Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA)
| Ano de defesa: | 2020 |
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| Autor(a) principal: | |
| Orientador(a): | |
| Banca de defesa: | |
| Tipo de documento: | Dissertação |
| Tipo de acesso: | Acesso aberto |
| Idioma: | por |
| Instituição de defesa: |
Universidade do Estado do Amazonas
Brasil UEA PPGH -PROGRAMA DE PÓS-GRADUAÇÃO EM CIÊNCIAS APLICADAS À HEMATOLOGIA |
| Programa de Pós-Graduação: |
Não Informado pela instituição
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| Departamento: |
Não Informado pela instituição
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| País: |
Não Informado pela instituição
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| Palavras-chave em Português: | |
| Link de acesso: | https://ri.uea.edu.br/handle/riuea/2253 |
Resumo: | Acute lymphoblastic leukemia (ALL) is the most common hematological neoplasm and the main cause of childhood mortality. Single Nucleotide Polymorphisms (SNPs) in key molecules of the immune system, such as Toll-Like receptors, are associated with the development of various diseases, however, their role in ALL is unknown. Objective: In this study, we described the frequency of Toll-Like receptor polymorphisms in patients with acute lymphoblastic leukemia and their association with clinical prognosis. Material and Methods: A case-control study was carried out with 152 DNA samples from patients with ALL and 187 samples from individuals without the disease (control group). Genotypic and allelic discrimination was performed using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism method (PCR-RFLP) for the TLR1 S602I (rs5743618), TLR4 A299G and I399T (rs4986790 and rs4986791), TLR5 R392S (rs5744105), TLR6 S249P (rs5743810), TLR9 -1237C/T and -1486C/T (rs5743836 and rs187084) and CD14 -159 (rs2569191) polymorphisms. Descriptive and statistical analysis was performed using Microsoft Excel 2013 and GraphPad Prism v.5.0 software. Results: The C/C genotype from -1486C/T polymorphism (TLR9) was associated with the risk of development acute lymphoblastic leukemia (TLR9: T/T + C/T vs. C/C OR = 2.0 [95% CI: 1.1 -3.5, p=0.01]; C/T vs. C/C OR = 2.2 [95% CI: 1.2–4.1, p=0.00]). In addition, the T/T genotype from - 1486 C/T (TLR9) was associated with the presence of comorbidities on diagnosis (TLR9: T/T C/T vs. C/C OR = 2.1 [95% CI: 1.1- 4.3, p=0.04]; T/T vs. C/T OR = 2.2 [95% CI: 1.0-4.7, p=0.04]). Conclusion: Our findings suggested a significant role for SNP -1486 C/T (TLR9) without the development and presence of infectious comorbidities in acute lymphoblastic leukemia |
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Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA)Study of polymorphisms in TLRS genes in patients diagnosed with Acute Lymphoblastic Leukemia (ALL)Leucemia Linfoide AgudaImunidade InataSNPsTLRsAcute lymphoid leukemiaAcute lymphoblastic leukemia (ALL) is the most common hematological neoplasm and the main cause of childhood mortality. Single Nucleotide Polymorphisms (SNPs) in key molecules of the immune system, such as Toll-Like receptors, are associated with the development of various diseases, however, their role in ALL is unknown. Objective: In this study, we described the frequency of Toll-Like receptor polymorphisms in patients with acute lymphoblastic leukemia and their association with clinical prognosis. Material