Clinical Imaging.(2000); (24): 104 106.
[4]  Kalof AN, Cooper K. D2-40 immunohistochemistry-so far. Adv Anat Pathol. (2009); (16): 62-4.
[5]  L. A. Erickson, R. V. Lloyd, R. Hartman, and G. Thompson. Cystic adrenal neoplasms. Cancer. (2004);(101): 1537-1544.
Show More References
[6]  Y. Tanuma, M. Kimura, and S. Sakai. Adrenal cyst: a review of the japanese literature and report of a case. International Journal of Urology. (2001); (8): 500-503.
[7]  J.M. Longo, S.Z. Jafri, andK. B. Bis. Adrenal lymphangioma: acase report. Clinical Imaging. (2000);(24): 104-106.
[8]  Y.-K. Guo, Z.-G. Yang, Y. Li et al.Uncommon adrenal masses: CT and MRI features with histopathologic correlation. European Journal of Radiology.(2007); (62): 359-370.
[9]  Satou T, Uesugi T, Nakai Y, Hayashi Y, Imano M, Hashimoto S. Case of adrenal lymphangioma with atypical lymphocytes in aspirate cytology. Diagn Cytopathol. (2003); ( 29): 87-90.
[10]  Goel MC, Agarwal MR, Misra A. Percutaneous drainage of renal hydatid cyst: early results and follow-up. Br J Urol. (1995); (75):724-8.
[11]  A. A. Kasperlik-Załuska, M. Otto, A. Cichocki et al.1,161 patients with adrenal incidentalomas: indications for surgery. Langenbeck’s Archives of Surgery. (2008); (393): 121-126.
Show Less References


Researches on the Pharmacological Effects of Eicosapentaenoic Acid

1School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, People’s Republic of China

American Journal of Medicine Studies. 2015, 3(1), 4-7
doi: 10.12691/ajms-3-1-2
Copyright © 2015 Science and Education Publishing

Cite this paper:
Zunting Pang, Qiang Zhang, Zhixiang Tian, Chunchao Han. Researches on the Pharmacological Effects of Eicosapentaenoic Acid. American Journal of Medicine Studies. 2015; 3(1):4-7. doi: 10.12691/ajms-3-1-2.

Correspondence to: Chunchao  Han, School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, People’s Republic of China. Email:


Fish oils are the most common source of omega-3 polyunsaturated fatty acids (n-3 PUFAs), mainly eicosapentaenoic acid(EPA). It has been pointed out protective effects and beneficial effects of EPA on body weight reduction, heart health, blood lipid profile, cardiovascular diseases and other diseases. Based on its biological activities, EPA may be developed to a complementary and alternative medicine through further research. In this paper, the pharmacological effects of EPA were summarized by reviewing the recent related literatures.



