{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T21:05:16Z","timestamp":1777928716397,"version":"3.51.4"},"reference-count":33,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2017,2,1]],"date-time":"2017-02-01T00:00:00Z","timestamp":1485907200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/3.0\/"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Tumour Biol."],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:p>Hepatocellular carcinoma is one of the most common cancers, and approximately 80% develop from cirrhotic livers. We have previously shown that the aspartate salt of adenosine prevents and reverses carbon tetrachloride\u2013induced liver fibrosis in rats. Considering the hepatoprotective role of this adenosine derivative in fibrogenesis, we were interested in evaluating its effect in a hepatocarcinogenesis model induced by diethylnitrosamine in rats, where multinodular cancer is preceded by cirrhosis. Rats were injected with diethylnitrosamine for 12\u2009weeks to induce cirrhosis and for 16\u2009weeks to induce hepatocarcinogenesis. Groups of rats were treated with aspartate salt of adenosine from the beginning of carcinogen administration for 12 or 18\u2009weeks total, and another group received the compound from weeks 12 to 18. Fibrogenesis was estimated and the proportion of preneoplastic nodules and tumors was measured. The apoptotic and proliferation rates in liver tissues were evaluated, as well as the expression of cell signaling and cell cycle proteins participating in hepatocarcinogenesis. The adenosine derivative treatment reduced diethylnitrosamine-induced collagen expression and decreased the proportion of nodules positive for the tumor marker \u03b3-glutamyl transferase. This compound down-regulated the expression of thymidylate synthase and hepatocyte growth factor, and augmented the protein level of the cell cycle inhibitor p27; these effects could be part of its chemopreventive mechanism. These findings suggest a hepatoprotective role of aspartate salt of adenosine that could be used as a therapeutic compound in the prevention of liver tumorigenesis as described earlier for hepatic fibrosis.<\/jats:p>","DOI":"10.1177\/1010428317691190","type":"journal-article","created":{"date-parts":[[2017,2,24]],"date-time":"2017-02-24T04:55:45Z","timestamp":1487912145000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":19,"title":["Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats"],"prefix":"10.1177","volume":"39","author":[{"given":"Gabriela","family":"Velasco-Loyden","sequence":"first","affiliation":[{"name":"Departamento de Biolog\u00eda Celular y Desarrollo, Instituto de Fisiolog\u00eda Celular (IFC), Universidad Nacional Aut\u00f3noma de M\u00e9xico (UNAM), M\u00e9xico City, M\u00e9xico"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lidia","family":"P\u00e9rez-Mart\u00ednez","sequence":"additional","affiliation":[{"name":"Departamento de Biolog\u00eda Celular y Desarrollo, Instituto de Fisiolog\u00eda Celular (IFC), Universidad Nacional Aut\u00f3noma de M\u00e9xico (UNAM), M\u00e9xico City, M\u00e9xico"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susana","family":"Vidrio-G\u00f3mez","sequence":"additional","affiliation":[{"name":"Departamento de Biolog\u00eda Celular y Desarrollo, Instituto de Fisiolog\u00eda Celular (IFC), Universidad Nacional Aut\u00f3noma de M\u00e9xico (UNAM), M\u00e9xico City, M\u00e9xico"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julio Isael","family":"P\u00e9rez-Carre\u00f3n","sequence":"additional","affiliation":[{"name":"Laboratorio de Bioqu\u00edmica y Estructura de Prote\u00ednas, Instituto Nacional de Medicina Gen\u00f3mica (INMEGEN), M\u00e9xico City, M\u00e9xico"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victoria","family":"Chagoya de S\u00e1nchez","sequence":"additional","affiliation":[{"name":"Departamento de Biolog\u00eda Celular y Desarrollo, Instituto de Fisiolog\u00eda Celular (IFC), Universidad Nacional Aut\u00f3noma de M\u00e9xico (UNAM), M\u00e9xico City, M\u00e9xico"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2017,2,1]]},"reference":[{"key":"bibr1-1010428317691190","doi-asserted-by":"publisher","DOI":"10.1634\/theoncologist.2010-S4-14"},{"key":"bibr2-1010428317691190","doi-asserted-by":"publisher","DOI":"10.1007\/s00432-009-0591-7"},{"key":"bibr3-1010428317691190","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2008.01.008"},{"key":"bibr4-1010428317691190","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4402132"},{"key":"bibr5-1010428317691190","first-page":"31","volume-title":"Liver cirrhosis: causes, diagnosis and treatment (Hepatology Research and Clinical Developments)","author":"Chagoya de Sanchez V","year":"2011"},{"key":"bibr6-1010428317691190","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2009.11.005"},{"key":"bibr7-1010428317691190","first-page":"212530","volume":"2012","author":"Chagoya de","year":"2012","journal-title":"Int J Hepatol"},{"key":"bibr8-1010428317691190","unstructured":"Chagoya-Hazas VE, Hernandez Munoz R-E, Villa-Trevino S, et al. 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