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1.
J Gastroenterol Hepatol ; 35(6): 1032-1041, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31783428

RESUMO

BACKGROUND AND AIM: Nowadays, anti-inflammation treatment is a promising approach for preventing tumorigenesis, and human microflora is closely related to inflammation. This study aimed to investigate the gastric cardiac microbiome and identify inflammation-related microorganisms for gastric cardiac inflammation. METHODS: We performed 16S rRNA sequencing on a total of 11 healthy individuals and 89 individuals with different degree of gastric cardiac inflammation. Immunohistochemistry was used for verifying candidate bacteria. Phylogenetic reconstruction of unobserved states (picrust) was used for predicting the pathways involved by cardiac microflora. RESULTS: The resident phyla in normal were Proteobacteria, Firmicutes, Bacteroides, and Actinobacteria, and the dominant genus in normal were Halomonas, shewanella, and Comamonas. In the progression of gastric cardiac inflammation, the diversity of cardiac microflora did not change (P > 0.05). However, the composition structure of cardiac microflora varied between healthy and inflamed tissues (P < 0.05). Meanwhile, there were 64 species parallel increased with inflammation degree, especially Helicobacter pylori, Lactobacillus spp. Additionally, inflammation-related species were detected (P < 0.05), including H. pylori, Acinetobacter ursingii, and Streptococcus agalactiae. Higher H. pylori colonization was positively related to the progression of cardiac inflammation (γ coefficient = 0.678, P < 0.001), and it also influenced the cardiac microbial community structure. Cardiac microflora also participated in DNA repair pathways and is affected by the relative abundance of H. pylori (P < 0.0001). CONCLUSIONS: Cardiac microflora dysbiosis, especially the increasing of the relevant abundance of H. pylori, promotes the progression of cardiac inflammation.


Assuntos
Cárdia/microbiologia , Disbiose , Inflamação/etiologia , Inflamação/microbiologia , Microbiota , Acinetobacter , Adulto , Idoso , Idoso de 80 Anos ou mais , Reparo do DNA , Feminino , Helicobacter pylori , Humanos , Lactobacillus , Masculino , Pessoa de Meia-Idade
2.
Gastroenterology ; 153(1): 166-177, 2017 07.
Artigo em Inglês | MEDLINE | ID: mdl-28365443

RESUMO

BACKGROUND & AIMS: Esophageal squamous cell carcinoma (ESCC) is the most common subtype of esophageal cancer. Little is known about the genetic changes that occur in esophageal cells during the development of ESCC. We performed next-generation sequence analyses of esophageal nontumor, intraepithelial neoplasia (IEN), and ESCC tissues from the same patients to track genetic changes during tumor development. METHODS: We performed whole-genome, whole-exome, or targeted sequence analyses of 227 esophageal tissue samples from 70 patients with ESCC undergoing resection at Shantou University Medical College in China from 2012 through 2015 (no patients had received chemotherapy or radiation therapy); we analyzed normal tissues, tissues with simple hyperplasia, dysplastic tissues (IEN), and ESCC tissues collected from different regions of the esophagus at the same time. We also obtained 1191 nontumor esophageal biopsy specimens from the Chaoshan region (a high-risk region for ESCC) of China (a high-risk region for ESCC) and performed immunohistochemical and histologic analyses to detect inflammation. RESULTS: IEN and ESCC tissues had similar mutations and copy number alterations, at similar frequencies; these differed from mutations detected in tissues with simple hyperplasia. IEN tissues had mutations associated with apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like-mediated mutagenesis (a DNA damage mutational signature). Genetic analyses indicated that most ESCCs were formed from early stage IEN clones. Trunk mutations (mutations shared by >10% of paired IEN and ESCC tissues) were in genes that regulate DNA repair and cell apoptosis, proliferation and adhesion. Mutations in TP53 and CDKN2A and copy number alterations in 11q (contains CCND1), 3q (contains SOX2), 2q (contains NFE2L2), and 9p (contains CDKN2A) were considered to be trunk variants; these were dominant mutations detected at high frequencies in clones of paired IEN and ESCC samples. In the esophageal biopsy samples from high-risk individuals (residing in the Chaoshan region), 68.9% had an evidence of chronic inflammation; the level of inflammation was correlated with atypical cell structures and markers of DNA damage. CONCLUSIONS: We analyzed mutations and gene copy number changes in nontumor, IEN, and ESCC samples, collected from 70 patients. IEN and ESCCs each had similar mutations and markers of genomic instability, including apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like. Genomic changes observed in precancerous lesions might be used to identify patients at risk for ESCC.


Assuntos
Carcinoma in Situ/genética , Carcinoma de Células Escamosas/genética , Neoplasias Esofágicas/genética , Esofagite/metabolismo , Esôfago/patologia , Desaminases APOBEC/genética , Apoptose/genética , Adesão Celular/genética , Proliferação de Células/genética , Cromossomos Humanos Par 11/genética , Cromossomos Humanos Par 2/genética , Cromossomos Humanos Par 3/genética , Cromossomos Humanos Par 9/genética , Inibidor p16 de Quinase Dependente de Ciclina , Inibidor de Quinase Dependente de Ciclina p18/genética , Variações do Número de Cópias de DNA , Análise Mutacional de DNA , Reparo do DNA/genética , Esofagite/patologia , Esôfago/metabolismo , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Hiperplasia/genética , Fator 2 Relacionado a NF-E2/genética , Filogenia , Fatores de Transcrição SOXB1/genética , Proteína Supressora de Tumor p53/genética
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