[1]  Dyerberg J, Bang HO. (1970).Lipid metabolism, atherogenesis, and haemostasis in Eskimos: The role of the prostaglandin-3 family. Haemostasis 8(3-5):227-233.
[2]  Eunice Molinar-Toribio1, Jara Pe ´rez-Jime ´nez1, Sara Ramos-Romero, et al. (2015) Effect of n-3 PUFA supplementation at different EPA:DHA ratios on the spontaneously hypertensive obese rat model of the metabolic syndrome. British Journal of Nutrition 113: 878-887
[3]  WHIMS-MRI. (2014) Higher RBC EPA+DHA corresponds with larger total brain and hippocampal volumes. American Academy of Neurology 82(5):435-42.
[4]  Hajime Ishii, Yasuo Horie, Shigetoshi Ohshima, et al. (2009). Eicosapentaenoic acid ameliorates steatohepatitis and hepatocellular carcinoma in hepatocytespecific Pten-deficient mice. J Hepatol 50(3):562-71.
[5]  Y.A. Carpentier, L. Portois, W.J. Malaisse. (2006). N-3 fatty acids and the metabolic syndrome. Am. J. Clin. Nutr 83:1499S-1504S.
Show More References
[6]  G. Schmitz, J. Ecker. (2008). The opposing effects of n-3 and n-6 fatty acids. Prog Lipid Res 47(2):147-55.
[7]  Kunesova M. (2006). The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women. Physiol Res Acad Sci Bohemoslov 55:63-72.
[8]  Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, et al. (2007). Randomized trial of weight-loss-diets for young adults varying in fish and fish oil content. Int J Obes 31:1560-1566.
[9]  LeMieux MJ, Kalupahana NS, Scoggin S, Moustaid-Moussa N. (2015) Eicosapentaenoic acid reduces adipocyte hypertrophy and inflammation in diet-induced obese mice in an adiposity-independent manner. J Nutr 145(3):411-7.
[10]  Huerta AE, Navas-Carretero S, et al. (2015) Effects of α-lipoic acid and eicosapentaenoic acid in overweight and obese women during weight loss.Obesity (Silver Spring) 23(2):313-21.
[11]  Balk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P, Lau J. (2006) Effects of omega-3 fatty acids on serum markers of cardiovascular disease risk: a systematic review. Atherosclerosis 189(1):19-30.
[12]  Jacobson TA. (2008)Role of n-3 fatty acids in the treatment of hypertriglyceridemia and cardiovascular disease. Am J Clin Nutr 87 (Suppl):S1981-S1990.
[13]  Fletcher B, Berra K, Ades P, et al. (2005)Managing abnormal blood lipids: a collaborative approach. Circulation 112:3184-3209.
[14]  Musa-VelosoK, Binns MA, Kocenas AC, et al. (2010) Long-chain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid dose-dependentlyreduce fasting serum triglycerides. Nutr Rev 68(3):155-67.
[15]  Durante W. (2010). Targeting heme oxygenase-1 in vascular disease. Curr Drug Targets 11(12):1504-1516.
[16]  Idriss NK, Blann AD, Lip GY. (2008)Hemoxygenase-1 in cardiovascular disease. J Am Coll Cardiol 52(12):971-978.
[17]  Lee SE, Kim GD, Yang H, Son GW, Park HR, Cho JJ, Ahn HJ, Park CS, Park YS. (2015)Effects of eicosapentaenoic acid (EPA) on the cytoprotection via Nrf2-mediated heme oxygenase-1 inhuman endothelial cells. J Cardiovasc Pharmacol 26.
[18]  H. Chamras, A. Ardashian, D. Heber, J.A. Glaspy. (2002)Fatty acid modulation of MCF-7 human breast cancer cell proliferation, apoptosis and differentiation. J Nutr Biochem 13:711-717.
[19]  Eser PO, Vanden Heuvel JP, Araujo J, Thompson JT. (2013) Marineand plant-derived omega-3 fatty acids differentially regulate prostate cancer cell proliferation. Mol Clin Oncol 1(3):444-452.
[20]  Fukui M, Kang KS, Okada K , Zhu BT. (2013)EPA, an omega-3fatty acid, induces apoptosis in human pancreatic cancer cells:role of ROS accumulation, caspase-8 activation, and autophagyinduction. J Cell Biochem 114(1):192-203.
[21]  Hossain Z, Hosokawa M, Takahashi K. (2009)Growth inhibition and induction of apoptosis of colon cancer cell lines by applying marine phospholipid. Nutr Cancer 61:123-130.
