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Comment
. 2015 May;61(5):1767-8.
doi: 10.1002/hep.27405. Epub 2014 Dec 24.

Reply: To PMID 24027047

Affiliations
Comment

Reply: To PMID 24027047

Amy S Lee et al. Hepatology. 2015 May.
No abstract available

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Figures

Fig. 1
Fig. 1
Heterogeneous GRP94 expression in cPtenf/fGrp94f/f tumors at 8–9 months. (A) H&E and GRP94 immunohistochemical staining (brown) in WT livers as well as hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) in cPtenf/fGrp94f/f livers. Black and white arrows indicate examples of GRP94-positive and -negative cells, respectively. (C) Triple immunofluorescent staining with GRP94 (red), CC marker panCK (green), and HCC marker HepPar1 (blue) in the liver of WT mice and tumors of cPtenf/fGrp94f/f mice. Nuclei were stained with DAPI (blue). Scale bars: 100 μm.

Comment on

References

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    1. Chiba T, Seki A, Aoki R, Ichikawa H, Negishi M, Miyagi S, Oguro H, et al. Bmi1 promotes hepatic stem cell expansion and tumorigenicity in both Ink4a/Arf-dependent and -independent manners in mice. Hepatology. 2010;52:1111–1123. - PubMed
    1. Chen WT, Ha D, Kanel G, Lee AS. Targeted deletion of ER chaperone GRP94 in the liver results in injury, repopulation of GRP94-positive hepatocytes, and spontaneous hepatocellular carcinoma development in aged mice. Neoplasia. 2014 doi: 10.1016/j.neo.2014.07.005. (in press) - DOI - PMC - PubMed
    1. Sekine S, Ogawa R, Kanai Y. Hepatomas with activating Ctnnb1 mutations in ‘Ctnnb1-deficient’ livers: a tricky aspect of a conditional knockout mouse model. Carcinogenesis. 2011;32:622–628. - PubMed
    1. Chen WT, Zhu G, Pfaffenbach K, Kanel G, Stiles B, Lee AS. GRP78 as a regulator of liver steatosis and cancer progression mediated by loss of the tumor suppressor PTEN. Oncogene. 2014 doi: 10.1038/onc.2013.437. [Epub ahead of print] - DOI - PMC - PubMed

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