Abstract Background Pharmacogenetics promises better control of diseases such as cardiovascular disease (CVD). Acetylsalicylic acid, aspirin, prevents the formation of an activating agent of platelet aggregation and vasoconstriction, and it is used to prevent CVD. Nevertheless, patients may have treatment failure due to genetic variants that modify the metabolism of the drug causing aspirin resistance (AR). Objectives To realize a systematic literature review to determine the impact of genetic variants on AR. Methods Articles published in the MEDLINE/PubMed, Cochrane, Scopus, LILACS, and SCIELO databases were systematically screened. A total of 290 articles were identified and 269 articles were excluded because they did not comply with the previously established inclusion criteria. A total of 20 case-control studies and 1 cohort was included. Results The genetic variants rs1126643 (ITGA2), rs3842787 (PTGS1), rs20417 (PTGS2), and rs5918 (ITGB3) were the most studied. As for relevance, of the 64 genetic variants evaluated by the articles, 14 had statistical significance (p< 0.05; 95% confidence interval [CI]) in at least one article. Among them, the following have had unanimous results: rs1371097 (P2RY1), rs1045642 (MDR1), rs1051931 and rs7756935 (PLA2G7), rs2071746 (HO1), rs1131882 and rs4523 (TBXA2R), rs434473 (ALOX12), rs9315042 (ALOX5AP), and rs662 (PON1), while these differ in real interference in AR: rs5918 (ITGB3), rs2243093 (GP1BA), rs1330344 (PTGS1), and rs20417 (PTGS2). As study limitations, we highlight the nonuniform methodologies of the analyzed articles and population differences. Conclusion It is noteworthy that pharmacogenetics is an expanding area. Therefore, further studies are needed to better understand the association between genetic variants and AR. CVD . (CVD) acid vasoconstriction Nevertheless AR (AR) MEDLINEPubMed MEDLINE PubMed MEDLINE/PubMed Cochrane Scopus LILACS screened 29 26 criteria 2 casecontrol case included rs rs112664 ITGA2, ITGA2 ITGA , (ITGA2) rs384278 PTGS1, PTGS1 PTGS (PTGS1) rs2041 PTGS2, PTGS2 (PTGS2) rs591 ITGB3 ITGB (ITGB3 studied relevance 6 p< p (p 0.05 005 0 05 95 CI [CI] article them results rs137109 P2RY1, P2RY1 PRY P RY (P2RY1) rs104564 MDR1, MDR1 MDR (MDR1) rs105193 rs775693 PLA2G7, PLA2G7 PLAG PLA G (PLA2G7) rs207174 HO1, HO1 HO (HO1) rs113188 rs452 TBXA2R, TBXA2R TBXAR TBXA R (TBXA2R) rs43447 ALOX12, ALOX12 ALOX (ALOX12) rs931504 ALOX5AP, ALOX5AP ALOXAP AP (ALOX5AP) rs66 PON1, PON1 PON (PON1) ITGB3, rs224309 GP1BA, GP1BA GPBA GP BA (GP1BA) rs133034 PTGS2. limitations differences area Therefore (CVD (AR rs11266 (ITGA2 rs38427 (PTGS1 rs204 (PTGS2 rs59 (ITGB 0.0 00 9 [CI rs13710 P2RY (P2RY1 rs10456 (MDR1 rs10519 rs77569 PLA2G (PLA2G7 rs20717 (HO1 rs11318 rs45 (TBXA2R rs4344 ALOX1 (ALOX12 rs93150 (ALOX5AP rs6 (PON1 rs22430 (GP1BA rs13303 rs1126 (ITGA rs3842 (PTGS rs20 rs5 0. rs1371 (P2RY rs1045 (MDR rs1051 rs7756 (PLA2G rs2071 (HO rs1131 rs4 rs434 (ALOX1 rs9315 (PON rs2243 rs1330 rs112 rs384 rs2 rs137 rs104 rs105 rs775 rs207 rs113 rs43 (ALOX rs931 rs224 rs133 rs11 rs38 rs13 rs10 rs77 rs93 rs22 rs1 rs3 rs7 rs9

