Abstract
In the DDC feeding mouse model where liver cells proliferate, Mallory-Denk bodies (MDBs) form and later, after DDC withdrawal, hepatocellular carcinomas (HCCs) develop (1). Similarly, patients who abuse alcohol develop alcoholic liver disease (ALD), MDBs form (2) and later, after alcohol abstinence, the patients develop HCCs (2). Also MDBs form in many of the HCCs, both in the mouse model and in ALD. Because of this, it has been suggested that MDBs are a preneoplastic change formed in balloon hepatocytes which transform into cancer cells (3-6). But there may be other links to the preneoplastic process in ALD-induced HCCs such as the role that macrophages play in the TLR4 pathway response to LPS (4) or the transformation of stem cells seen in both cirrhosis and the associated HCC in ALD (7). In this review the role played by the following is discussed: (I) cell cycle arrest, (II) TLR signaling macrophages and stem cell transformation to form cancer stem cells, (III) ballooned hepatocytes that form Mallory-Denk bodies as progenitor pre-cancer cells in the pathogenesis of the ALD/HCC transformation.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