[22]  B.E.S. Hashem, K.L. Rudolph. (2007)Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. J Gastroenterol 132:2557-2576.
[23]  J. Whang Peng, A.L. Cheng, C. Hsu, C.M. Chen. (2010)Clinical development and future direction for the treatment of hepatocellular carcinoma. J Exp Clin Med 2:93-103.
[24]  Zhang Y, Han L, Qi W, Cheng D, Ma X, Hou L, Cao X, Wang C. (2015) Eicosapentaenoic acid (EPA) induced apoptosis in HepG2 cells through ROS-Ca(2+)-JNK mitochondrial pathways. Biochem Biophys Res Commun 456(4):926-32.
[25]  Fietkau R, Lewitzki V, Kuhnt T, Holscher T, Hess CF, Berger B, Wiegel T, Rodel C, Niewald M, Hermann RM , Lubgan D. (2013)A disease-specific enteral nutrition formula improves nutritional status and functional performance in patients with head and neck and esophageal cancer undergoing chemoradiotherapy: results of a randomized, controlled, multicenter trial. Cancer 119: 3343-3353.
[26]  Mizoguchi K, Ishiguro H, Takahashi H, Sakamoto N, et al. (2014)Induction of apoptosis by eicosapentaenoic acid in esophageal squamous cell carcinoma. Anticancer Res 34(12):7145-9.
[27]  Jump DB. (2002)The biochemistry of n-3 polyunsaturated fatty acids. J Biol Chem 277: 8755-8758.
[28]  Konuma K, Itoh M, Suganami T, Kanai S, et al. (2015)Eicosapentaenoic Acid ameliorates non-alcoholic steatohepatitis in a novel mouse model using melanocortin 4 receptor-deficient mice. PLoS One 27, 10(3):e0121528.
[29]  Wirth S, Ribes-Koninckx C, Calzado MA, et al. (2010)High sustained virologic response rates in children with chronic hepatitis C receiving peginterferon alfa-2b plus ribavirin. J Hepatol 52:501-7.
[30]  Sokal EM, Bourgois A, Stephenne X, et al. (2010)Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection in children andadolescents. J Hepatol 52: 827-31.
[31]  Tajiri H, Inui A, Kiyohara Y, et al. (2009)Peginterferon alpha-2b and ribavirin for the treatment of chronic hepatitis C in Japanese pediatric and young adult patients: a survey of the Japan Society of Pediatric Hepatology. Eur J Gastroenterol Hepatol 21:1256-60.
[32]  Baker RD, Dee D, Baker SS. (2007) Response to pegylated interferon alpha-2b and ribavirin in children with chronic hepatitis C. J Clin Gastroenterol 41: 111-4.
[33]  McHutchison JG, Manns MP, Longo DL. (2006)Definition and management of anemia in patients infected with hepatitis C virus. Liver Int 26: 389-98.
[34]  Suzuki M, Inage E, et al. (2012)Prophylaxis for ribavirin-related anemia using eicosapentaenoic acid in chronic hepatitis C patients. Pediatr Int 54(4):528-31.
[35]  Rowan AD. (2001)Cartilage catabolism in arthritis: factors that influence homeostasis. Expert Rev Mol Med 1-20.
[36]  Hashimoto S, Nishiyama T, Hayashi S, et al. (2009)Role of p53 in human chondrocyte apoptosis in response to shear strain. Arthritis Rheum 60:2340-2349.
[37]  Takebe K, Nishiyama T, Hayashi S, et al. (2011)Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress. Int J Mol Med 27:329-335.
[38]  Sakata S, Hayashi S, Fujishiro T, et al. (2015)Oxidative Stress-induced Apoptosis and Matrix Loss of Chondrocytes Is Inhibited by Eicosapentaenoic Acid. J Orthop Res 33(3):359-65.
[39]  Jump DB, Depner CM, Tripathy S. (2012)Omega-3 fatty acid supplementation and cardiovascular disease. J Lipid Res 53:2525–2545.
[40]  Eslick GD, Howe PR, Smith C, Priest R, Bensoussan A. (2009) Benefits of fish oil supplementation in hyperlipidemia: a systematic review and metaanalysis. Int J Cardiol 136(1):4-16.
[41]  Verduci E, Agostoni C, et al. (2014)Blood lipids profile in hyperlipidemic children undergoing different dietary long chain polyunsaturated supplementations: a preliminary clinical trial. Int J Food Sci Nutr 65(3):375-9.
[42]  Angela Pirillo. (2013)Omega-3 polyunsaturated fatty acids in the treatment of hypertriglyceridaemia. Int J Cardiol.
Show Less References


