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1.
Epidemiol Health ; 42: e2020004, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32023777

RESUMO

OBJECTIVES: This report provides information on 14 behavioral and nutritional factors that can be addressed in stomach cancer prevention programs. METHODS: PubMed, Web of Science, and Scopus were searched through December 2018. Reference lists were also screened. Observational studies addressing the associations between stomach cancer and behavioral factors were analyzed. Between-study heterogeneity was investigated using the χ2, τ2, and I2 statistics. The likelihood of publication bias was explored using the Begg and Egger tests and trim-and-fill analysis. Effect sizes were expressed as odds ratios (ORs) with 95% confidence intervals (CIs) using a random-effects model. RESULTS: Of 52,916 identified studies, 232 (including 33,831,063 participants) were eligible. The OR (95% CI) of factors associated with stomach cancer were as follows: Helicobacter pylori infection, 2.56 (95% CI, 2.18 to 3.00); current smoking, 1.61 (95% CI, 1.49 to 1.75); former smoking 1.43 (95% CI, 1.29 to 1.59); current drinking, 1.19 (95% CI, 1.10 to 1.29); former drinking, 1.73 (95% CI, 1.17 to 2.56); overweight/obesity, 0.89 (95% CI, 0.74 to 1.08); sufficient physical activity, 0.83 (95% CI, 0.68 to 1.02); consumption of fruits ≥3 times/wk, 0.48 (95% CI, 0.37 to 0.63); consumption of vegetables ≥3 times/wk, 0.62 (95% CI, 0.49 to 0.79); eating pickled vegetables, 1.28 (95% CI, 1.09 to 1.51); drinking black tea, 1.00 (95% CI, 0.84 to 1.20); drinking green tea, 0.88 (95% CI, 0.80 to 0.97); drinking coffee, 0.99 (95% CI, 0.88 to 1.11); eating fish ≥1 time/wk 0.79 (95% CI, 0.61 to 1.03); eating red meat ≥4 times/wk 1.31 (95% CI, 0.87 to 1.96), and high salt intake 3.78 (95% CI, 1.74 to 5.44) and 1.34 (95% CI, 0.88 to 2.03), based on two different studies. CONCLUSIONS: This meta-analysis provided a clear picture of the behavioral and nutritional factors associated with the development of stomach cancer. These results may be utilized for ranking and prioritizing preventable risk factors to implement effective prevention programs.


Assuntos
Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/prevenção & controle , Comportamentos de Risco à Saúde , Humanos , Estado Nutricional , Fatores de Risco
3.
N Engl J Med ; 382(5): 427-436, 2020 01 30.
Artigo em Inglês | MEDLINE | ID: mdl-31995688

RESUMO

BACKGROUND: Helicobacter pylori infection and a family history of gastric cancer are the main risk factors for gastric cancer. Whether treatment to eradicate H. pylori can reduce the risk of gastric cancer in persons with a family history of gastric cancer in first-degree relatives is unknown. METHODS: In this single-center, double-blind, placebo-controlled trial, we screened 3100 first-degree relatives of patients with gastric cancer. We randomly assigned 1838 participants with H. pylori infection to receive either eradication therapy (lansoprazole [30 mg], amoxicillin [1000 mg], and clarithromycin [500 mg], each taken twice daily for 7 days) or placebo. The primary outcome was development of gastric cancer. A prespecified secondary outcome was development of gastric cancer according to H. pylori eradication status, assessed during the follow-up period. RESULTS: A total of 1676 participants were included in the modified intention-to-treat population for the analysis of the primary outcome (832 in the treatment group and 844 in the placebo group). During a median follow-up of 9.2 years, gastric cancer developed in 10 participants (1.2%) in the treatment group and in 23 (2.7%) in the placebo group (hazard ratio, 0.45; 95% confidence interval [CI], 0.21 to 0.94; P = 0.03 by log-rank test). Among the 10 participants in the treatment group in whom gastric cancer developed, 5 (50.0%) had persistent H. pylori infection. Gastric cancer developed in 0.8% of participants (5 of 608) in whom H. pylori infection was eradicated and in 2.9% of participants (28 of 979) who had persistent infection (hazard ratio, 0.27; 95% CI, 0.10 to 0.70). Adverse events were mild and were more common in the treatment group than in the placebo group (53.0% vs. 19.1%; P<0.001). CONCLUSIONS: Among persons with H. pylori infection who had a family history of gastric cancer in first-degree relatives, H. pylori eradication treatment reduced the risk of gastric cancer. (Funded by the National Cancer Center, South Korea; ClinicalTrials.gov number, NCT01678027.).


