Zobrazení zdroje stránky Bredahlgormsen0577

In this review, we will discuss the important molecular pathways through which various metabolites and other signaling substances released by the GM regulate liver biology, under both physiological and pathological conditions. Finally, we highlight numerous therapeutic attempts, such as probiotics, prebiotics, and fecal microbial transplantation (FMT), to reprogram the gut-liver axis for decreasing liver diseases.Liver cancer is the 6th leading cause of cancer related deaths in the US even though it ranks 14th in incidence. More men are diagnosed with liver cancer than women, and the number of projected deaths among men (20,020) is almost double that among women (10,140) in the US. Infections like hepatitis and metabolic conditions like obesity are believed to be major risk factors for the onset of liver cancer. Hepatocellular carcinoma (HCC), the most common type of liver cancer, accounts for 75% of all cases. Chemotherapy has not been effective in treating HCC. Targeted therapies are being used in advanced HCC patients due to a better survival and less side effects when compared to traditional chemotherapy. Therapeutic agents targeting the regulators of growth factor signaling pathways and the mediators of downstream signaling-for example, inhibitors of the tyrosine kinase receptor-are used as targeted molecular therapies. Kinase inhibitors that modulate growth signals, such as sorafenib and lenvatinib, are commonly employed in targeted molecular therapy for HCC patients. This review covers these agents, highlighting modes of action and providing details on clinical trials.Liver cancer is a particularly aggressive group of malignancies with historically low survival rates. Despite advancements in cancer treatments in general in the last few decades, incidence and mortality have not changed. Even though some phase 1 and 2 studies have shown promising results, many medication have failed to reach a sustainable level of efficacy to move into the clinical setting. Immunotherapy drugs have shown impressive results in the treatment of specific immunogenic cancers, prompting the possibility of their use in liver cancers. Immunotherapy medications approved for other cancers have received FDA accelerated approval for treatment of hepatocellular carcinoma. [https://www.selleckchem.com/products/nt157.html https://www.selleckchem.com/products/nt157.html] But, these approvals are contingent upon verification and description of clinical benefit in confirmatory trials. With more treatments in development involving cancer vaccines and natural killer cell-mediated therapy, liver cancer treatment is being reinvigorated with a broad array of new treatment angles. In this review article, we discuss these treatments, focusing on mechanism of action and clinical trials. Much needed advancements in treating late- and early-stage liver cancers will require new and innovative immunotherapeutic treatments.Autophagy is a self-destructive process that occurs in the cells during abnormal conditions like protein aggregation due to misfolding, nutrient deprivation, damage to vital cell organelles, pathogenic infections, and during cancer. Typically, autophagy plays a key role in the renovation of new cells by balancing the equilibrium between cell death and cell renewal. Dysregulation of autophagy has a profound effect on protein turnover, mitochondrial homeostasis, clearance of damaged organelles, and cellular metabolism, which lead to neurodegenerative, metabolic, and proliferative diseases. Despite its antitumorigenic role, autophagy can promote cell proliferation by enhancing chemotherapeutic resistance in liver cancer. In the present review, we provide a comprehensive overview and discussion on the role of autophagy in the drug-resistant mechanisms of liver cancer.Hepatocellular carcinoma (HCC) is one of the most common primary hepatic tumors, and it is ranked as the third most common cause of cancer-linked deaths. Although the precise etiology of HCC is unknown, inflammation has been considered the foremost cause of HCC. Previous studies indicated that tumor necrosis factor-alpha (TNF-α) is associated with increased risk of HCC, but the results are conflicting. In the present study, we assessed the correlation between TNF-α G-308A polymorphism as well as HCC risk via a meta-analysis. We searched databases such as PubMed, EMBASE, and Web of Science for articles related to this subject. To evaluate the correlation between TNF-α G-308A polymorphism and HCC, the odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Between-study heterogeneity was assessed using Cochrane Q test and I2 statistics. To assess the robustness of data, sensitivity analysis, publication bias, and subgroup analysis were conducted. Approximately 30 articles with 4,753 cases of HCC and 6,667 controls were included for the meta-analysis. Overall, the TNF-α G-308A polymorphism notably correlated with increased risk of HCC in the dominant model (OR = 1.41, 95% CI 1.02-1.94, P = 0.036). Furthermore, a subgroup investigation showed significant correlation between TNF-α G-308A polymorphisms and HCC risk only in Asian populations (dominant model OR = 1.55, 95% CI 1.05-2.23, P = 0.025). Studies in ethnic groups showed significant heterogeneity (I2 &gt; 50%). Funnel plot and Eggers p values did not reveal publication bias. The present meta-analysis suggested that TNF-α G-308A polymorphisms are correlated with an elevated risk of HCC in Asian populations.The tumor microenvironment (TME) favors the complex interaction of tumor cells with stromal cells that are recognized to be the regulators of hallmarks of liver cancer growth and metastasis. The most common components of TME include cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), and tumor-associated extracellular matrix (ECM) are involved in facilitating the enhancement of liver cancer and can be exploited as potential targets. In addition, cancer stem cells (CSCs) that are known to regulate tumor initiation and progression are present in the TME. All these accumulated factors of the TME represent the driving force for liver cancer progression. This review is focused on the functions of each of the above-mentioned components of the TME and their roles as potential key players in targeting liver cancer.