The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Nonalcoholic Fatty Liver Disease and Hepatocellular Carcinoma: A Weighty Connection
Open accessAbstract
Hepatocellular carcinoma (HCC) is a common and deadly malignancy that is increasing in incidence in developed countries. The emergence of hepatitis C virus (HCV) accounts for about half of this increase in HCC, although the etiology of HCC in 15%-50% of new HCC cases remains unclear. The most common form of chronic liver disease in developed countries is nonalcoholic fatty liver disease (NAFLD), which encompasses a broad spectrum of histopathology. The prevalence of NAFLD, including the more aggressive nonalcoholic steatohepatitis (NASH), is increasing with the growing epidemics of diabetes and obesity. NASH can progress to cirrhosis and its related complications. Growing evidence suggests that NASH accounts for a large proportion of idiopathic or cryptogenic cirrhosis, which is associated with the typical risk factors for NASH. HCC is a rare, although important complication of NAFLD. Diabetes and obesity have been established as independent risk factors for the development of HCC. New evidence also suggests that hepatic iron deposition increases the risk of HCC in NASH-derived cirrhosis. Multiple case reports and case reviews of HCC in the setting of NASH support the associations of diabetes and obesity with the risk of HCC, as well as suggest age and advanced fibrosis as significant risks. Insulin resistance and its subsequent inflammatory cascade that is associated with the development of NASH appear to play a significant role in the carcinogenesis of HCC. The complications of NASH, including cirrhosis and HCC, are expected to increase with the growing epidemic of diabetes and obesity. (Hepatology 2010;51:1820–1832)
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Cites
Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. Adults
Calle, E. E., Rodriguez, C., Walker-Thurmond, K., & Thun, M. J. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa021423 · Cited by 7,696
Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms
Calle, E. E., & Kaaks, R. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1408 · Cited by 3,613
A central role for JNK in obesity and insulin resistance
Hirosumi, J., Tuncman, G., Chang, L., Görgün, C. Z., Uysal, K. T., Maeda, K., Karin, M., & Hotamisligil, G. S. (2002) · Nature · doi:10.1038/nature01137 · Cited by 3,359
The Natural History of Nonalcoholic Fatty Liver Disease: A Population-Based Cohort Study
Adams, L. A., Lymp, J. F., St. Sauver, J., Sanderson, S. O., Lindor, K. D., Feldstein, A., & Angulo, P. (2005) · Gastroenterology · doi:10.1053/j.gastro.2005.04.014 · Cited by 2,890
Ursodeoxycholic acid for treatment of nonalcoholic steatohepatitis: results of a randomized trial
Lindor, K. D., Kowdley, K. V., Heathcote, J. E., Harrison, E. M., Jorgensen, R., Angulo, P., Lymp, J. F., Burgart, L., & Colin, P. (2004) · Hepatology · doi:10.1002/hep.20092 · Cited by 727
Wideroff, L., Gridley, G., Chow, W. H., Linet, M., Mellemkjaer, L., Olsen, J. H., Keehn, S., & Borch-Johnsen, K. (1997) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/89.18.1360 · Cited by 627
A prospective study of obesity and cancer risk (Sweden)
Wolk, A., Gridley, G., Svensson, M., Nyrén, O., McLaughlin, J. K., Fraumeni, J. F., & Adami, H.-O. (2001) · Cancer Causes & Control · doi:10.1023/a:1008995217664 · Cited by 581
Metabolic syndrome and hepatocellular carcinoma: Two growing epidemics with a potential link
Siegel, A. B., & Zhu, A. X. (2009) · Cancer · doi:10.1002/cncr.24687 · Cited by 399
JNK1 but not JNK2 promotes the development of steatohepatitis in mice
Schattenberg, J. M., Singh, R., Wang, Y., Lefkowitch, J. H., Rigoli, R. M., Scherer, P. E., & Czaja, M. J. (2006) · Hepatology · doi:10.1002/hep.20999 · Cited by 384 · cited 1×
“Mouse models have also demonstrated that JNK1 promotes the development of steatohepatitis.(126) One mouse model demonstrated a protective effect with JNK1 ablation.”
BackgroundHepatocellular carcinoma in patients with nonalcoholic steatohepatitis
Hashimoto, E., Yatsuji, S., Tobari, M., Taniai, M., Torii, N., Tokushige, K., & Shiratori, K. (2009) · Journal of Gastroenterology · doi:10.1007/s00535-008-2262-x · Cited by 308
Cited by
Human Fatty Liver Disease: Old Questions and New Insights
Cohen, J. C., Horton, J. D., & Hobbs, H. H. (2011) · Science · doi:10.1126/science.1204265 · Cited by 2,089
Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis
Anstee, Q. M., Targher, G., & Day, C. P. (2013) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2013.41 · Cited by 1,747
Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome
Yki-Järvinen, H. (2014) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(14)70032-4 · Cited by 1,259
Stern, J. H., Rutkowski, J. M., & Scherer, P. E. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2016.04.011 · Cited by 1,031
Martin, P., DiMartini, A., Feng, S., Brown, R., & Fallon, M. (2014) · Hepatology · doi:10.1002/hep.26972 · Cited by 1,045
Metadata
- Authors
- Starley, B. Q., Calcagno, C. J., & Harrison, S. A.
- Venue
- Hepatology
- Published
- 2010-05
- Volume
- 51
- Issue
- 5
- Pages
- 1820-1832
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2136795008
- Cited by
- 1,336
- References
- 10
- FWCI
- 73.17
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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