Activation of β-catenin provides proliferative and invasive advantages in c-myc /TGF-α hepatocarcinogenesis promoted by phenobarbital

Author:

Calvisi Diego F.,Ladu Sara,Factor Valentina M.,Thorgeirsson Snorri S.

Publisher

Oxford University Press (OUP)

Subject

Cancer Research,General Medicine

Reference40 articles.

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2. Brockenbrough,J.S., Meyer,S.A., Li,C.X. and Jirtle,R.L. ( 1991 ) Reversible and phorbol ester-specific defect of protein kinase C translocation in hepatocytes isolated from phenobarbital-treated rats. Cancer Res. , 51 , 130 –136.

3. Bursch,W., Lauer,B., Timmermann-Trosiener,I., Barthel,G., Schuppler,J. and Schulte-Hermann,R. ( 1984 ) Controlled death (apoptosis) of normal and putative preneoplastic cells in rat liver following withdrawal of tumor promoters. Carcinogenesis , 5 , 453 –458.

4. Guppy,M.J., Wilton,J.C., Sharma,R., Coleman,R. and Chipman,J.K. ( 1994 ) Modulation of phenobarbitone-induced loss of gap junctional intercellular communication in hepatocyte couplets. Carcinogenesis , 15 , 1917 –1921.

5. Murakami,H., Sanderson,N.D., Nagy,P., Marino,P.A., Merlino,G. and Thorgeirsson,S.S. ( 1993 ) Transgenic mouse model for synergistic effects of nuclear oncogenes and growth factors in tumorigenesis: interaction of c-myc and transforming growth factor alpha in hepatic oncogenesis. Cancer Res. , 53 , 1719 –1723.

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