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dc.contributor.authorSzabo, Gyongyi
dc.contributor.authorSaha, Banishree
dc.contributor.authorBukong, Terence N.
dc.date2022-08-11T08:08:32.000
dc.date.accessioned2022-08-23T15:58:10Z
dc.date.available2022-08-23T15:58:10Z
dc.date.issued2015-01-01
dc.date.submitted2015-05-29
dc.identifier.citationAdv Exp Med Biol. 2015;815:197-216. doi: 10.1007/978-3-319-09614-8_12. <a href="http://dx.doi.org/10.1007/978-3-319-09614-8_12">Link to article on publisher's site</a>
dc.identifier.issn0065-2598 (Linking)
dc.identifier.doi10.1007/978-3-319-09614-8_12
dc.identifier.pmid25427909
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30370
dc.description.abstractLiver cancers are one of the deadliest known malignancies which are increasingly becoming a major public health problem in both developed and developing countries. Overwhelming evidence suggests a strong role of infection with hepatitis B and C virus (HBV and HCV), alcohol abuse, as well as metabolic diseases such as obesity and diabetes either individually or synergistically to cause or exacerbate the development of liver cancers. Although numerous etiologic mechanisms for liver cancer development have been advanced and well characterized, the lack of definite curative treatments means that gaps in knowledge still exist in identifying key molecular mechanisms and pathways in the pathophysiology of liver cancers. Given the limited success with current therapies and preventive strategies against liver cancer, there is an urgent need to identify new therapeutic options for patients. Targeting HCV and or alcohol-induced signal transduction, or virus-host protein interactions may offer novel therapies for liver cancer. This review summarizes current knowledge on the mechanistic development of liver cancer associated with HCV infection and alcohol abuse as well as highlights potential novel therapeutic strategies.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=25427909&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1007/978-3-319-09614-8_12
dc.subjectAnimals
dc.subjectEthanol
dc.subjectHepatitis C
dc.subjectHumans
dc.subjectImmunity, Innate
dc.subjectKiller Cells, Natural
dc.subjectLiver Neoplasms
dc.subjectMicroRNAs
dc.subjectOxidative Stress
dc.subjectVirus Replication
dc.subjectDigestive System Diseases
dc.subjectGastroenterology
dc.subjectHepatology
dc.subjectImmune System Diseases
dc.subjectImmunology and Infectious Disease
dc.subjectInfectious Disease
dc.subjectNeoplasms
dc.subjectOncology
dc.titleAlcohol and HCV: implications for liver cancer
dc.typeBook Chapter
dc.source.booktitleAdvances in experimental medicine and biology
dc.source.volume815
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/642
dc.identifier.contextkey7158521
html.description.abstract<p>Liver cancers are one of the deadliest known malignancies which are increasingly becoming a major public health problem in both developed and developing countries. Overwhelming evidence suggests a strong role of infection with hepatitis B and C virus (HBV and HCV), alcohol abuse, as well as metabolic diseases such as obesity and diabetes either individually or synergistically to cause or exacerbate the development of liver cancers. Although numerous etiologic mechanisms for liver cancer development have been advanced and well characterized, the lack of definite curative treatments means that gaps in knowledge still exist in identifying key molecular mechanisms and pathways in the pathophysiology of liver cancers. Given the limited success with current therapies and preventive strategies against liver cancer, there is an urgent need to identify new therapeutic options for patients. Targeting HCV and or alcohol-induced signal transduction, or virus-host protein interactions may offer novel therapies for liver cancer. This review summarizes current knowledge on the mechanistic development of liver cancer associated with HCV infection and alcohol abuse as well as highlights potential novel therapeutic strategies.</p>
dc.identifier.submissionpathfaculty_pubs/642
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.source.pages197-216


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