and Methods: A case-control study was carried out with 152 DNA samples from patients with ALL and 187 samples from individuals without the disease (control group). Genotypic and allelic discrimination was performed using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism method (PCR-RFLP) for the TLR1 S602I (rs5743618), TLR4 A299G and I399T (rs4986790 and rs4986791), TLR5 R392S (rs5744105), TLR6 S249P (rs5743810), TLR9 -1237C/T and -1486C/T (rs5743836 and rs187084) and CD14 -159 (rs2569191) polymorphisms. Descriptive and statistical analysis was performed using Microsoft Excel 2013 and GraphPad Prism v.5.0 software. Results: The C/C genotype from -1486C/T polymorphism (TLR9) was associated with the risk of development acute lymphoblastic leukemia (TLR9: T/T + C/T vs. C/C OR = 2.0 [95% CI: 1.1 -3.5, p=0.01]; C/T vs. C/C OR = 2.2 [95% CI: 1.2–4.1, p=0.00]). In addition, the T/T genotype from - 1486 C/T (TLR9) was associated with the presence of comorbidities on diagnosis (TLR9: T/T C/T vs. C/C OR = 2.1 [95% CI: 1.1- 4.3, p=0.04]; T/T vs. C/T OR = 2.2 [95% CI: 1.0-4.7, p=0.04]). Conclusion: Our findings suggested a significant role for SNP -1486 C/T (TLR9) without the development and presence of infectious comorbidities in acute lymphoblastic leukemiaAs Leucemias Agudas são neoplasias malignas graves, que acometem crianças e adultos e tem grande incidência no Amazonas. Sua etiologia e patogênese ainda permanecem incertas, sendo considerada uma doença multifatorial. Frente, a essa necessidade de informações, autores como, Leo Kinlen e Mel Greaves, tem sugerido, por meio de ponto vistas diferentes, que o modo como o sistema imunológico de alguns indivíduos reconhece antígenos e responde aos mesmos representa um fator de risco para a leucogênese. Polimorfismos nos genes dos receptores TLRs, presentes na imunidade inata, podem conter grande influência na alteração do padrão de resposta do indivíduo, contribuindo para a resistência ou suscetibilidade de doenças infecciosas. Objetivo: Assim, nosso objetivo foi de avaliar a influência dos polimorfismos nos genes dos receptores TLRs no prognostico clínico de pacientes diagnosticados com Leucemia Linfoide Aguda (LLA). Material e Métodos: Um estudo de caso- controle foi realizado com 152 amostras de DNA de pacientes com LLA e 187 amostras de indivíduos sem a doença (grupo controle). A discriminação genotípica e alélica foi realizada pelo método PCR-RFLP dos SNPs rs5743618 (TLR1 S602I), rs4986790 e rs4986791 (TLR4 A299G e I399T), rs5744105 (TLR5 R392S), rs5743810 (TLR6 S249P), rs5743836 e rs187084 (TLR9 -1237C/T e -1486C/T) e molécula rs2569191 (CD14 -159). A análise descritiva e estatística foi realizada com os softwares Microsoft Excel 2013 e GraphPadPrism v.5.0. Resultados: O genótipo C/C do polimorfismo -1486 C/T (TLR9) foi associado com o risco de desenvolvimento de leucemia linfoide aguda (TLR9: T/T+C/T vs. C/C OR = 2,0 [95% CI: 1,1-3,5, p = 0,014]; C/T vs. C/C OR = 2,2, [IC 95%: 1,2–4,1, p = 0,006]). Além disso, o genótipo TT do SNP -1486 C/T (TLR9) foi associado com a presença de comorbidades ao diagnóstico (TLR9: T/T + C/T vs. C/C OR = 2,1 [95% CI: 1,1-4,3, p=0,04]; T/T vs. C/T OR = 2,2 [95% CI: 1,0-4,7, p=0,04]). Conclusão: Nossos achados sugerem um papel significativo do SNP -1486C/T (TLR9) no desenvolvimento e presença de comorbidades infecciosas na leucemia linfoide agudaUniversidade do Estado do AmazonasBrasilUEAPPGH -PROGRAMA DE PÓS-GRADUAÇÃO EM CIÊNCIAS APLICADAS À HEMATOLOGIACosta, Allyson Guimarães daMarie, Adriana Malheiro AllePassos, Leny Nascimento da MottaMourão , Lucivania Prata de SouzaRamasawmy, RajendranathXabregas, Lilyane de Amorim2022-08-11T17:01:20Z2024-09-05T18:56:30Z2022-08-102022-08-11T17:01:20Z2020-07-29info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisapplication/pdfhttps://ri.uea.edu.br/handle/riuea/2253por1. Bawazir A, Al-Zamel N, Amen A, Akiel MA, Alhawiti NM, Alshehri A. The burden of leukemia in the Kingdom of Saudi Arabia: 15 years period (1999- 2013). BMC Cancer. 2019;19(1):1-10. doi:10.1186/s12885-019-5897-5 2. INCA. ESTIMATIVA 2020/ Incidência de Câncer No Brasil.; 2020. 3. Alves S, Wendell M, Id ALS, et al. Acute lymphoid and myeloid leukemia in a Brazilian Amazon population : Epidemiology and predictors of comorbidity and deaths. PLoS One. 2019;14(e0221518):1-16. doi:https://doi.org/10.1371/journal. pone.0221518 4. Reis RDS, Camargo B De, Santos MDO, et al. Childhood Leukemia Incidence in Brazil According to Different Geographical Regions. Pediatr blood cancer. 2011;56(2011):58-64. doi:10.1002/pbc 5. Abboud MR, Ghanem K, Muwakkit S. Acute lymphoblastic leukemia in low and middle-income countries. Curr Opin Oncol. 2014;26(6):650-655. doi:10.1097/CCO.0000000000000125 6. Zuckerman T, Rowe J. Pathogenesis and prognostication in acute lymphoblastic leukemia. F1000Prime Rep. 2014;6(July):3-7. doi:10.12703/P6- 59 7. Ladines-Castro W, Barragán-Ibañez G, Luna-Pérez MA, et al. Morphology of leukaemias. Rev Médica del Hosp Gen México. 2016;79(2):107- 113. doi:10.1016/j.hgmx.2015.06.007 8. Greaves MF. Differentiation-Linked Leukemogenesis Origins of Phenotypic Diversity in. Science (80- ). 1986;234. 9. Greaves MF. Aetiology of acute leukaemia. Lancet. 1997;349(9048):344- 349. doi:10.1016/S0140-6736(96)09412-3 61 10. Greaves M. The ‘delayed infection’ (aka ‘hygiene’) hypothesis for childhood leukaemia. In: The Hygiene Hypothesis and Darwinian Medicine. Basel: Birkhäuser Basel; 2009:239-255. doi:10.1007/978-3-7643-8903-1_13 11. Greaves M. A causal mechanism for childhood acute lymphoblastic leukaemia. Nat Rev Cancer. 2018;18(8):471-484. doi:10.1038/s41568-018- 0015-6 12. Kinlen L. Childhood leukaemia, nuclear sites, and population mixing. Br J Cancer. 2011;104(1):12-18. doi:10.1038/sj.bjc.6605982 13. Kinlen LJ. Childhood leukemia and population mixing. Cancer Causes Control. 2016;27(12):1499. doi:10.1007/s10552-016-0819-1 14. Monlish DA, Bhatt ST, Schuettpelz LG. The Role of Toll-Like Receptors in Hematopoietic Malignancies. Front Immunol. 2016;7(SEP):390. doi:10.3389/fimmu.2016.00390 15. Saborit-Villarroya I, Vaisitti T, Rossi D, et al. E2A is a transcriptional regulator of CD38 expression in chronic lymphocytic leukemia. Leukemia. 2011;25:479-488. doi:10.1038/leu.2010.291 16. Jacqueline C, Tasiemski A, Sorci G, et al. Infections and cancer: The “fifty shades of immunity” hypothesis. BMC Cancer. 2017;17(1):1-11. doi:10.1186/s12885-017-3234-4 17. El-Zayat SR, Sibaii H, Mannaa FA. Toll-like receptors activation, signaling, and targeting: an overview. Bull Natl Res Cent. 2019;43(1). doi:10.1186/s42269-019-0227-2 18. Lakshmi Narendra B, Eshvendar Reddy K, Shantikumar S, Ramakrishna S. Immune system: A double-edged sword in cancer. Inflamm Res. 2013;62(9):823-834. doi:10.1007/s00011-013-0645-9 19. Porcelli SA. EFFECTOR MECHANISMS IN AUTOIMMUNITY AND INFLAMMATION CHAPTER 17 Innate Immunity. Tenth Edit. Elsevier Inc.; 2017. doi:10.1016/B978-0-323-31696-5.00017-6 20. Mcdonald DR, Levy O. 3 - Innate Immunity. Fifth Edit. Elsevier Ltd doi:10.1016/B978-0-7020-6896-6.00003-X 21. Ishii KJ, Akira S. Cap 3 – Innate Immunity. Third Edit. Elsevier; 2008. doi:10.1016/B978-0-323-04404-2.10003-X 22. Kaisho T, Akira S. Toll-like receptor function and signaling. J Allergy Clin Immunol. 