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1.
Front Pharmacol ; 15: 1391562, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38783944

RESUMO

Gastric/gastroesophageal junction (G/GEJ) cancer represents a significant global health challenge. Radical surgery remains the cornerstone of treatment for resectable G/GEJ cancer. Supported by robust evidence from multiple clinical studies, therapeutic approaches, including adjuvant chemotherapy or chemoradiation, and perioperative chemotherapy, are generally recommended to reduce the risk of recurrence and enhance long-term survival outcomes post-surgery. In recent years, immune checkpoint inhibitors (ICIs) have altered the landscape of systemic treatment for advanced or metastatic G/GEJ cancer, becoming the standard first-line therapy for specific patients. Consequently, exploring the efficacy of ICIs in the adjuvant or neoadjuvant setting for resectable G/GEJ cancer is worthwhile. This review summarizes the current advances in the application of ICIs for resectable G/GEJ cancer.

2.
JAMA Netw Open ; 7(3): e243812, 2024 Mar 04.
Artigo em Inglês | MEDLINE | ID: mdl-38546641

RESUMO

Importance: Whether anti-Helicobacter pylori treatment can provide survival benefits for patients with gastric cancer who are diagnosed with H pylori infection is an area with limited research. Objective: To explore the potential survival benefits of anti-H pylori treatment after radical gastrectomy in patients with gastric cancer and presurgical confirmation of H pylori infection. Design, Setting, and Participants: This retrospective cohort study was conducted using data from patients with gastric cancer treated between January 1, 2010, and December 31, 2018, and followed up for outcome ascertainment until May 19, 2021. Propensity score matching was performed in patients treated with or without anti-H pylori treatment. This study involved a single institute in a comprehensive cancer treatment and research center located in Guangzhou, Guangdong Province, China. The study included patients with gastric or esophagogastric junction adenocarcinoma who underwent curative gastrectomy with D2 lymphadenectomy and tested positive for H pylori infection. Data were analyzed from March to June 2023. Exposure: Anti-H pylori treatment, which primarily includes triple therapy regimens consisting of amoxicillin, clarithromycin, and omeprazole for 14 days. Main Outcomes and Measures: Clinical outcomes, including overall survival (OS) and disease-free survival (DFS), were analyzed by Kaplan-Meier method, log-rank test, and Cox proportional hazards regression model. Subgroup analysis based on crucial clinical information was also conducted. Results: All 1293 patients (median [IQR] age, 59 [50-65] years; 860 [66.5%] male) were divided into 2 groups, with 125 patients in the anti-H pylori treatment group and 1168 patients in the non-anti-H pylori treatment group based on whether they received anti-H pylori treatment during the perioperative period and the follow-up. Survival analysis showed that the 5-year OS rates were 94.1% (95% CI, 89.3%-99.2%) in the anti-H pylori group and 73.8% (95% CI, 70.7%-77.0%) in the non-anti-H pylori group, and the hazard ratio (HR) of these 2 groups was 0.33 (95% CI, 0.18-0.60; P < .001). The survival benefit remained after propensity score matching (HR, 0.50; 95% CI, 0.26-0.99; P = .048). Multivariable analysis for OS and DFS further showed the survival benefit of anti-H pylori treatment, with HRs of 0.38 (95% CI, 0.17-0.87; P = .02) and 0.48 (95% CI, 0.28-0.83; P = .008), respectively. Among patients with TNM stage II/III disease who received adjuvant chemotherapy, anti-H pylori treatment was associated with survival benefits (OS: HR, 0.49; 95% CI, 0.24-0.99; P = .046), whereas among those who did not receive adjuvant chemotherapy, anti-H pylori treatment was not associated with survival benefits (OS: HR, 0.29; 95% CI, 0.04-2.08; P = .22). Conclusions and Relevance: This cohort study indicates that anti-H pylori treatment may be associated with improved survival in patients with gastric cancer who have H pylori infections. The study reinforces the importance of including H pylori screening and treatment in the surgical treatment of these patients.


