Association between Polymorphisms in Inflammatory Response-Related Genes and the Susceptibility, Progression and Prognosis of the Diffuse Histological Subtype of Gastric Cancer

Imagem de Miniatura
Arquivos
art_FURUYA_Association_between_Polymorphisms_in_Inflammatory_ResponseRelated_Genes_and_2018.PDF (359.53 KB)
Citações na Scopus
18
Tipo de produção
article
Data de publicação
2018
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
MDPI
Autores
Citação
GENES, v.9, n.12, article ID 631, 22p, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
The chronic inflammatory microenvironment and immune cell dysfunction have been described as critical components for gastric tumor initiation and progression. The diffuse subtype is related to poor clinical outcomes, pronounced inflammation, and the worst prognosis. We investigated the association of polymorphisms in inflammatory response-related genes (COX-2, OGG1, TNFB, TNFA, HSPA1L, HSPA1B, VEGFA, IL17F, LGALS3, PHB, and TP53) with gastric cancer susceptibility, progression and prognosis in a Brazilian sample, focusing on the diffuse subtype. We also performed the analysis regarding the total sample of cases (not stratified for tumor subtypes), allowing the comparison between the findings. We further investigated the polymorphisms in linkage disequilibrium and performed haplotype association analyses. In the case-control study, rs1042522 (TP53) was associated with a stronger risk for developing gastric cancer in the sample stratified for diffuse subtype patients when compared to the risk observed for the total cases; CTC haplotype (rs699947 / rs833061 / rs2010963 VEGFA) was associated with risk while rs699947 was associated with protection for gastric malignancy in the total sample. Regarding the associations with the clinicopathological features of gastric cancer, for the diffuse subtype we found that rs699947 and rs833061 (VEGFA) were associated with outcomes related to a worse progression while rs5275 (COX-2), rs909253 (TNFB), and rs2227956 (HSPA1L) were associated to a better progression of the disease. In the total sample, rs699947 and rs833061 (VEGFA), rs4644 (LGALS3), and rs1042522 (TP53) were able to predict a worse progression while rs5275 (COX-2), rs2227956 (HSPA1L), and rs3025039 (VEGFA) a better progression. Besides, rs909253 (TNFB) predicted protection for the overall and disease-free survivals for gastric cancer. In conclusion, these results helped us to clarify the potential role of these polymorphisms in genes involved in the modulation of the inflammatory response in the pathogenesis of gastric cancer.
Palavras-chave
gastric cancer, diffuse histological subtype of Lauren, genetic polymorphisms, haplotypes, inflammation, genetic association studies, genetic predisposition to disease, disease progression, prognosis
URI
https://observatorio.fm.usp.br/handle/OPI/30889
Referências
  1. Achatz MI, 2016, CSH PERSPECT MED, V6, DOI 10.1101/cshperspect.a026195
  2. Adzhubei IA, 2010, NAT METHODS, V7, P248, DOI 10.1038/nmeth0410-248
  3. Assumpcao JG, 2008, BMC CANCER, V8, DOI 10.1186/1471-2407-8-357
  4. Balan V, 2008, CANCER RES, V68, P10045, DOI 10.1158/0008-5472.CAN-08-3224
  5. Baniak N, 2016, WORLD J SURG ONCOL, V14, DOI 10.1186/s12957-016-0969-3
  6. Barrett JC, 2005, BIOINFORMATICS, V21, P263, DOI 10.1093/bioinformatics/bth457
  7. Bass AJ, 2014, NATURE, V513, P202, DOI 10.1038/nature13480
  8. Borges LM, 2015, GENET MOL RES, V14, P17034, DOI 10.4238/2015.December.16.4
  9. Bornschein J, 2011, LANGENBECK ARCH SURG, V396, P729, DOI 10.1007/s00423-011-0810-y
  10. Bray F, 2018, CA-CANCER J CLIN, V68, P394, DOI 10.3322/caac.21492
  11. Chen C, 2014, CLIN RES HEPATOL GAS, V38, P346, DOI 10.1016/j.clinre.2013.12.009
  12. Da MX, 2008, ARCH MED RES, V39, P92, DOI 10.1016/j.arcmed.2007.06.021
  13. Dicken BJ, 2005, ANN SURG, V241, P27, DOI 10.1097/01.sla.0000149300.28588.23