Deletion Polymorphism of Glutathione S-transferases M1 and T1 genes in the Sudanese Population

1Department of Biochemistry, College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Bahrain

2Central Laboratory, Ministry of Science and Technology, Khartoum, Sudan

3College of Animal Production Science and Technology, Sudan University of Science and Technology, Khartoum, Sudan

4Department of Anatomy, College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Bahrain

5Department of Anatomy, Faculty of Medicine, Suez Canal University, Ismailia, Egypt

American Journal of Medicine Studies. 2015, 3(1), 8-12
doi: 10.12691/ajms-3-1-3
Copyright © 2015 Science and Education Publishing

Cite this paper:
Muhalab Ali, Amir T. Ibrahim, Mohamed T. Ibrahim, Abdel Halim A. Salem. Deletion Polymorphism of Glutathione S-transferases M1 and T1 genes in the Sudanese Population. American Journal of Medicine Studies. 2015; 3(1):8-12. doi: 10.12691/ajms-3-1-3.

Correspondence to: Abdel  Halim A. Salem, Department of Anatomy, College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Bahrain. Email:


Glutathione S-transferases (GSTs) play a major role in the detoxification of various compounds. Polymorphic variants in GST genes were reported for different populations. The main objective of this study was to determine the frequencies of GSTM1 and GSTT1 null genotypes in the Sudanese population. GST genotyping was carried out using multiplex PCR. Study population included 114 unrelated healthy Sudanese subjects. The results showed that the prevalence of GSTM1 and GSTT1 deletion homozygosity among Sudanese were 54.7% and 42.1%, respectively. There are no significant differences in allelic distribution of GSTM1 gene between the Sudanese and other ethnic groups except for sub-Saharan Africans. As regards the allelic distribution of GSTT1 genes, the Sudanese population is similar to sub-Saharan Africans but significantly different from Europeans. Combined analysis of both genes revealed that 24.6% of Sudanese harbor the deleted genotype of both genes and it is the highest reported so far for an Arab and African population. This is the first study that addresses deletion polymorphism of GST genes in Sudanese. We provide a reference database of allelic frequencies of the GSTM1 and GSTT1 genotypes among Sudanese.