Assuntos
Neoplasias Gástricas , Humanos , Masculino , Pessoa de Meia-Idade , Feminino , Neoplasias Gástricas/cirurgia , Estudos de Coortes , Estudos Retrospectivos , Gastrectomia , Academias e Institutos
3.
Microbiol Spectr ; 11(3): e0007623, 2023 06 15.
Artigo em Inglês | MEDLINE | ID: mdl-37199635

RESUMO

Fetuses diagnosed with fetal growth restriction (FGR) are at an elevated risk of stillbirth and adulthood morbidity. Gut dysbiosis has emerged as one of the impacts of placental insufficiency, which is the main cause of FGR. This study aimed to characterize the relationships among the intestinal microbiome, metabolites, and FGR. Characterization was conducted on the gut microbiome, fecal metabolome, and human phenotypes in a cohort of 35 patients with FGR and 35 normal pregnancies (NP). The serum metabolome was analyzed in 19 patients with FGR and 31 normal pregnant women. Multidimensional data was integrated to reveal the links between data sets. A fecal microbiota transplantation mouse model was used to determine the effects of the intestinal microbiome on fetal growth and placental phenotypes. The diversity and composition of the gut microbiota were altered in patients with FGR. A group of microbial species altered in FGR closely correlated with fetal measurements and maternal clinical variables. Fecal and serum metabolism profiles were distinct in FGR patients compared to those in the NP group. Altered metabolites were identified and associated with clinical phenotypes. Integrated multi-omics analysis revealed the interactions among gut microbiota, metabolites, and clinical measurements. Microbiota from FGR gravida transplanted to mice progestationally induced FGR and placental dysfunction, including impaired spiral artery remodeling and insufficient trophoblast cell invasion. Taken together, the integration of microbiome and metabolite profiles from the human cohort indicates that patients with FGR endure gut dysbiosis and metabolic disorders, which contribute to disease pathogenesis. IMPORTANCE Downstream of the primary cause of fetal growth restriction are placental insufficiency and fetal malnutrition. Gut microbiota and metabolites appear to play an important role in the progression of gestation, while dysbiosis induces maternal and fetal complications. Our study elaborates the significant differences in microbiota profiles and metabolome characteristics between women with FGR and normal pregnancies. This is the first attempt so far that reveals the mechanistic links in multi-omics in FGR, providing a novel insight into host-microbe interaction in placenta-derived diseases.


Assuntos
Retardo do Crescimento Fetal , Microbioma Gastrointestinal , Animais , Feminino , Humanos , Camundongos , Gravidez , Disbiose , Retardo do Crescimento Fetal/metabolismo , Retardo do Crescimento Fetal/microbiologia , Placenta/patologia , Estudos de Coortes , Fezes/microbiologia , RNA Ribossômico 16S/genética , Bactérias/classificação , Bactérias/genética , Bactérias/metabolismo , Adulto , Biodiversidade , Soro/metabolismo
4.
Front Genet ; 13: 1004665, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36276936

RESUMO

Background: Associations between irregular diet and the risk of esophageal cancer remain unclear. The current meta-analysis was performed to determine whether the presence of irregular diet increases the risk of esophageal cancer. Methods: The data from PubMed, Cochrane Libraries, and Embase up to 23 January 2022 were included in our analysis to identify studies that investigated associations between irregular diet and the risk of esophageal cancer. Summary relative risk (RR) and 95% confidence intervals (CIs) were calculated using a random-effects model. Results: Five cohort studies and one case-control study investigating associations between irregular diet and the risk of esophageal cancer were included. None of the articles demonstrated publication bias. The summary RR was 4.181 (95% CI 2.196-7.960, I2 = 66.1%, p = 0.011). In the subgroup analysis, we found significant heterogeneity in the Non-disease-causing group, nurse group and Asian group. The above three that produce heterogeneity may be the source of heterogeneity in the results of this study. Conclusion: The current meta-analysis indicates that irregular diet increase the risk of esophageal cancer. Trial registration: (https://www.crd.york.ac.uk/prospero/), (PROSPERO, CRD42022306407).

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