  14. Dumont P, 2003, NAT GENET, V33, P357, DOI 10.1038/ng1093
  15. Eng L, 2013, PHARMACOGENOMICS, V14, P1659, DOI 10.2217/pgs.13.165
  16. Faul F, 2007, BEHAV RES METHODS, V39, P175, DOI 10.3758/BF03193146
  17. Ferrer-Ferrer M, 2013, ARCH MED RES, V44, P467, DOI 10.1016/j.arcmed.2013.08.008
  18. Francisco G, 2011, INT J CANCER, V129, P920, DOI 10.1002/ijc.25710
  19. Garritano S, 2010, HUM MUTAT, V31, P143, DOI 10.1002/humu.21151
  20. Ge S, 2018, NAT COMMUN, V9, DOI 10.1038/s41467-018-03121-2
  21. Hanahan D, 2011, CELL, V144, P646, DOI 10.1016/j.cell.2011.02.013
  22. He L, 2014, SCI WORLD J, DOI 10.1155/2014/540309
  23. Henderson NC, 2009, IMMUNOL REV, V230, P160, DOI 10.1111/j.1600-065X.2009.00794.x
  24. Howell WM, 2002, P NUTR SOC, V61, P447, DOI 10.1079/PNS2002186
  25. Instituto Nacional de Cancer Jose Alencar Gomes da Silva (INCA), EST 2018 IND CANC BR
  26. Joo YE, 2002, DIGESTION, V66, P222, DOI 10.1159/000068366
  27. Ke Q, 2008, MOL CARCINOGEN, V47, P647, DOI 10.1002/mc.20435
  28. Kim SJ, 2011, CLIN EXP METASTAS, V28, P743, DOI 10.1007/s10585-011-9406-8
  29. Krippl P, 2003, INT J CANCER, V106, P468, DOI 10.1002/ijc.11238
  30. Kumar P, 2009, NAT PROTOC, V4, P1073, DOI 10.1038/nprot.2009.86
  31. LAUREN P, 1965, ACTA PATHOL MIC SC, V64, P31, DOI 10.1111/apm.1965.64.1.31
  32. Lewis Cathryn M, 2012, Cold Spring Harb Protoc, V2012, P297, DOI 10.1101/pdb.top068163
  33. Li M, 2006, ACTA ONCOL, V45, P1115, DOI 10.1088/02841860601043066
  34. Liu FT, 2005, INT ARCH ALLERGY IMM, V136, P385, DOI 10.1159/000084545
  35. Liu H, 2012, CURR PHARM DESIGN, V18, P2395, DOI 10.2174/13816128112092395
  36. Liu H, 2011, ASIAN PAC J CANCER P, V12, P1979
  37. Ma HY, 2016, WORLD J GASTROENTERO, V22, P6619, DOI 10.3748/wjg.v22.i29.6619
  38. Makhatadze NJ, 1998, HUM IMMUNOL, V59, P571, DOI 10.1016/S0198-8859(98)00056-1
  39. MESSER G, 1991, J EXP MED, V173, P209, DOI 10.1084/jem.173.1.209
  40. Milne AN, 2009, HUM GENET, V126, P615, DOI 10.1007/s00439-009-0722-x
  41. Moore AE, 2012, ONCOGENE, V31, P1592, DOI 10.1038/onc.2011.349
  42. Nangia-Makker P, 2007, CANCER RES, V67, P11760, DOI 10.1158/0008-5472.CAN-07-3233
  43. Palmero EI, 2008, CANCER LETT, V261, P21, DOI 10.1016/j.canlet.2007.10.044
  44. Partida-Rodriguez O, 2010, INT J CANCER, V126, P1861, DOI 10.1002/ijc.24773
  45. Pasini FS, 2014, J GASTROENTEROL, V49, P1453, DOI 10.1007/s00535-013-0904-0
  46. Pinto Emilia M., 2004, Arq Bras Endocrinol Metab, V48, P647, DOI 10.1590/S0004-27302004000500009
  47. Purcell S, 2007, AM J HUM GENET, V81, P559, DOI 10.1086/519795
  48. Renner W, 2000, J VASC RES, V37, P443, DOI 10.1159/000054076
  49. RIPPMANN F, 1991, EMBO J, V10, P1053, DOI 10.1002/j.1460-2075.1991.tb08044.x
  50. Tahara Eiichi, 2004, IARC Sci Publ, P327
  51. Tang WR, 2012, BIOMARKERS, V17, P597, DOI 10.3109/1354750X.2012.704646
  52. Thomas M, 1999, MOL CELL BIOL, V19, P1092
  53. Van Cutsem E, 2016, LANCET, V388, P2654, DOI 10.1016/S0140-6736(16)30354-3
  54. Vauhkonen M, 2006, BEST PRACT RES CL GA, V20, P651, DOI 10.1016/j.bpg.2006.03.016
  55. Washington K, 2010, ANN SURG ONCOL, V17, P3077, DOI 10.1245/s10434-010-1362-z
  56. Werner M, 2001, J CANCER RES CLIN, V127, P207, DOI 10.1007/s004320000195
  57. Wunsch V, 2006, BRAZ J MED BIOL RES, V39, P545, DOI 10.1590/S0100-879X2006000400016
  58. Xiang B, 2012, ASIAN PAC J CANCER P, V13, P1787, DOI 10.7314/APJCP.2012.13.5.1787
  59. Zabaleta Jovanny, 2012, Methods Mol Biol, V863, P411, DOI 10.1007/978-1-61779-612-8_26
  60. Zhang XM, 2005, GASTROENTEROLOGY, V129, P565, DOI 10.1053/j.gastro.2005.05.003
  61. Zhou LP, 2011, EXP THER MED, V2, P931, DOI 10.3892/etm.2011.278

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPR
Artigos e Materiais de Revistas Científicas - FM/MDR
Artigos e Materiais de Revistas Científicas - FM/MGT
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Carregar mais