Assuntos
Antibacterianos/uso terapêutico , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori , Inibidores da Bomba de Prótons/uso terapêutico , Neoplasias Gástricas/prevenção & controle , Adenoma/epidemiologia , Adenoma/etiologia , Adenoma/prevenção & controle , Adulto , Idoso , Amoxicilina/uso terapêutico , Claritromicina/uso terapêutico , Método Duplo-Cego , Quimioterapia Combinada , Feminino , Infecções por Helicobacter/complicações , Humanos , Incidência , Estimativa de Kaplan-Meier , Lansoprazol/uso terapêutico , Masculino , Pessoa de Meia-Idade , República da Coreia , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/genética
5.
Gastroenterology ; 158(3): 527-536.e7, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31654635

RESUMO

BACKGROUND & AIMS: Nearly all studies of gastric adenocarcinoma in the United States have relied on national cancer databases, which do not include data on Helicobacter pylori infection, the most well-known risk factor for gastric cancer. We collected data from a large cohort of patients in the United States to calculate the incidence of and risk factors for nonproximal gastric adenocarcinomas after detection of H pylori. Secondary aims included identifying how treatment and eradication affect cancer risk. METHODS: We performed a retrospective cohort study, collecting data from the Veterans Health Administration on 371,813 patients (median age 62 years; 92.3% male) who received a diagnosis of H pylori infection from January 1, 1994, through December 31, 2018. The primary outcome was a diagnosis of distal gastric adenocarcinoma 30 days or more after detection of H pylori infection. We performed a time to event with competing risk analysis (with death before cancer as a competing risk). RESULTS: The cumulative incidence of cancer at 5, 10, and 20 years after detection of H pylori infection was 0.37%, 0.5%, and 0.65%, respectively. Factors associated with cancer included older age at time of detection of H pylori infection (subhazard ratio [SHR], 1.13; 95% confidence interval [CI], 1.11-1.15; P < .001), black/African American race (SHR, 2.00; 95% CI, 1.80-2.22), Asian race (SHR, 2.52; 95% CI, 1.64-3.89) (P < .001 for race), Hispanic or Latino ethnicity (SHR, 1.59; 95% CI, 1.34-1.87; P < .001), and history of smoking (SHR, 1.38; 95% CI, 1.25-1.52; P < .001). Women had decreased risk of gastric adenocarcinoma compared with men (SHR, 0.52; 95% CI, 0.40-0.68; P < .001); patients whose H pylori infection was detected based on serum antibody positivity also had a reduced risk of cancer (SHR 0.74; 95% CI, 0.54-1.04; P = .04). Patients who received treatment for their H pylori infection still had an increased risk of gastric cancer (SHR, 1.16; 95% CI, 0.74-1.83; P = .51) but confirmed H pylori eradication after treatment reduced risk of gastric cancer (SHR, 0.24; 95% CI, 0.15-0.41; P < .001). CONCLUSIONS: In a study of 371,813 veterans with a diagnosis of H pylori infection, we found significantly higher risks of gastric cancer in racial and ethnic minorities and smokers. Treatment of H pylori infection decreased risk only if eradication was successful. Studies are needed on the effects of screening high-risk persons and to identify quality measures for diagnosis, resistance patterns, and treatment efficacy.