2006;117(5):979-987. doi:10.1016/j.jaci.2006.02.023 23. Harsini S, Beigy M, Akhavan-Sabbagh M, Rezaei N. Toll-like receptors in lymphoid malignancies: Double-edged sword. Crit Rev Oncol Hematol. 2014;89(2):262-283. doi:10.1016/j.critrevonc.2013.08.010 62 24. Messaritakis I, Stogiannitsi M, Koulouridi A, et al. Evaluation of the detection of Toll-like receptors (TLRs) in cancer development and progression in patients with colorectal cancer. PLoS One. 2018;13(6):1-14. doi:10.1371/journal.pone.0197327 25. Zhao S, Zhang Y, Zhang Q, Wang F, Zhang D. Toll-Like Receptors and Prostate Cancer. Front Immunol. 2014;5(JUL):1-6. doi:10.3389/fimmu.2014.00352 26. Rahman HAA, Khorshied MM, Khorshid OMR, Mahgoub SM. Toll-like receptor 2 and 9 genetic polymorphisms and the susceptibility to B cell Non- Hodgkin Lymphoma in Egypt. Ann Hematol. 2014;93(11):1859-1865. doi:10.1007/s00277-014-2131-z 27. Costa AG, Ramasawmy R, Ibiapina HNS, et al. Association of TLR variants with susceptibility to Plasmodium vivax malaria and parasitemia in the Amazon region of Brazil. PLoS One. 2017;12(8):1-14. doi:10.1371/journal.pone.0183840 28. Azevedo-Silva F, De Camargo B, Pombo-de-Oliveira MS. Implications of infectious diseases and the adrenal hypothesis for the etiology of childhood acute lymphoblastic leukemia. Brazilian J Med Biol Res. 2010;43(3):226-229. doi:10.1590/S0100-879X2010007500011 29. Chan LC, Lam TH, Li CK, et al. Is the timing of exposure to infection a major determinant of acute lymphoblastic leukaemia in Hong Kong? Paediatr Perinat Epidemiol. 2002;16(2):154-165. doi:10.1046/j.1365-3016.2002.00406.x 30. Pui C-H, Robison LL, Look AT. Acute lymphoblastic leukaemia. Lancet. 2008;371(9617):1030-1043. doi:10.1016/S0140-6736(08)60457-2 31. Takeda K, Akira S. Toll-like receptors in innate immunity. Int Immunol. 2005;17(1):1-14. doi:10.1093/intimm/dxh186 32. Wolska A, Lech-Marańda E, Robak T. Toll-like receptors and their role in carcinogenesis and anti-tumor treatment. Cell Mol Biol Lett. 2009;14(2). doi:10.2478/s11658-008-0048-z 33. Trejo-De La O A, Hernández-Sancén P, Maldonado-Bernal C. Relevance of single-nucleotide polymorphisms in human TLR genes to infectious and inflammatory diseases and cancer. Genes Immun. 2014;15(4):199-209. doi:10.1038/gene.2014.10 34. Redaelli A, Corporation P, Redaelli A, et al. The clinical and epidemiological burden of chronic lymphocytic leukaemia. Eur J Cancer Care (Engl). 2004;13(10):279-287. 35. Hamann L, Glaeser C, Hamprecht A, Gross M, Gomma A, Schumann RR. Toll-like receptor (TLR)-9 promotor polymorphisms and atherosclerosis. Clin Chim Acta. 2006;364(1-2):303-307. doi:10.1016/j.cca.2005.07.017 63 36. Roszak A, Lianeri M, Sowińska A, Jagodziński PP. Involvement of toll- like receptor 9 polymorphism in cervical cancer development. Mol Biol Rep. 2012;39(8):8425-8430. doi:10.1007/s11033-012-1695-8 37. Ng MTH, Van’t Hof R, Crockett JC, et al. Increase in NF-κB binding affinity of the variant C allele of the toll-like receptor 9 -1237T/C polymorphism is associated with Helicobacter pylori-induced gastric disease. Infect Immun. 