Role of TGF-β in Alcohol-Induced Liver Disease

被引:3
|
作者
Jogunoori, Wilma [1 ,2 ,3 ]
Mishra, Lopa [1 ,2 ,3 ]
机构
[1] George Washington Univ, Ctr Translat Med, Dept Surg, Washington, DC 20052 USA
[2] George Washington Univ, George Washington Canc Ctr, Washington, DC 20052 USA
[3] Vet Affairs Med Ctr, 50 Irving St NW, Washington, DC 20422 USA
来源
ALCOHOL AND CANCER | 2018年 / 1032卷
关键词
Hepatocellular; Carcinoma; Cirrhosis; TGF-beta; Beckwith-Wiedemann syndrome; GROWTH-FACTOR-BETA; INTERSTRAND CROSS-LINK; TUMOR-SUPPRESSOR; CELL-MEMBRANE; STEM-CELLS; RECEPTOR; CANCER; SMAD4; PHOSPHORYLATION; PATHWAYS;
D O I
10.1007/978-3-319-98788-0_7
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Over 90% of hepatocellular carcinoma (HCC) occurs against a background of chronic liver disease or cirrhosis induced from viral hepatitis to alcohol injury. One third of patients with cirrhosis will develop HCC during their lifetime, with a 3-5% annual incidence. However, little is known about the key mechanisms by which toxins mediate DNA damage in the liver. Recent studies support a central role for TGF-beta signaling in conferring genomic stability yet the precise mechanism of action and the specific stages of tumor suppression remain unclear (Bornstein S, White R, Malkoski S, Oka M, Han G, Cleaver T, Reh D, Andersen P, Gross N, Olson S, Deng C, Lu SL, Wang XJ. J Clin Invest 119:3408-3419 (2009); Korc M. J Clin Invest 119:3208-3211 (2009); Glick A, Popescu N, Alexander V, Ueno H, Bottinger E, Yuspa SH. Proc Natl Acad Sci U S A 96:14949-14954 (1999)). Furthermore, it has recently been shown that beta 2SP(+/-) and beta 2SP(+/-)/Smad3(+/-) mice phenocopy a hereditary human cancer syndrome, the Beckwith-Wiedemann syndrome (BWS), which has an 800 fold risk of cancers including HCC, hepatoblastoma, and a range of liver disorders. Identifying key biological pathways and mechanisms for suppressing alcohol-induced stem cell injury and HCC will be critical for enhancing patient care and the employment of new therapeutic approaches.
引用
收藏
页码:93 / 104
页数:12
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