Assuntos
Adenocarcinoma/epidemiologia , Infecções por Helicobacter/epidemiologia , Helicobacter pylori/isolamento & purificação , Neoplasias Gástricas/epidemiologia , Adenocarcinoma/etiologia , Adenocarcinoma/prevenção & controle , Fatores Etários , Idoso , Antiácidos/uso terapêutico , Antibacterianos/uso terapêutico , Quimioterapia Combinada/métodos , Grupos Étnicos/estatística & dados numéricos , Feminino , Seguimentos , Disparidades nos Níveis de Saúde , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/tratamento farmacológico , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Inibidores da Bomba de Prótons/uso terapêutico , Fatores Raciais , Estudos Retrospectivos , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/prevenção & controle , Fatores de Tempo , Estados Unidos/epidemiologia , United States Department of Veterans Affairs/estatística & dados numéricos , Veteranos/estatística & dados numéricos
10.
Int J Mol Sci ; 20(20)2019 Oct 09.
Artigo em Inglês | MEDLINE | ID: mdl-31600923

RESUMO

Germline pathogenic variants in the CDH1 gene are a well-established cause of hereditary diffuse gastric cancer (HDGC) syndrome. The aim of this study was to characterize CDH1 mutations associated with HDGC from Chile, a country with one of the highest incidence and mortality rates in the world for gastric cancer (GC). Here, we prospectively include probands with family history/early onset of diffuse-type of GC. The whole coding sequence of the CDH1 gene was sequenced from genomic DNA in all patients, and a multidisciplinary team managed each family member with a pathogenic sequence variant. Thirty-six cases were included (median age 44 years/male 50%). Twenty-seven (75%) patients had diffuse-type GC at ≤50 years of age and 19 (53%) had first or second-degree family members with a history of HDGC. Two cases (5.5%) carried a non-synonymous germline sequence variant in the CDH1 gene: (a) The c.88C>A missense variant was found in a family with three diffuse-type GC cases; and (b) c.1531C>T a nonsense pathogenic variant was identified in a 22-year-old proband with no previous family history of HDGC. Of note, six family members carry the same nonsense pathogenic variant. Prophylactic gastrectomy in the proband's sister revealed stage I signet-ring cell carcinoma. The finding of 1531C>T pathogenic variant in the CDH1 in proband with no previous family history of HDGC warrants further study to uncover familial clustering of disease in CDH1 negative patients. This finding may be particularly relevant in high incidence countries, such as the case in this report.


Assuntos
Alelos , Antígenos CD/genética , Caderinas/genética , Predisposição Genética para Doença , Mutação em Linhagem Germinativa , Síndromes Neoplásicas Hereditárias/genética , Neoplasias Gástricas/genética , Adulto , Feminino , Gastrectomia/métodos , Estudos de Associação Genética , Humanos , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Síndromes Neoplásicas Hereditárias/diagnóstico , Síndromes Neoplásicas Hereditárias/prevenção & controle , Linhagem , Procedimentos Cirúrgicos Profiláticos , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/prevenção & controle , Adulto Jovem
12.
Biomed Pharmacother ; 120: 109427, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31648165

RESUMO

Gastric cancer is recognized as one of the most common cancer. In-depth research of gastric precancerous lesions (GPL) plays an important role in preventing the occurrence of gastric cancer. Meanwhile, traditional treatment provides a novel sight in the prevention of occurrence and development of gastric cancer. The current study was designed to assess the effects of therapy with Weipixiao (WPX) decoction on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced GPL rats and the underlying molecular mechanisms. After 10-weeks treatment, all rats were sacrificed. Histopathological changes of gastric tissue were assessed via hematoxylin-eosin (HE) and High-iron diamine-Alcian blue-Periodic acid-Schiff (HID-AB-PAS) staining. To be fully evidenced, RT-qPCR, Western blot and immunohistochemistry were used to detect the expressions of LDHA, CD147, HIF-1α, MCT4, PI3K, AKT, mTOR and miRNA-34a, which were crucial factors for evaluating GPL in the aspect of glycolysis pathogenesis. According to the results of HE and HID-AB-PAS staining, it could be confirmed that MNNG-induced GPL rats were obviously reversed by WPX decoction. Additionally, the increased gene levels of LDHA, CD147, MCT4, PI3K, AKT, mTOR and HIF-1α in model group were down-regulated by WPX decoction, while miRNA-34a expression was decreased and up-regulated by WPX decoction. The significantly increased protein levels of LDHA, CD147, MCT4, PI3K, AKT, mTOR and HIF-1α induced by MNNG were attenuated in rats treated with WPX decoction. In brief, the findings of this study imply that abnormal glycolysis in MNNG-induced GPL rats was relieved by WPX decoction via regulation of the expressions of LDHA, CD147, HIF-1α, MCT4, PI3K, AKT, mTOR and miRNA-34a.


