Hepatic OV-6 expression in human liver disease and rat experiments: evidence for hepatic progenitor cells in man

Accumulation of Hedgehog-Responsive Progenitors Parallels Alcoholic Liver Disease Severity in Mice and Humans

“…5 Studies in experimental animals and humans with various types of chronic liver disease consistently demonstrate high proliferative activity in these stromal and ductular cells and show that many of them express markers of immature cells. 6,7 These findings support the concept that the ductular reaction represents an expansion of the progeny of typically inconspicuous liver progenitors that reside along Canals of Hering in healthy adult livers and suggest that the ductular reaction is involved in liver repair. 8 Fortunately, knowledge about the mechanisms that regulate the ductular response to liver injury is growing [9][10][11][12][13] because such information might suggest novel therapeutic targets to reduce fibrosis and improve regeneration in individuals with alcoholinduced liver injury.…”

Two pathologic types of hepatocellular carcinoma with lymph node metastasis with distinct prognosis on the basis of CK19 expression in tumor

“…Despite that OV-6 was positive in some bile duct cells that always shared immunoreactivity for CK19 in cirrhotic liver, OV-6 was regarded as a specific marker of liver progenitor cells that have the capacity to differentiate into either hepatocytes or biliary cells. 8,[17][18][19][20][21] Moreover, increasing evidence indicated that HCC with ICC differentiation was derived from a hepatic progenitor cell. 4,17,20 During its neoplastic transformation the progenitor cell marker (OV-6) and biliary marker (CK19) could partially be retained in HCC cells, 6 which resemble hepatic progenitor cells with coexpression of CK19 and OV-6, 22 and was consistent with the present study.…”

Oval cell‐mediated liver regeneration: Role of cytokines and growth factors

“…52 Evidently, this situation also occurs in humans, as elevated levels of serum HGF are present in individuals with chronic hepatitis and cirrhosis, [55][56][57] both conditions in which oval cell proliferation is well documented. 7,18,38,40,58,59 In situ hybridization has revealed that oval cells and basophilic hepatocytes, in addition to hepatic stellate cells, express aFGF transcripts. 60 A marked increase in hepatic aFGF levels has been reported at the peak of oval cell proliferation in the 2-AAF/PH model, and levels greatly exceeded those observed after PH alone, suggesting a more prominent role for aFGF in oval cellmediated regeneration.…”