Hepatitis B virus (HBV) is a significant cause of liver disease and cancer worldwide. Understanding the genetic factors influencing HBV evolution is crucial for developing effective prevention and treatment strategies. Host genetic and environmental factors particularly influence the evolution of this infection. Recent studies have implicated the ECM1 gene in HBV pathogenesis, mainly two specific polymorphisms (rs3834087 and rs3754217). In an African cohort, we comprehensively analyzed these ECM1 gene polymorphisms and their association with HBV evolution.In this case-control analysis, 167 samples, consisting of 59 controls and 108 cases, were examined. The cases included 50 patients with Chronic Hepatitis B(CHB), 16 with cirrhosis, and 42 with hepatocellular carcinoma (HCC). Genomic DNA extraction was executed using INVITROGEN and FAVORGEN kits. Genotyping of rs3834087 and rs3754217 polymorphisms in the ECM1 gene was accomplished via real-time PCR on the QuantStudioTM 5 Real-Time instrument, followed by allelic discrimination using TaqMan Genotyper Software. Data was interpreted using SPSS version 20 and Epi info version 7.5.2.0. Odds ratios (OR), confidence intervals (CI), and p-values were derived for risk and significance evaluation.In our study, the heterozygous genotype (GT) of rs3754217 could confer protection to controls against the onset of chronic hepatitis in the event of infection (OR=0.05; CI=0.006-0.46; p=0.002). In addition, carriage of mutated alleles of the two (2) polymorphisms was associated with the course of infection and may influence the appearance of severe forms at certain stages of the disease.Our study is the first to assess the association between polymorphisms (rs3834087 and rs3754217) in the ECM1 gene and the course of HBV infection in Burkina Faso. It showed that combining specific genotypes of the two (2) polymorphisms would be associated with protection against chronic hepatitis.
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http://dx.doi.org/10.14715/cmb/2024.70.12.5 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
January 2025
Université Joseph KI-ZERBO, Laboratoire de Biologie Moléculaire et de Génétique (LABIOGENE), 03 BP 7021 Ouagadougou 03, Burkina Faso.
Cancer Cell Int
December 2024
Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Hepato-Pancreato-Biliary Surgery, Peking University Cancer Hospital & Institute, Beijing, 100142, P. R. China.
Background: Retroperitoneal liposarcoma (RLPS) is a mesenchymal malignant tumor characterized by different degrees of adipocytic differentiation. Well-differentiated liposarcoma (WDLPS) and dedifferentiated liposarcoma (DDLPS) are two of the most common subtypes of RLPS, exhibiting clear differences in biological behaviors and clinical prognosis. The metabolic features and genomic characteristics remain unclear.
View Article and Find Full Text PDFBMC Cancer
December 2024
Institute of Integrative Medicine, Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha, 410008, People's Republic of China.
Background: The NTRK fusion gene is a rare cancer driver and a typical representative "diamond mutation". Its unique role in tumor progression is highly important for the clinical diagnosis and treatment of patients with tumors. We searched for NTRK fusion-positive patients in our hospital.
View Article and Find Full Text PDFRespir Res
December 2024
Department of Respiratory Diseases, Medical School, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, People's Republic of China.
Cell Oncol (Dordr)
November 2024
Department of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Purpose: Leiomyosarcoma (LMS) is an aggressive mesenchymal malignant tumor with poor therapeutic options, but the molecular mechanisms underlying LMS remain largely unknown. Increasing evidence indicates that transient receptor potential vanilloid 4 (TRPV4) levels are closely related to the advancement of various malignant tumors through diverse molecular mechanisms. However, the roles and regulatory mechanisms of TRPV4 in LMS progression remain unclear.
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