Resumo Antecedentes A farmacogenética promete melhorar o controle de doenças como as cardiovasculares. O ácido acetilsalicílico, a aspirina, previne a formação de um agente ativador da agregação plaquetária e vasoconstrição e é usado na prevenção de tais doenças. No entanto, os pacientes podem ter falha no tratamento devido a variantes genéticas que modificam o metabolismo da droga causando resistência à aspirina (RA). Objetivos Realizar uma revisão sistemática da literatura para determinar o impacto das variantes genéticas na resistência à aspirina. Métodos Artigos publicados nos bancos de dados MEDLINE/PubMed, Cochrane, Scopus, LILACS e SCIELO foram sistematicamente selecionados. Foram identificados 290 artigos e, destes, 269 artigos foram excluídos por não atenderem aos critérios de inclusão previamente estabelecidos. Um total de 20 estudos caso-controles e 1 coorte foi incluído. Resultados As variantes genéticas rs1126643 (ITGA2), rs3842787 (PTGS1), rs20417 (PTGS2) e rs5918 (ITGB3) foram as mais estudadas. Quanto à relevância, das 64 variantes genéticas avaliadas pelos artigos, 14 tiveram significância estatística (p< 0,05; intervalo de confiança [IC] de 95%) em pelo menos um artigo. Entre eles, os seguintes tiveram resultados unânimes: rs1371097 (P2RY1), rs1045642 (MDR1), rs1051931 e rs7756935 (PLA2G7), rs2071746 (HO1), rs1131882 e rs4523 (TBXA2R), rs434473 (ALOX12), rs9315042 (ALOX5AP) e rs662 (PON1), enquanto estes diferiram na interferência real na RA: rs5918 (ITGB3), rs2243093 (GP1BA), rs1330344 (PTGS1) e rs20417 (PTGS2). Como limitações do estudo, destacam-se as metodologias não uniformes dos artigos analisados e as diferenças populacionais. Conclusão Vale ressaltar que a farmacogenética é uma área em expansão. Portanto, mais estudos são necessários para entender melhor a associação entre variantes genéticas e RA. cardiovasculares acetilsalicílico entanto RA . (RA) MEDLINEPubMed MEDLINE PubMed MEDLINE/PubMed Cochrane Scopus selecionados 29 destes 26 estabelecidos 2 casocontroles caso controles incluído rs rs112664 ITGA2, ITGA2 ITGA , (ITGA2) rs384278 PTGS1, PTGS1 PTGS rs2041 PTGS2 (PTGS2 rs591 ITGB3 ITGB (ITGB3 estudadas relevância 6 p< p (p 0,05 005 0 05 IC [IC 95% 95 artigo eles unânimes rs137109 P2RY1, P2RY1 PRY P RY (P2RY1) rs104564 MDR1, MDR1 MDR (MDR1) rs105193 rs775693 PLA2G7, PLA2G7 PLAG PLA G (PLA2G7) rs207174 HO1, HO1 HO (HO1) rs113188 rs452 TBXA2R, TBXA2R TBXAR TBXA R (TBXA2R) rs43447 ALOX12, ALOX12 ALOX (ALOX12) rs931504 ALOX5AP ALOXAP AP (ALOX5AP rs66 PON1, PON1 PON (PON1) ITGB3, rs224309 GP1BA, GP1BA GPBA GP BA (GP1BA) rs133034 (PTGS1 PTGS2. estudo destacamse destacam se populacionais expansão Portanto (RA rs11266 (ITGA2 rs38427 rs204 (PTGS rs59 (ITGB 0,0 00 9 rs13710 P2RY (P2RY1 rs10456 (MDR1 rs10519 rs77569 PLA2G (PLA2G7 rs20717 (HO1 rs11318 rs45 (TBXA2R rs4344 ALOX1 (ALOX12 rs93150 rs6 (PON1 rs22430 (GP1BA rs13303 rs1126 (ITGA rs3842 rs20 rs5 0, rs1371 (P2RY rs1045 (MDR rs1051 rs7756 (PLA2G rs2071 (HO rs1131 rs4 rs434 (ALOX1 rs9315 (PON rs2243 rs1330 rs112 rs384 rs2 rs137 rs104 rs105 rs775 rs207 rs113 rs43 (ALOX rs931 rs224 rs133 rs11 rs38 rs13 rs10 rs77 rs93 rs22 rs1 rs3 rs7 rs9