[1]  Ginsberg G, Smolenski S, Hattis D, Guyton KZ, Johns DO, Sonawane B. Genetic Polymorphism in Glutathione Transferases (GST): Population distribution of GSTM1, T1, and P1 conjugating activity. J Toxicol Environ Health B Crit Rev. 2009;12:389-439.
[2]  McIlwain CC, Townsend DM, Tew KD. Glutathione S-transferase polymorphisms: cancer incidence and therapy. Oncogene. 2006;25:1639-48.
[3]  Bolt HM, Thier R. Relevance of the deletion polymorphisms of the glutathione S-transferases GSTT1 and GSTM1 in pharmacology and toxicology. Curr Drug Metab. 2006;7:613-28.
[4]  Xu S, Wang Y, Roe B, Pearson WR. Characterization of the human class Mu glutathione S-transferase gene cluster and the GSTM1 deletion. J Biol Chem. 1998;273:3517-27.
[5]  Pemble S, Schroeder KR, Spencer SR, Meyer DJ, Hallier E, Bolt HM, et al. Human glutathione S-transferase theta (GSTT1): cDNA cloning and the characterization of a genetic polymorphism. Biochem J. 1994;300:271-6.
Show More References
[6]  Strange RC, Fryer AA. The glutathione S-transferases: influence of polymorphism on cancer susceptibility. IARC Sci Publ. 1999:231-49.
[7]  Hayes JD, Pulford DJ. The glutathione S-transferase supergene family: regulation of GST and the contribution of the isoenzymes to cancer chemoprotection and drug resistance. Crit Rev Biochem Mol Biol. 1995;30:445-600.
[8]  Lear J, Heagerty A, Smith A, Bowers B, Jones P, Gilford J, et al. Polymorphism in detoxifying enzymes and susceptibility to skin cancer. Photochem Photobiol. 1996;63:424-8.
[9]  Fryer AA, Bianco A, Hepple M, Jones PW, Strange RC, Spiteri MA. Polymorphism at the glutathione S-transferase GSTP1 locus. A new marker for bronchial hyperresponsiveness and asthma. Am J Respir Crit Care Med. 2000;161:1437-42.
[10]  Relling MV, Giacomini KM. Pharmacogenetics. In: Brunton L, Chabner B, Knollaman B, editors. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 12 ed. New York: McGraw Hill; 2011. p. 140.
[11]  Townsend D, Tew K. Cancer drugs, genetic variation and the glutathione-S-transferase gene family. Am J Pharmacogenomics. 2003;3:157-72.
[12]  Yu L, Wang CY, Xi B, Sun L, Wang RQ, Yan YK, et al. GST polymorphisms are associated with hepatocellular carcinoma risk in Chinese population. World J Gastroenterol. 2011;17:3248-56.
[13]  Davies SM, Robison LL, Buckley JD, Tjoa T, Woods WG, Radloff GA, et al. Glutathione S-transferase polymorphisms and outcome of chemotherapy in childhood acute myeloid leukemia. J Clin Oncol. 2001;19:1279-87.
[14]  Bailey LR, Roodi N, Verrier CS, Yee CJ, Dupont WD, Parl FF. Breast cancer and CYPIA1, GSTM1, and GSTT1 polymorphisms: evidence of a lack of association in Caucasians and African Americans. Cancer Res. 1998;58:65-70.
[15]  Abdel-Rahman SZ, el-Zein RA, Anwar WA, Au WW. A multiplex PCR procedure for polymorphic analysis of GSTM1 and GSTT1 genes in population studies. Cancer Lett. 1996;107:229-33.
[16]  Salem AH, Yaqoob A, Ali M, Handu S, Fadel R, Abu-Hijleh M, et al. Genetic polymorphism of the glutathione S-transferase M1 and T1 genes in three distinct Arab populations. Dis Markers. 2011;31:311-6.
[17]  Hamdy SI, Hiratsuka M, Narahara K, Endo N, El-Enany M, Moursi N, et al. Genotype and allele frequencies of TPMT, NAT2, GST, SULT1A1 and MDR-1 in the Egyptian population. Br J Clin Pharmacol. 2003;55:560-9.
[18]  Siraj AK, Ibrahim M, Al-Rasheed M, Abubaker J, Bu R, Siddiqui SU, et al. Polymorphisms of selected xenobiotic genes contribute to the development of papillary thyroid cancer susceptibility in Middle Eastern population. BMC Med Genet. 2008;9:61.
[19]  Ada AO, Suzen SH, Iscan M. Polymorphisms of cytochrome P450 1A1, glutathione S-transferases M1 and T1 in a Turkish population. Toxicology letters. 2004;151:311-5.
[20]  Girisha KM, Gilmour A, Mastana S, Singh VP, Sinha N, Tewari S, et al. T1 and M1 polymorphism in glutathione S-transferase gene and coronary artery disease in North Indian population. Indian J Med Sci. 2004;58:520-6.