2010;78(3):1345-1352. doi:10.1128/IAI.01226-09 38. Zhang L, Qin H, Guan X, Zhang K, Liu Z. The TLR9 gene polymorphisms and the risk of cancer: evidence from a meta-analysis. PLoS One. 2013;8(8):e71785. doi:10.1371/journal.pone.0071785 39. Nieters A, Beckmann L, Deeg E, Becker N. Gene polymorphisms in Toll- like receptors , interleukin-10 , and interleukin-10 receptor alpha and lymphoma risk. Genes Immun. 2006;7:615-624. doi:10.1038/sj.gene.6364337 40. Pandey N o., Chauhan A, Pandey N, et al. Association of TLR4 and TLR9 gene polymorphisms and haplotypes with cervicitis susceptibility. PLoS One. 2019;14(7):1-11. doi:10.1371/journal.pone.0220330 41. Carvalho A, Cunha C, Almeida A, et al. The rs5743836 polymorphism in TLR9 confers a population- based increased risk of non-Hodgkin lymphoma. Genes Immun. 2012;13(2):1-9. doi:10.1038/gene.2011.59 42. Ashton KA, Proietto A, Otton G, et al. Toll-Like Receptor ( TLR ) and Nucleosome-binding Oligomerization Domain ( NOD ) gene polymorphisms and endometrial cancer risk. BMC Cancer. 2010;10:1-7. doi:10.1186/1471-2407-10- 382 43. Mollaki V, Georgiadis T, Tassidou A, et al. Polymorphisms and haplotypes in TLR9 and MYD88 are associated with the development of Hodgkin’s lymphoma: A candidate-gene association study. J Hum Genet. 2009;54(11):655-659. doi:10.1038/jhg.2009.90 44. Rybka J, Gębura K, Wróbel T, et al. Variations in genes involved in regulation of the nuclear factor - κ B pathway and the risk of acute myeloid leukaemia. Int J Immunogenet. 2016;43(2):101-106. doi:10.1111/iji.12255 45. Pandey S, Mittal B, Srivastava M, et al. Evaluation of Toll-like receptors 3 (c.1377C/T) and 9 (G2848A) gene polymorphisms in cervical cancer susceptibility. Mol Biol Rep. 2011;38(7):4715-4721. doi:10.1007/s11033-010- 0607-z 46. Lazarus R, Klimecki WT, Raby BA, et al. Single-nucleotide polymorphisms in the Toll-like receptor 9 gene ( TLR9 ): frequencies , pairwise linkage disequilibrium , and haplotypes in three U . S . ethnic groups and exploratory case – control disease association studies ૾ . Genomics. 2003;81:85-91. doi:10.1016/S0888-7543(02)00022-8 64 47. Batar B, Mutlu T, Özdemİr N, Celkan T, Güven M. TLR4 ve NOD2 Polimorfizmlerinin Çocukluk Çağı Akut Lenfoblastik Lösemi ile İlişkisiq/ Association of the TLR4 and NOD2 Polymorphisms with Childhood. Bezmialem Sci. 2018;6:119-125. doi:10.14235/bs.2018.1678 48. Sheng WY, Yong Z, Yun Z, Hong H, Hai LL. Systematic review / Meta- analysis Toll-like receptor 4 gene polymorphisms and susceptibility to colorectal cancer : a meta-analysis and review. Arch Med Sci 2015;. 2015;11(4):699–707. doi:10.5114/aoms.2015.53288info:eu-repo/semantics/openAccessreponame:Repositório Institucional da Universidade do Estado do Amazonas (UEA)instname:Universidade do Estado do Amazonas (UEA)instacron:UEA2024-09-25T21:10:47Zoai:ri.uea.edu.br:riuea/2253Repositório InstitucionalPUBhttps://ri.uea.edu.br/server/oai/requestbibliotecacentral@uea.edu.bropendoar:2024-09-25T21:10:47Repositório Institucional da Universidade do Estado do Amazonas (UEA) - Universidade do Estado do Amazonas (UEA)false |
| dc.title.none.fl_str_mv |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) Study of polymorphisms in TLRS genes in patients diagnosed with Acute Lymphoblastic Leukemia (ALL) |
| title |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) |