RESUMO Antecedentes: O acidente vascular cerebral isquêmico (AVCI) é uma doença multifatorial que apresenta altas taxas de morbimortalidade no Brasil. Vários estudos provaram que existe uma ligação entre o sistema ABO de grupos sanguíneos e a ocorrência de eventos trombóticos. No entanto, sua associação com AVCI não está bem estabelecida. Objetivo: Por essa razão, o objetivo deste trabalho foi investigar a relação entre os grupos sanguíneos ABO e a ocorrência de AVCI em uma coorte brasileira de doenças cerebrovasculares. Métodos: Ao longo de 12 meses foram incluídos 529 indivíduos, dos quais 275 apresentaram um episódio de AVCI e 254 compuseram o grupo controle. Amostras de sangue foram coletadas para sorotipagem direta e reversa. Os grupos controle e AVCI foram comparados em relação aos fatores de risco tradicionais e à distribuição dos grupos sanguíneos ABO. Resultados: O grupo AVCI apresentou maior prevalência de hipertensão arterial sistêmica (HAS), diabetes mellitus, tabagismo, história familiar, cardiopatia e estilo de vida sedentário em comparação ao grupo controle. O tipo sanguíneo AB prevaleceu entre os pacientes (5,1 vs. 1,6%; p<0,05) e apresentou mais casos de HAS em comparação ao tipo O (92,9 vs. 67,3%; p<0,05). Conclusões: Nossos resultados sugerem que a ocorrência de AVCI é mais frequente entre os pacientes do tipo sanguíneo AB.

ABSTRACT Background: Ischemic stroke (IS) is a multifactorial disease that presents high rates of morbimortality in Brazil. Several studies proved that there is a link between the ABO blood group system and the occurrence of thrombotic events. Nonetheless, its association with IS is not well established. Objective: For that reason, the purpose hereof was to investigate the relation between the ABO blood groups and the occurrence of IS in a Brazilian cohort of cerebrovascular diseases. Methods: Five hundred and twenty-nine subjects were included over 12 months, from which 275 presented an IS episode and 254 composed the control group. Blood samples were drawn for direct and reverse serotyping. The control and IS groups were compared regarding the traditional risk factors and the distribution of the ABO blood groups. Results: The IS group presented a higher prevalence of systemic arterial hypertension (SAH), diabetes mellitus, smoking habits, family history, cardiopathy, and sedentary lifestyle in comparison with the control group. The AB blood type prevailed among the patients (5.1 vs. 1.6%; p<0.05) and this group had more SAH cases in comparison with the O type group (92.9 vs. 67.3%; p<0.05). Conclusions: Our results suggest that the occurrence of IS is more frequent among patients of the AB blood type.

RESUMO Com o objetivo de contribuir para estudos que utilizam informações clínicas e genômicas de biobancos, apresentamos os resultados iniciais do primeiro Biobanco Latinoamericano em Acidente Vascular Cerebral (AVC). Métodos: Foram coletadas amostras de sangue de pacientes recrutados pelo Registro de AVC de Joinville e posteriormente de quatro cidades brasileiras. Foram registrados dados socioeconômicos demográficos, fatores de risco cardiovasculares, Causative Classification System (CCS), Trial of Org 10172 in Acute Stroke Treatment, National Institutes of Health, estado funcional (Rankin modificado) e imagens cerebrais. Adicionalmente, foram recrutados controles das regiões geográficas correspondentes. Obteve-se DNA genômico de todos participantes. Resultados: Foram incluídos 2688 pacientes e 3282 controles. Entre os pacientes, 76% tiveram AVC isquêmico, 12% ataques isquêmicos transitórios, 9% AVC hemorrágico e 3% hemorragia subaracnóidea. Os casos indeterminados foram os mais frequentes e classificados de acordo com TOAST (40%) e CCS (47%). Um quarto dos pacientes tinham menos de 55 anos no primeiro evento. Conclusões: Estabelecemos o Joinville Stroke Biobank, e discutimos aqui seu potencial na compreensão dos fatores de risco do AVC.