Assuntos
Anticarcinógenos/farmacologia , Medicamentos de Ervas Chinesas/farmacologia , Glicólise/efeitos dos fármacos , Metilnitronitrosoguanidina , Lesões Pré-Cancerosas/prevenção & controle , Neoplasias Gástricas/prevenção & controle , Estômago/efeitos dos fármacos , Animais , Citoproteção , Modelos Animais de Doenças , Regulação Enzimológica da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Masculino , Lesões Pré-Cancerosas/induzido quimicamente , Lesões Pré-Cancerosas/enzimologia , Lesões Pré-Cancerosas/patologia , Ratos Sprague-Dawley , Transdução de Sinais , Estômago/enzimologia , Estômago/patologia , Neoplasias Gástricas/induzido quimicamente , Neoplasias Gástricas/enzimologia , Neoplasias Gástricas/patologia
13.
BMJ ; 366: l5016, 2019 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-31511230

RESUMO

OBJECTIVE: To assess the effects of Helicobacter pylori treatment, vitamin supplementation, and garlic supplementation in the prevention of gastric cancer. DESIGN: Blinded randomized placebo controlled trial. SETTING: Linqu County, Shandong province, China. PARTICIPANTS: 3365 residents of a high risk region for gastric cancer. 2258 participants seropositive for antibodies to H pylori were randomly assigned to H pylori treatment, vitamin supplementation, garlic supplementation, or their placebos in a 2×2×2 factorial design, and 1107 H pylori seronegative participants were randomly assigned to vitamin supplementation, garlic supplementation, or their placebos in a 2×2 factorial design. INTERVENTIONS: H pylori treatment with amoxicillin and omeprazole for two weeks; vitamin (C, E, and selenium) and garlic (extract and oil) supplementation for 7.3 years (1995-2003). MAIN OUTCOME MEASURES: Primary outcomes were cumulative incidence of gastric cancer identified through scheduled gastroscopies and active clinical follow-up through 2017, and deaths due to gastric cancer ascertained from death certificates and hospital records. Secondary outcomes were associations with other cause specific deaths, including cancers or cardiovascular disease. RESULTS: 151 incident cases of gastric cancer and 94 deaths from gastric cancer were identified during 1995-2017. A protective effect of H pylori treatment on gastric cancer incidence persisted 22 years post-intervention (odds ratio 0.48, 95% confidence interval 0.32 to 0.71). Incidence decreased significantly with vitamin supplementation but not with garlic supplementation (0.64, 0.46 to 0.91 and 0.81, 0.57 to 1.13, respectively). All three interventions showed significant reductions in gastric cancer mortality: fully adjusted hazard ratio for H pylori treatment was 0.62 (95% confidence interval 0.39 to 0.99), for vitamin supplementation was 0.48 (0.31 to 0.75), and for garlic supplementation was 0.66 (0.43 to 1.00). Effects of H pylori treatment on both gastric cancer incidence and mortality and of vitamin supplementation on gastric cancer mortality appeared early, but the effects of vitamin supplementation on gastric cancer incidence and of garlic supplementation only appeared later. No statistically significant associations were found between interventions and other cancers or cardiovascular disease. CONCLUSIONS: H pylori treatment for two weeks and vitamin or garlic supplementation for seven years were associated with a statistically significant reduced risk of death due to gastric cancer for more than 22 years. H pylori treatment and vitamin supplementation were also associated with a statistically significantly reduced incidence of gastric cancer. TRIAL REGISTRATION: ClinicalTrials.gov NCT00339768.


