Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxyradical overload disease develops in conditions involving chronic inflammation and may be of inherited etiology, e.g. haemochromatosis and Wilson disease, be acquired, e.g. infection with hepatitis B or C virus or Helicobactor pylori, or be chemically induced, e.g. acid reflux in Barrett oesophagus. Susceptibility to cancer is frequently a pathological consequence of extensive oxyradical damage that leads to a cycle of cell death and regeneration and causes mutations in cancer-related genes. In this brief review, we focus on the possible interactive effects of nitric oxide and the p53 tumour suppressor gene in human carcinogenesis.
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PMID:Cancer-prone oxyradical overload disease. 1062 29

A variety of carcinogens, in particular smoking, alcohol abuse and infections, are associated with an increased risk for the development of cancer of the upper gastrointestinal tract. Cancer prevention should start here, in particular since cessation of nicotine abuse, only moderate consumption of alcohol, and weight loss also have other positive effects on health. Where the indication is appropriate, H. pylori eradication, vaccination against hepatitis B and avoidance of exposure to hepatitis are well-founded prophylactic measures. Further screening measures make good sense only in high-risk groups, and are based on recommendations. It has, however, not yet been demonstrated that the screening of patients with Barrett's esophagus, liver cirrhosis, chronic hepatitis or gastric risk diseases actually can lower cancer-related deaths.
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PMID:[Esophagus, stomach, liver, pancreas carcinoma. What recommendations for prevention?]. 1460 99

Gastrointestinal (GI) cancers are the leading cause of mortality worldwide. These cancers are the end result of a complex interplay between gene and environment. Bacteria, parasites, and viruses have been implicated in some cancers. Recent data have put at focus the gut microbiome as the key player firing tumorigenesis. Experimental and human studies have provided evidence on the role of microbiota in cancer development. Although subject to changes in different settings such as antibiotic treatment, diet or lifestyle, our microbiome is quite stable and is capable of increasing susceptibility to cancer or decrease and halt its progression. The crucial event in carcinogenesis triggered by microbiome seems to be chronic inflammation influencing the genomic stability of host cells and activating immune mechanisms. Infection-related cancers represent 5.5% of the global cancer burden. Chronic inflammation predisposes to cancer in various GI organs, including hepatocellular carcinoma caused by hepatitis B or hepatitis C virus-related chronic hepatitis, gastric cancer (GC) caused by Helicobacter pylori-associated chronic gastritis, colorectal cancer caused by inflammatory bowel disease, bile duct cancer by primary sclerosing cholangitis, and esophageal cancer caused by Barrett esophagus. Apart from its impact in GI cancer development microbiota can also play an important role in the progression of cancer, response to chemotherapy or cancer prevention. In this review we will discuss the role of microbiome in GI cancers in the light of the current literature and the possible therapeutic options targeting microbiota in the near future.
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PMID:Gut Microbiome and Gastrointestinal Cancer: Les liaisons Dangereuses. 2774 Nov 73