ABSTRACT Aiming to contribute to studies that use detailed clinical and genomic information of biobanks, we present the initial results of the first Latin American Stroke Biobank. Methods: Blood samples were collected from patients included in the Joinville Stroke Registry and four Brazilian cities. Demographic socio-economic data, cardiovascular risk factors, Causative Classification System for Ischemic Stroke, Trial of Org 10172 in Acute Stroke Treatment and National Institutes of Health scores, functional stroke status (modified Rankin) and brain images were recorded. Additionally, controls from both geographic regions were recruited. High-molecular-weight genomic DNA was obtained from all participants. Results: A total of 2,688 patients and 3,282 controls were included. Among the patients, 76% had ischemic stroke, 12% transient ischemic attacks, 9% hemorrhagic stroke and 3% subarachnoid hemorrhage. Patients with undetermined ischemic stroke were most common according the Trial of Org 10172 in Acute Stroke Treatment (40%) and Causative Classification System for Ischemic Stroke (47%) criteria. A quarter of the patients were under 55 years of age at the first-ever episode. Conclusions: We established the Joinville Stroke Biobank and discuss its potential for contributing to the understanding of the risk factors leading to stroke.

Abstract: INTRODUCTION: Members of the Acinetobacter genus are key pathogens that cause healthcare-associated infections, and they tend to spread and develop new antibiotic resistance mechanisms. Oxacillinases are primarily responsible for resistance to carbapenem antibiotics. Higher rates of carbapenem hydrolysis might be ascribed to insertion sequences, such as the ISAba1 sequence, near bla OXA genes. The present study examined the occurrence of the genetic elements bla OXA and ISAba1 and their relationship with susceptibility to carbapenems in clinical isolates of the Acinetobacter calcoaceticus-Acinetobacter baumannii complex. METHODS: Isolates identified over 6 consecutive years in a general hospital in Joinville, Southern Brazil, were evaluated. The investigation of 5 families of genes encoding oxacillinases and the ISAba1 sequence location relative to bla OXA genes was conducted using polymerase chain reaction. RESULTS: All isolates presented the bla OXA-51-like gene (n = 78), and 91% tested positive for the bla OXA-23-like gene (n = 71). The presence of ISAba1 was exclusively detected in isolates carrying the bla OXA-23-like gene. All isolates in which ISAba1 was found upstream of the bla OXA-23-like gene (n = 69) showed resistance to carbapenems, whereas the only isolate in which ISAba1 was not located near the bla OXA-23-like gene was susceptible to carbapenems. The ISAba1 sequence position of another bla OXA-23-like-positive isolate was inconclusive. The isolates exclusively carrying the bla OXA-51-like gene (n = 7) showed susceptibility to carbapenems. CONCLUSIONS: The presence of the ISAba1 sequence upstream of the bla OXA-23-like gene was strongly associated with carbapenem resistance in isolates of the A. calcoaceticus-A. baumannii complex in the hospital center studied.

Abstract: INTRODUCTION: Carbapenems are the therapy of choice for treating severe infections caused by the Acinetobacter calcoaceticus-Acinetobacter baumannii complex. We aimed to assess the prevalence and antimicrobial susceptibility profiles of producers of distinct oxacillinases among nosocomial isolates of the A. calcoaceticus-A. baumannii complex in a 249-bed general hospital located in Joinville, Southern Brazil. METHODS: Of the 139 A. baumannii clinical isolates with reduced susceptibility to carbapenems between 2010 and 2013, 118 isolates from varying anatomical sites and hospital sectors were selected for genotypic analysis. Five families of genes encoding oxacillinases, namely blaOXA-23-like, blaOXA-24-like, blaOXA-51-like, blaOXA-58-like, and blaOXA-143-like, wereinvestigated by multiplex polymerase chain reaction (PCR). RESULTS: Most (87.3%) isolates simultaneously carried the blaOXA-23-likeand blaOXA-51-likegenes, whereas three (2.5%) isolates harbored only blaOXA-51-likeones. The circulation of carbapenem-resistant isolates increased during the study period: from none in 2010, to 22 in 2011, 64 in 2012, and 53 in 2013. CONCLUSIONS: Isolates carrying the blaOXA-23-likeand blaOXA-51-likegenes were widely distributed in the hospital investigated. Because of the worsening scenario, the implementation of preventive measures and effective barriers is needed.