Assuntos
Infecções por Helicobacter/terapia , Lesões Pré-Cancerosas/terapia , Neoplasias Gástricas/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Antiulcerosos/administração & dosagem , Biópsia , China/epidemiologia , Suplementos Nutricionais , Quimioterapia Combinada/métodos , Feminino , Seguimentos , Alho/química , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Gastroscopia , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Extratos Vegetais/administração & dosagem , Lesões Pré-Cancerosas/microbiologia , Lesões Pré-Cancerosas/patologia , Inibidores da Bomba de Prótons/administração & dosagem , Neoplasias Gástricas/patologia , Neoplasias Gástricas/prevenção & controle , Análise de Sobrevida , Taxa de Sobrevida , Fatores de Tempo , Resultado do Tratamento , Vitaminas/administração & dosagem
14.
Biomed Pharmacother ; 118: 109144, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31545234

RESUMO

Gastric cancer is one of the most common cancers leading to tumor-related deaths worldwide. Chicoric acid (CA) exhibits a variety of protective effects in different diseases. However, its role in regulating tumor progression has not been reported. Autophagy, as a conserved catabolic process, sustains cellular homoeostasis responding to stress to modulate cell fate. In the study, the effects of CA on gastric cancer were investigated. The results indicated that CA treatment markedly reduced the cell viability and induced apoptosis in gastric cancer cells, and prevented tumor growth in an established xenograft gastric cancer model. Furthermore, CA exposure significantly induced autophagy both in gastric cancer cells and tumor samples, as evidenced by the up-regulated expression of LC3II. Moreover, phosphorylated AMP-activated protein kinase (AMPK) and p70S6 kinase (p70s6k) expression were obviously promoted by CA in vitro and in vivo. Importantly, blocking AMPK activation abrogated CA-induced expression of LC3II in gastric cancer cells. In addition, endoplasmic reticulum (ER) stress in tumor samples or cells was markedly induced by CA treatment through promoting the expression of associated signals such as Parkin, protein kinase RNA-like ER kinase (PERK), activating transcription factors 4 (ATF4) and ATF6. Importantly, these effects were abolished by the inhibition of AMPK signaling. Collectively, our findings indicated that CA prevents human gastric cancer progression by inducing autophagy partly through the activation of AMPK, and represents an effective therapeutic strategy against gastric cancer development.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Anticarcinógenos/farmacologia , Autofagia/efeitos dos fármacos , Ácidos Cafeicos/farmacologia , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Células Epiteliais/efeitos dos fármacos , Neoplasias Gástricas/prevenção & controle , Succinatos/farmacologia , Animais , Anticarcinógenos/sangue , Ácidos Cafeicos/sangue , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Humanos , Camundongos Endogâmicos BALB C , Camundongos Nus , Ratos , Ratos Sprague-Dawley , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Succinatos/sangue
15.
Klin Onkol ; 32(Supplementum2): 109-117, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31409086

RESUMO

Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) is a rare variant of familial adenomatous polyposis. It is an autosomal-dominant cancer-predisposition syndrome with massive polyposis of the stomach and a significant risk of gastric adenocarcinoma. Li et al., 2016, described point mutations in the Ying Yang 1 binding site of the APC gene 1B promoter associated with GAPPS syndrome. The first GAPPS syndrome in a Czech family was described in 2016. At Masaryk Memorial Cancer Institute, GAPPS syndrome was diagnosed in eight families using Sanger sequencing. In all families, one mutation in promoter 1B of APC gene NM_001127511: c.-191T>C was detected. This mutation was not found in any patient with multiple colon polyposis without a detected classic mutation in the APC gene. In total, 24 carriers of this mutation in promoter 1B of the APC gene were detected. Out of those 24 carriers, 20 had massive gastric polyposis with more than 100 fundic glandular polyps diagnosed between the age of 22 and 65, 5 had already died of adenocarcinoma of the stomach (at the ages of 29, 40, 59, 60 and 64, respectively) and another woman was treated at the age of 29. Two female carriers do not yet have polyposis of the stomach at the ages of 31 and 65, respectively; one female carrier has incipient polyposis at the age of 58. A male carrier does not have any clinical symptoms, gastroscopy was not indicated because of his age. Prophylactic total gastrectomy with D2 lymphadenectomy has already been performed 6 times at Masaryk Memorial Cancer Institute, in 5 cases without adenocarcinoma at the ages of 27, 34, 44, 51 and 66, respectively; in one female carrier adenocarcinoma of the stomach was detected in a histology specimen. Two prophylactic gastrectomies with D1 lymphadenectomy were performed at University Hospital Brno at the ages of 42 and 50, respectively. In the Czech Republic point mutation c.-191T>C (rs879253783) in the 1B promoter of the APC gene is a frequent cause of gastric polyposis with a high risk of gastric adenocarcinoma, even at a young age. Positively tested individuals are recommended to high-risk oncology clinic. A necessary part of the discussion with the patient is information about a preventive gastrectomy.