| spellingShingle |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) Xabregas, Lilyane de Amorim Leucemia Linfoide Aguda Imunidade Inata SNPs TLRs Acute lymphoid leukemia |
| title_short |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) |
| title_full |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) |
| title_fullStr |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) |
| title_full_unstemmed |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) |
| title_sort |
Estudo dos polimorfismos nos genes dos TLRS em pacientes diagnósticados com Leucemia Linfoide Aguda (LLA) |
| author |
Xabregas, Lilyane de Amorim |
| author_facet |
Xabregas, Lilyane de Amorim |
| author_role |
author |
| dc.contributor.none.fl_str_mv |
Costa, Allyson Guimarães da Marie, Adriana Malheiro Alle Passos, Leny Nascimento da Motta Mourão , Lucivania Prata de Souza Ramasawmy, Rajendranath |
| dc.contributor.author.fl_str_mv |
Xabregas, Lilyane de Amorim |
| dc.subject.por.fl_str_mv |
Leucemia Linfoide Aguda Imunidade Inata SNPs TLRs Acute lymphoid leukemia |
| topic |
Leucemia Linfoide Aguda Imunidade Inata SNPs TLRs Acute lymphoid leukemia |
| description |
Acute lymphoblastic leukemia (ALL) is the most common hematological neoplasm and the main cause of childhood mortality. Single Nucleotide Polymorphisms (SNPs) in key molecules of the immune system, such as Toll-Like receptors, are associated with the development of various diseases, however, their role in ALL is unknown. Objective: In this study, we described the frequency of Toll-Like receptor polymorphisms in patients with acute lymphoblastic leukemia and their association with clinical prognosis. Material and Methods: A case-control study was carried out with 152 DNA samples from patients with ALL and 187 samples from individuals without the disease (control group). Genotypic and allelic discrimination was performed using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism method (PCR-RFLP) for the TLR1 S602I (rs5743618), TLR4 A299G and I399T (rs4986790 and rs4986791), TLR5 R392S (rs5744105), TLR6 S249P (rs5743810), TLR9 -1237C/T and -1486C/T (rs5743836 and rs187084) and CD14 -159 (rs2569191) polymorphisms. Descriptive and statistical analysis was performed using Microsoft Excel 2013 and GraphPad Prism v.5.0 software. Results: The C/C genotype from -1486C/T polymorphism (TLR9) was associated with the risk of development acute lymphoblastic leukemia (TLR9: T/T + C/T vs. C/C OR = 2.0 [95% CI: 1.1 -3.5, p=0.01]; C/T vs. C/C OR = 2.2 [95% CI: 1.2–4.1, p=0.00]). In addition, the T/T genotype from - 1486 C/T (TLR9) was associated with the presence of comorbidities on diagnosis (TLR9: T/T C/T vs. C/C OR = 2.1 [95% CI: 1.1- 4.3, p=0.04]; T/T vs. C/T OR = 2.2 [95% CI: 1.0-4.7, p=0.04]). Conclusion: Our findings suggested a significant role for SNP -1486 C/T (TLR9) without the development and presence of infectious comorbidities in acute lymphoblastic leukemia |
| publishDate |
2020 |
| dc.date.none.fl_str_mv |
2020-07-29 2022-08-11T17:01:20Z 2022-08-10 2022-08-11T17:01:20Z 2024-09-05T18:56:30Z |
| dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
| dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
| format |
masterThesis |
| status_str |
publishedVersion |
| dc.identifier.uri.fl_str_mv |
https://ri.uea.edu.br/handle/riuea/2253 |
| url |
https://ri.uea.edu.br/handle/riuea/2253 |
| dc.language.iso.fl_str_mv |
por |
| language |
por |