ContextoA doença de Crohn caracteriza-se por uma desordem inflamatória, crônica e debilitante do trato gastrointestinal. Diversos fatores contribuem para seu desenvolvimento. A partir da realização de estudos amplos do genoma, o polimorfismo T300A do gene ATG16L1 (autophagy-related 16-like 1) tem sido relacionado com aumento de susceptibilidade ao desenvolvimento desta doença.ObjetivosAnalisar a incidência do polimorfismo T300A (rs2241880) em pacientes com doença de Crohn.MétodosForam analisadas 238 amostras de doadores de sangue (grupo controle) e 106 amostras de pacientes com doença de Crohn, procedentes de cinco centros. A genotipagem consistiu em amplificação do segmento gênico T300A, via reação em cadeia da polimerase, seguidos da análise de polimorfismo de comprimentos dos fragmentos de restrição. Os amplicons e fragmentos foram separados via eletroforese em gel de agarose e visualizados sob luz ultravioleta.ResultadosO genótipo AG foi mais prevalente entre os pacientes e controles (50% vs 44,8%), seguido dos genótipos AA (26,4% vs 35,1%) e GG (23,6% vs 20,1%). A freqüência do alelo G do polimorfismo T300A foi maior no grupo de pacientes com doença de Crohn (48,6%) do que nos controles (42,4%), embora sem significância estatística.ConclusõesNão foi possível confirmar o aumento de susceptibilidade à doença de Crohn conferido pelo polimorfismo T300A.

ContextCrohn’s disease is characterized by a chronic and debilitating inflammatory disorder of the gastrointestinal tract. Several factors may contribute to its development. From extensive studies of the human genome, the polymorphism T300A of the gene ATG16L1 (autophagy-related 16-like 1) has been related to increased risk of developing this disease.ObjectivesAnalyze the role of polymorphism T300A (rs2241880) in patients with Crohn’s disease.Methods238 samples from (control group) and 106 samples from patients with Crohn’s disease recruited at five Southern Brazilian reference centers were evaluated. The genotyping consisted of the amplification via Polymerase Chain Reaction of the genomic segment encompassing T300A, followed by Restriction Fragment Length Polymorphism analysis. The amplicons and fragments were separated by agarose gel electrophoresis and confirmed under ultraviolet light.ResultsThe genotype AG was more prevalent among patients and controls (50% vs 44.8%), followed by genotypes AA (26.4% vs 35.1%) and GG (23.6% vs 20.1%). The frequency of the allele G of the polymorphism T300A was higher in the group of patients with Crohn’s disease (48.6%) than in controls (42.4%), although not reaching statistical significance.ConclusionsIt was not possible to confirm the increased susceptibility on development of Crohn’s disease conferred by polymorphism T300A.

CONTEXTO: A utilização de drogas tiopurinas como a azatioprina e a 6-mercaptopurina tem se tornado bastante frequente no tratamento de doenças inflamatórias intestinais, transplantes e leucemias agudas. Apesar de sua efetividade, estas drogas são capazes de causar toxicidade droga-induzida com risco de morte através de mielossupressão. Sabe-se hoje que estas complicações ocorrem em decorrência de polimorfismos genéticos da enzima tiopurina metiltransferase (TPMT), responsável por sua metabolização. OBJETIVOS: Avaliar a prevalência do polimorfismo do gene da TPMT na população de Joinville, SC. MÉTODOS: Foi analisada a frequência das quatro principais variantes alélicas do gene da TPMT em 199 doadores de sangue da cidade de Joinville, SC, no período de fevereiro a abril de 2010. RESULTADOS: O alelo normal ("selvagem") foi encontrado em 93,9% dos indivíduos estudados. Variantes da TPMT foram detectadas em 12 sujeitos (6,03%). CONCLUSÕES: A partir do presente estudo, pode-se estimar em cerca de 6% o risco de toxicidade na administração de azatioprina e 6-mercaptopurina a pacientes em Joinville.

CONTEXT: The use of thiopurine drugs such as azathioprine and 6-mercaptopurine has become quite common in the treatment of inflammatory bowel disease, transplantation and acute leukemias. Despite their effectiveness, these drugs are capable of causing drug-induced toxicity with the risk of death by myelosuppression. It is now known that these complications occur because of genetic polymorphisms of the thiopurinemethyltransferase (TPMT) enzyme, responsible for its metabolism. OBJECTIVE: To assess the prevalence of thiopurine methyltransferase polymorphisms in the population of Joinville, SC, Brazil. METHODS: We analyzed the frequency of four main allelic variants of the TPMT gene in 199 blood donors from Joinville, from February to April 2010. RESULTS: The normal allele ("wild-type") was found in 93.9% of subjects studied. TPMT variants were detected in 12 subjects (6.03%). CONCLUSIONS: From this study, it was estimated at 6% the risk of toxicity by the administration of azathioprine and 6-mercaptopurine to patients in Joinville.