Assuntos
Adenocarcinoma , Síndromes Neoplásicas Hereditárias , Neoplasias Gástricas , Adenocarcinoma/genética , Adenocarcinoma/prevenção & controle , Proteína da Polipose Adenomatosa do Colo/genética , Adulto , Idoso , Institutos de Câncer , República Tcheca , Feminino , Gastrectomia , Humanos , Masculino , Pessoa de Meia-Idade , Mutação , Síndromes Neoplásicas Hereditárias/genética , Síndromes Neoplásicas Hereditárias/prevenção & controle , Procedimentos Cirúrgicos Profiláticos , Neoplasias Gástricas/genética , Neoplasias Gástricas/prevenção & controle , Adulto Jovem
16.
World J Gastroenterol ; 25(25): 3183-3195, 2019 Jul 07.
Artigo em Inglês | MEDLINE | ID: mdl-31333310

RESUMO

Helicobacter pylori (H. pylori) is the causative agent of gastritis, peptic ulcer disease, mucosa associated lymphoid tissue lymphoma and gastric cancer (GC). While this bacterium infects 50% of the world's population, in Africa its prevalence reach as high as 80% as the infection is acquired during childhood. Risk factors for H. pylori acquisition have been reported to be mainly due to overcrowding, to have infected siblings or parent and to unsafe water sources. Despite this high H. pylori prevalence there still does not exist an African guideline, equivalent to the Maastricht V/Florence Consensus Report of the European Helicobacter and Microbiota Study Group for the management of this infection. In this continent, although there is a paucity of epidemiologic data, a contrast between the high prevalence of H. pylori infection and the low incidence of GC has been reported. This phenomenon is the so-called "African Enigma" and it has been hypothesized that it could be explained by environmental, dietary and genetic factors. A heterogeneity of data both on diagnosis and on therapy have been published. In this context, it is evident that in several African countries the increasing rate of bacterial resistance, mainly to metronidazole and clarithromycin, requires continental guidelines to recommend the appropriate management of H. pylori. The aim of this manuscript is to review current literature on H. pylori infection in Africa, in terms of prevalence, risk factors, impact on human health, treatment and challenges encountered so as to proffer possible solutions to reduce H. pylori transmission in this continent.


Assuntos
Antibacterianos/farmacologia , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori/patogenicidade , Neoplasias Gástricas/epidemiologia , África/epidemiologia , Antibacterianos/uso terapêutico , Claritromicina/farmacologia , Claritromicina/uso terapêutico , Farmacorresistência Bacteriana/efeitos dos fármacos , Gastroenterologia/normas , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/microbiologia , Helicobacter pylori/efeitos dos fármacos , Helicobacter pylori/isolamento & purificação , Humanos , Incidência , Metronidazol/farmacologia , Metronidazol/uso terapêutico , Guias de Prática Clínica como Assunto , Prevalência , Fatores de Risco , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/prevenção & controle
17.
Medicina (Kaunas) ; 55(7)2019 Jul 19.
Artigo em Inglês | MEDLINE | ID: mdl-31330954