| dc.relation.none.fl_str_mv |
1. Bawazir A, Al-Zamel N, Amen A, Akiel MA, Alhawiti NM, Alshehri A. The burden of leukemia in the Kingdom of Saudi Arabia: 15 years period (1999- 2013). BMC Cancer. 2019;19(1):1-10. doi:10.1186/s12885-019-5897-5 2. INCA. ESTIMATIVA 2020/ Incidência de Câncer No Brasil.; 2020. 3. Alves S, Wendell M, Id ALS, et al. Acute lymphoid and myeloid leukemia in a Brazilian Amazon population : Epidemiology and predictors of comorbidity and deaths. PLoS One. 2019;14(e0221518):1-16. doi:https://doi.org/10.1371/journal. pone.0221518 4. Reis RDS, Camargo B De, Santos MDO, et al. Childhood Leukemia Incidence in Brazil According to Different Geographical Regions. Pediatr blood cancer. 2011;56(2011):58-64. doi:10.1002/pbc 5. Abboud MR, Ghanem K, Muwakkit S. Acute lymphoblastic leukemia in low and middle-income countries. Curr Opin Oncol. 2014;26(6):650-655. doi:10.1097/CCO.0000000000000125 6. Zuckerman T, Rowe J. Pathogenesis and prognostication in acute lymphoblastic leukemia. F1000Prime Rep. 2014;6(July):3-7. doi:10.12703/P6- 59 7. Ladines-Castro W, Barragán-Ibañez G, Luna-Pérez MA, et al. Morphology of leukaemias. Rev Médica del Hosp Gen México. 2016;79(2):107- 113. doi:10.1016/j.hgmx.2015.06.007 8. Greaves MF. Differentiation-Linked Leukemogenesis Origins of Phenotypic Diversity in. Science (80- ). 1986;234. 9. Greaves MF. Aetiology of acute leukaemia. Lancet. 1997;349(9048):344- 349. doi:10.1016/S0140-6736(96)09412-3 61 10. Greaves M. The ‘delayed infection’ (aka ‘hygiene’) hypothesis for childhood leukaemia. In: The Hygiene Hypothesis and Darwinian Medicine. Basel: Birkhäuser Basel; 2009:239-255. doi:10.1007/978-3-7643-8903-1_13 11. Greaves M. A causal mechanism for childhood acute lymphoblastic leukaemia. Nat Rev Cancer. 2018;18(8):471-484. doi:10.1038/s41568-018- 0015-6 12. Kinlen L. Childhood leukaemia, nuclear sites, and population mixing. Br J Cancer. 2011;104(1):12-18. doi:10.1038/sj.bjc.6605982 13. Kinlen LJ. 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J Hum Genet. 2009;54(11):655-659. doi:10.1038/jhg.2009.90 44. Rybka J, Gębura K, Wróbel T, et al. Variations in genes involved in regulation of the nuclear factor - κ B pathway and the risk of acute myeloid leukaemia. Int J Immunogenet. 2016;43(2):101-106. doi:10.1111/iji.12255 45. Pandey S, Mittal B, Srivastava M, et al. Evaluation of Toll-like receptors 3 (c.1377C/T) and 9 (G2848A) gene polymorphisms in cervical cancer susceptibility. Mol Biol Rep. 2011;38(7):4715-4721. doi:10.1007/s11033-010- 0607-z 46. Lazarus R, Klimecki WT, Raby BA, et al. Single-nucleotide polymorphisms in the Toll-like receptor 9 gene ( TLR9 ): frequencies , pairwise linkage disequilibrium , and haplotypes in three U . S . ethnic groups and exploratory case – control disease association studies ૾ . Genomics. 2003;81:85-91. doi:10.1016/S0888-7543(02)00022-8 64 47. Batar B, Mutlu T, Özdemİr N, Celkan T, Güven M. TLR4 ve NOD2 Polimorfizmlerinin Çocukluk Çağı Akut Lenfoblastik Lösemi ile İlişkisiq/ Association of the TLR4 and NOD2 Polymorphisms with Childhood. Bezmialem Sci. 2018;6:119-125. doi:10.14235/bs.2018.1678 48. Sheng WY, Yong Z, Yun Z, Hong H, Hai LL. Systematic review / Meta- analysis Toll-like receptor 4 gene polymorphisms and susceptibility to colorectal cancer : a meta-analysis and review. Arch Med Sci 2015;. 2015;11(4):699–707. doi:10.5114/aoms.2015.53288 |
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