INTRODUÇÃO: A sepse é uma resposta inflamatória sistêmica relacionada com altas taxas de mortalidade no meio hospitalar. O diagnóstico etiológico tardio e terapia antimicrobiana inadequada se associam a falhas do tratamento. Exames moleculares baseados na reação em cadeia da polimerase são considerados métodos mais rápidos e precisos do que técnicas de hemocultura para identificação microbiana, proporcionando uma taxa mais elevada de sucesso terapêutico. OBJETIVO: Desenvolver um painel de seqüências iniciadoras (primers) para fragmentos de DNA de microrganismos associados à sepse. MÉTODOS: Seqüências iniciadoras para amplificação de Enterobacter spp., Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus e Candida spp. foram desenvolvidos e testados quanto a sensibilidade e especificidade com base em suas respectivas cepas padrão. RESULTADOS: A especificidade pretendida foi obtida para os primers de P. aeruginosa, S. aureus e Candida spp. O teste de sensibilidade mostrou um limite de detecção de 5 ng a 500 fg em amostras de sangue contaminado com DNA microbiano. CONCLUSÕES: O painel molecular apresentado oferece a vantagem de constituir um sistema flexível "aberto" em comparação a outros métodos de detecção múltipla.

INTRODUCTION: Sepsis is a systemic inflammatory response related to high mortality rates in the hospital environment. Delayed etiological diagnosis and inadequate antimicrobial therapy are associated with treatment failures. Molecular tests based on polymerase chain reaction are regarded as faster and more accurate procedures than culture techniques for microbial identification, providing a higher rate of therapeutic success. OBJECTIVE: To develop a panel of primers for DNA fragments of sepsis-related microorganisms. METHODS: Primers for amplification of Enterobacter spp., Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus and Candida spp. were designed and tested for sensitivity and specificity on the basis of their respective standard strains. RESULTS: The intended specificity was obtained for P. aeruginosa, S. aureus and Candida spp primers. Sensitivity tests showed a threshold for detection from 5 ng to 500 fg in blood samples contaminated with microbial DNA. CONCLUSIONS: The molecular panel presented offers the advantage of a flexible 'open' system when compared to other multiplex detection methods.

Os estudos em biologia molecular desenvolvidos nas últimas décadas, possibilitaram grandes avanços para uma maior compreensão da carcinogênese colorretal. Na década de 80 pesquisadores descobriram uma proteína com a capacidade de aumentar a permeabilidade dos vasos sangüíneos. Inicialmente esta proteína foi denominada como fator de permeabilidade vascular. Estudos posteriores correlacionaram esta proteína com o crescimento de novos vasos sangüíneos (angiogênese), quando passou a ser chamada de fator de crescimento endotelial vascular (VEGF). A proteína VEGF tem sido apontada como o principal fator promotor da angiogênese, dentre os vários já conhecidos. Neste trabalho o objetivo foi quantificar a proteína VEGF, e correlacionar os resultados com o estadiamento tumoral em amostras de adenocarcinoma colorretal. Foram incluídos 56 adenocarcinomas colorretais, nos quais a detecção da proteína VEGF foi realizada por imunoistoquímica através da construção de uma matriz tecidual e sua quantificação com análise digital de imagens assistida por computador. Nossos resultados não evidenciaram relação estatisticamente significativa entre a expressão da proteína VEGF e o estadiamento tumoral, ou presença e número de linfonodos comprometidos. Baseado no nível de expressão da proteína VEGF não foi possível inferir a presença de linfonodos comprometidos nas amostras analisadas.

Development of studies in molecular biology over the last decades has contributed for better knowledge about colorectal carcinogenesis. An important landmark in this process was the identification of a protein with effect on vascular permeability eventually named as vascular endothelial growth factor (VEGF), which seems to be essential for the angiogenesis activation of tumor development. The aim of this study was to assess the VEGF expression and correlate to tumor staging in colorectal cancer. Surgical specimens from 56 colorectal cancer patients were analyzed by immunohistochemistry for VEGF expression using a multitissue array and a computer-assisted image system. No significant result was found between VEGF expression and tumor staging or lymph nodes metastasis. We concluded that no predictive value for lymph nodes metastasis could be demonstrated by VEGF immunostaining in this study.