RESUMO

Background and objectives: Human gastric adenocarcinoma (AGS) is one of the most common malignant cancers worldwide. The present study aimed to transfer oleuropein into cancer cells using synthetic paramagnetic nanoparticles and study their effect on the AGS (ATCC® CRL1739™) cell line. Materials and Methods: Paramagnetic nano-oleuropein was synthesized using four-stage co-precipitation by developing NH-connected bridges and was evaluated by EDS, SEM and FTIR methods. Different concentrations of magnetic oleuropein (0, 0.15, 0.45, 1.37, 4.12, 12.35, 37.04, 111.11, 333.33, 1000 µg/mL) were used to treat the AGS cell line in a completely randomized design using a statistical framework with three replicates. The relative expression rate of miR-200 and KRAS oncogenes was evaluated using real-time PCR. The inhibition rate of the AGS cells was assessed using the MTT test at 24, 48 and 72 h intervals. Results: The results showed that there was a significant difference between the inhibition rates of magnetic nano-oleuropein at IC50-24h (23.6 µg/mL), IC50-48h (15.2 µg/mL) and IC50-72h (9.2 µg/mL). Real-time PCR indicated that the relative expression of KRAS and miR-200 genes was highest at IC50 at these intervals. Conclusions: Magnetic nano-oleuropein can be subjected to objective testing and clinical evaluations as a natural antioxidant to prevent and treat gastric adenocarcinoma.


Assuntos
Adenocarcinoma/prevenção & controle , Expressão Gênica/efeitos dos fármacos , Iridoides/uso terapêutico , Proteínas Proto-Oncogênicas p21(ras)/biossíntese , Neoplasias Gástricas/prevenção & controle , Proliferação de Células/efeitos dos fármacos , Humanos , Iridoides/farmacologia , Nanopartículas/uso terapêutico , Olea/enzimologia , Olea/genética , Proteínas Proto-Oncogênicas p21(ras)/sangue , Espectrometria por Raios X/métodos
18.
Nutrients ; 11(8)2019 Jul 26.
Artigo em Inglês | MEDLINE | ID: mdl-31357492

RESUMO

To investigate the associations between dietary fatty acids and cholesterol consumption and stomach cancer (SC), we analyzed data from a population-based case-control study with a total of 1900 SC cases and 6532 controls. Dietary data and other risk or protective factors were collected by face-to-face interviews in Jiangsu Province, China, from 2003 to 2010. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple unconditional logistic regression models and an energy-adjusted method. The joint associations between dietary factors and known risk factors on SC were examined. We observed positive associations between dietary saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and total cholesterol and the development of SC, comparing the highest versus lowest quarters. Increased intakes of dietary SFAs (p-trend = 0.005; aOR, 1.11; 95% CI, 1.01-1.22 with a 7 g/day increase as a continuous variable) and total cholesterol (p-trend < 0.001; aOR, 1.13; 95% CI, 1.06-1.22 with a 250 mg/day increase as a continuous variable) were monotonically associated with elevated odds of developing SC. Our results indicate that dietary SFAs, MUFAs, and total cholesterol are associated with stomach cancer, which might provide a potential dietary intervention for stomach cancer prevention.


Assuntos
Colesterol na Dieta/efeitos adversos , Dieta/efeitos adversos , Ácidos Graxos/efeitos adversos , Neoplasias Gástricas/epidemiologia , Idoso , Estudos de Casos e Controles , China/epidemiologia , Colesterol na Dieta/administração & dosagem , Ácidos Graxos/administração & dosagem , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Proteção , Recomendações Nutricionais , Medição de Risco , Fatores de Risco , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/prevenção & controle
19.
Phytomedicine ; 63: 152968, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31280140