[21]  Moy KA, Yuan JM, Chung FL, Wang XL, Van Den Berg D, Wang R, et al. Isothiocyanates, glutathione S-transferase M1 and T1 polymorphisms and gastric cancer risk: a prospective study of men in Shanghai, China. Int J Cancer. 2009;125:2652-9.
[22]  Morinobu A, Kanagawa S, Koshiba M, Sugai S, Kumagai S. Association of the glutathione S-transferase M1 homozygous null genotype with susceptibility to Sjogren's syndrome in Japanese individuals. Arthritis Rheum. 1999;42:2612-5.
[23]  Cho HJ, Lee SY, Ki CS, Kim JW. GSTM1, GSTT1 and GSTP1 polymorphisms in the Korean population. J Korean Med Sci. 2005;20:1089-92.
[24]  Duncan H, Swan C, Green J, Jones P, Brannigan K, Alldersea J, et al. Susceptibility to ulcerative colitis and Crohn's disease: interactions between glutathione S-transferase GSTM1 and GSTT1 genotypes. Clin Chim Acta. 1995;240:53-61.
[25]  Jourenkova N, Reinikanen M, Bouchardy C, Husgafvel-Pursiainen K, Dayer P, Benhamou S, et al. Effects of glutathione S-transferases GSTM1 and GSTT1 genotypes on lung cancer risk in smokers. Pharmacogenetics. 1997;7:515-8.
[26]  Jahnke V, Matthias C, Fryer A, Strange R. Glutathione S-transferase and cytochrome-P-450 polymorphism as risk factors for squamous cell carcinoma of the larynx. Am J Surg. 1996;172:671-3.
[27]  Piacentini S, Polimanti R, Porreca F, Martinez-Labarga C, De Stefano GF, Fuciarelli M. GSTT1 and GSTM1 gene polymorphisms in European and African populations. Mol Biol Rep. 2011;38:1225-30.
[28]  Wild CP, Yin F, Turner PC, Chemin I, Chapot B, Mendy M, et al. Environmental and genetic determinants of aflatoxin-albumin adducts in the Gambia. Int J Cancer. 2000;86:1-7.
[29]  Santovito A, Burgarello C, Cervella P, Delpero M. Polymorphisms of cytochrome P450 1A1, glutathione s-transferases M1 and T1 genes in Ouangolodougou (Northern Ivory Coast). Genetics and Molecular Biology. 2010;33:434-7.
[30]  Nelson HH, Wiencke JK, Christiani DC, Cheng TJ, Zuo ZF, Schwartz BS, et al. Ethnic differences in the prevalence of the homozygous deleted genotype of glutathione S-transferase theta. Carcinogenesis. 1995;16:1243-5.
[31]  Garte S, Gaspari L, Alexandrie AK, Ambrosone C, Autrup H, Autrup JL, et al. Metabolic gene polymorphism frequencies in control populations. Cancer Epidemiol Biomarkers Prev. 2001;10:1239-48.
[32]  Bu R, Gutierrez MI, Al-Rasheed M, Belgaumi A, Bhatia K. Variable drug metabolism genes in Arab population. Pharmacogenomics J. 2004;4:260-6.
[33]  Hatagima A, Marques CF, Krieger H, Feitosa MF. Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms in a Brazilian mixed population. Hum Biol. 2004;76:937-42.
[34]  Rebbeck TR. Molecular epidemiology of the human glutathione S-transferase genotypes GSTM1 and GSTT1 in cancer susceptibility. Cancer Epidemiol Biomarkers Prev. 1997;6:733-43.
[35]  Saeed IE, Weng HY, Mohamed KH, Mohammed SI. Cancer incidence in Khartoum, Sudan: first results from the Cancer Registry, 2009-2010. Cancer Med. 2014;3:1075-84.
[36]  Revised global burden of disease (GBD) 2002 estimates. Geneva: World Health Organization; 2002.
[37]  Gsur A, Haidinger G, Hinteregger S, Bernhofer G, Schatzl G, Madersbacher S, et al. Polymorphisms of glutathione-S-transferase genes (GSTP1, GSTM1 and GSTT1) and prostate-cancer risk. Int J Cancer. 2001;95:152-5.
[38]  Liu D, Liu Y, Ran L, Shang H, Li D. GSTT1 and GSTM1 polymorphisms and prostate cancer risk in Asians: a systematic review and meta-analysis. Tumour Biol. 2013;34:2539-44.
[39]  Liu K, Lin X, Zhou Q, Ma T, Han L, Mao G, et al. The associations between two vital GSTs genetic polymorphisms and lung cancer risk in the Chinese population: evidence from 71 studies. PLoS One. 2014;9:e102372.
[40]  Zhao Y, Zeng J, Zhang Y, Lu S, Zhao E, Huang Z, et al. GSTM1 polymorphism and lung cancer risk among East Asian populations: a meta-analysis. Tumour Biol. 2014;35:6493-500.
[41]  Zhang H, Wu X, Xiao Y, Chen M, Li Z, Wei X, et al. Genetic polymorphisms of glutathione S-transferase M1 and T1, and evaluation of oxidative stress in patients with non-small cell lung cancer. Eur J Med Res. 2014;19:67.
Show Less References