Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The X protein (HBx) of hepatitis B virus (HBV) plays important roles in hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) during viral infection. In this study, we demonstrated that co-transfection of mouse embryo fibroblasts (STO) with HBx and activated Ras triggered apoptotic cell death, while HBx or activated Ras individually failed to induce apoptosis. In addition, STO cells were able to form colonies on soft agar after transfected with HBx or Ras, and cells co-transfected with both genes failed to transform. Moreover, nude mice injected with STO cells carrying either HBx or Ras could develop tumor, but tumor growth was inhibited by the injection of both STO cells harboring HBx and carrying Ras. These results suggested that HBx plays a role as a tumor inducer and stimulates neoplastic transformation of normal cells, but shifts its function to the induction of apoptosis in association with Ras.
 ...
PMID:Functional switch of viral protein HBx on cell apoptosis, transformation, and tumorigenesis in association with oncoprotein Ras. 1656 76

The complex aspects linking the nucleolus and ribosome biogenesis to cancer are reviewed here. The available evidence indicates that the morphological and functional changes in the nucleolus, widely observed in cancer tissues, are a consequence of both the increased demand for ribosome biogenesis, which characterizes proliferating cells, and the changes in the mechanisms controlling cell proliferation. In fact, the loss or functional changes in the two major tumor suppressor proteins pRB and p53 cause an up-regulation of ribosome biogenesis in cancer tissues. In this context, the association in human carcinomas of nucleolar hypertrophy with bad prognoses is worthy of note. Further, an increasing amount of data coming from studies on both hepatitis virus-induced chronic liver diseases and a subset of rare inherited disorders, including X-linked dyskeratosis congenita, suggests an active role of the nucleolus in tumorigenesis. Both an up-regulation of ribosome production and changes in the ribosome structure might causally contribute to neoplastic transformation, by affecting the balance of protein translation, thus altering the synthesis of proteins that play an important role in the genesis of cancer.
 ...
PMID:Nucleolus, ribosomes, and cancer. 1858 14

Cholangiocarcinoma (CCA), a cancer originating from the neoplastic transformation of the biliary epithelium, is characterized by a progressive increase in incidence and prevalence. A number of risk factors have been identified including primary sclerosing cholangitis, liver fluke infestation, and hepatolithiasis. More recently, hepatitis viruses (HCV, HBV) have been taken into consideration as risk factors for the intrahepatic CCA and this could explain the increased incidence seen in the last two decades. All these risk factors induce chronic inflammation in the biliary epithelium together with partial bile obstruction. These two conditions are considered the background (chronic inflammation) favouring the cancer development. The only effective treatment is the radical surgical resection but, this is applicable in less than 40% of the patients since CCA is mostly diagnosed at an advanced stage. This mainly occurs because, in the majority of the cases, CCA is clinically silent, with symptoms only developing at an advanced stage but also for the lack of effective biomarkers to be used for a screening purpose. A number of serum and bile biomarkers have been recently proposed for the diagnosis of CCA but, their impact on the early diagnosis is still under the evaluation.
 ...
PMID:Cholangiocarcinoma: risk factors and clinical presentation. 2049 49

Among cancers diagnosed worldwide on a yearly basis, 20% are thought to be associated with a viral infection. The viruses involved are, by order of decreasing incidence, the hepatitis viruses, the papillomaviruses and the Epstein-Barr virus. These virus-induced cancers generate a high level of interest not only for the study of mechanisms involved in the neoplastic transformation, but also for the set-up of specific immunotherapies including prophylactic and therapeutic antitumor vaccination.
 ...
PMID:[Virus-induced cancers: interplay between genetics and environment]. 2289 94

Chronic infection with hepatitis C virus (HCV) is one of the main causes of hepatocellular carcinoma. However, the molecular mechanisms linking the infection to cancer development remain poorly understood. Here we used HCV-infected cells and liver biopsies to study how HCV modulates the glutaminolysis pathway, which is known to play an important role in cellular energetics, stress defense, and neoplastic transformation. Transcript levels of glutaminolytic factors were quantified in Huh7.5 cells or primary human hepatocytes infected with the Japanese fulminant hepatitis 1 HCV strain as well as in biopsies of chronic HCV patients. Nutrient deprivation, biochemical analysis, and metabolite quantification were performed with HCV-infected Huh7.5 cells. Furthermore, short hairpin RNA vectors and small molecule inhibitors were used to investigate the dependence of HCV replication on metabolic changes. We show that HCV modulates the transcript levels of key enzymes of glutamine metabolism in vitro and in liver biopsies of chronic HCV patients. Consistently, HCV infection increases glutamine use and dependence. We finally show that inhibiting glutamine metabolism attenuates HCV infection and the oxidative stress associated with HCV infection.
 ...
PMID:Hepatitis C virus infection triggers a tumor-like glutamine metabolism. 2786 47

Virally induced liver cancer usually evolves over long periods of time in the context of a strongly oxidative microenvironment, characterized by chronic liver inflammation and regeneration processes. They ultimately lead to oncogenic mutations in many cellular signaling cascades that drive cell growth and proliferation. Oxidative stress, induced by hepatitis viruses, therefore is one of the factors that drives the neoplastic transformation process in the liver. This review summarizes current knowledge on oxidative stress and oxidative stress responses induced by human hepatitis B and C viruses. It focuses on the molecular mechanisms by which these viruses activate cellular enzymes/systems that generate or scavenge reactive oxygen species (ROS) and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on the initiation and establishment of chronic viral infection, as well as on the course and outcome of liver fibrosis and hepatocarcinogenesis will be discussed The review neither discusses reactive nitrogen species, although their metabolism is interferes with that of ROS, nor antioxidants as potential therapeutic remedies against viral infections, both subjects meriting an independent review.
 ...
PMID:Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis. 2796 66

Chronic inflammation is a causative factor of many cancers, although it originally acts as a protective host response to the loss of tissue homeostasis. Many inflammatory conditions predispose susceptible cells, most of which are of epithelial origin, to neoplastic transformation. There is a close correlation between digestive tract (DT) cancer and chronic inflammation, such as esophageal adenocarcinoma associated with Barrett's esophagus, helicobacter pylori infection as the cause of stomach cancer, hepatitis leading to liver cirrhosis and subsequent cancer, and colon cancer linking to inflammatory bowel diseases and schistosomiasis. A prominent feature of malignant transformation of DT tract epithelial cells is their adoption of somatic gene mutations resulting in abnormal expression of proteins that endow the cells with unlimited proliferation as well as increased motility and invasive capabilities. Many of these events are mediated by Gi-protein coupled chemoattractant receptors (GPCRs) including formyl peptide receptors (FPRs in human, Fprs in mice). In this article, we review the current understanding of FPRs (Fprs) and their function in DT cancer types as well as their potential as therapeutic targets.
 ...
PMID:The G-Protein Coupled Formyl Peptide Receptors and Their Role in the Progression of Digestive Tract Cancer. 3325 86


<< Previous 1 2