RESUMO

BACKGROUND: Gastric cancer has a high morbidity and is a leading cause of cancer-related mortality worldwide. Helicobacter pylori (H. pylori) infection is commonly found in the early stage of gastric cancer pathogenesis, which induces chronic gastritis. Artemisinin (ART) and its derivatives (ARTS, artesunate and DHA, dihydroartemisinin), a new class of potent antimalarials, have been reported to exert both preventive and anti-gastric cancer effects. However, the underlying mechanisms of the chemopreventive effects of ART and its derivatives in H. pylori infection induced-gastric cancer are not fully elucidated. PURPOSE: We investigated the effects of H. pylori infection in gastric cancer; and the preventive mechanisms of ART, ARTS and DHA. METHODS: The H. pylori growth was determined by the broth macro-dilution method, and its adhesion to gastric cancer cells was evaluated by using the urease assay. The protein and mRNA levels, reactive oxygen species (ROS) production, as well as the production of inflammatory cytokines were evaluated by Western blot, real-time PCR, flow cytometry and ELISA, respectively. Moreover, an in vivo MNU (N-methyl-N-nitroso-urea) and H. pylori-induced gastric adenocarcinoma mouse model was established for the investigation of the cancer preventive effects of ART and its derivaties, and the underlying mechanisms of action. RESULTS: ART, DHA and ARTS inhibited the growth of H. pylori and gastric cancer cells,suppressed H. pylori adhesion to the gastric cancer cells, and reduced the H. pylori-enhanced ROS production. Moreover, ART, DHA and ARTS significantly reduced tumor incidence, number of tumor nodules and tumor size in the mouse model. Among these three compounds, DHA exerted the most potent chemopreventive effect. Mechanistic studies showed that ART and its derivatives potently inhibited the NF-κB activation. CONCLUSION: ART, DHA and ARTS have potent preventive effects in H. pylori-induced gastric carcinogenesis. These effects are, at least in part, attributed to the inhibition of NF-κB signaling pathway. Our findings provide a molecular justification of using ART and its derivatives for the prevention and treatment of gastric cancer.


Assuntos
Anticarcinógenos/farmacologia , Artemisininas/farmacologia , Infecções por Helicobacter/complicações , Helicobacter pylori/efeitos dos fármacos , Neoplasias Gástricas/prevenção & controle , Animais , Artesunato/farmacologia , Aderência Bacteriana/efeitos dos fármacos , Linhagem Celular Tumoral , Citocinas/metabolismo , Helicobacter pylori/patogenicidade , Humanos , Camundongos Endogâmicos C57BL , Testes de Sensibilidade Microbiana , NF-kappa B/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/patologia
20.
Fam Cancer ; 18(4): 429-438, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31273560

RESUMO

Germline CDH1 mutation carriers are at risk for early-onset diffuse gastric cancer (DGC) and female carriers have an additional risk of lobular breast cancer. The reported literature GC risk of 70% has led to the recommendation for germline mutation carriers to undergo prophylactic total gastrectomy (PTG). The objective of this research was to examine post-surgical clinical outcomes and to identify which of the domains/symptoms from the European Organisation for Research and Treatment of Cancer QOL Questionnaire (EORTC QLQ-C30) were determinants of overall quality of life (QOL) in individuals undergoing PTG. Participants were recruited through multiple sources. Postsurgical clinical outcomes were obtained from hospital records. Participants completed validated questionnaires measuring generic and condition specific QOL (PROMIS, EORTC and SF 36v.II) at a single point in time. The mean QOL in this cohort was 70.6 (SD = 25.6), which is better than reference values from the general populations in USA and Canada Role and social function plus the symptoms anxiety, pain, taste, dyspnea and diarrhea were significant predictor variables for QOL (p < 0.05). Although this study reveals good overall QOL for individuals after PTG, attention should be given to managing symptoms as part of long term care to further enhance QOL. The function/symptom scores were associated with worse overall health and global health status and thus may mark a real need for more attentive post-surgical care.


Assuntos
Gastrectomia/psicologia , Complicações Pós-Operatórias/etiologia , Procedimentos Cirúrgicos Profiláticos/psicologia , Neoplasias Gástricas/prevenção & controle , Ansiedade/etiologia , Peso Corporal , Depressão/etiologia , Feminino , Gastrectomia/efeitos adversos , Humanos , Laparoscopia/efeitos adversos , Laparoscopia/métodos , Laparoscopia/psicologia , Tempo de Internação , Masculino , Pessoa de Meia-Idade , Satisfação do Paciente , Procedimentos Cirúrgicos Profiláticos/efeitos adversos , Qualidade de Vida , Estudos Retrospectivos , Resultado do Tratamento
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