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Gill J H
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http://hub.abes.fr/oup/periodical/carcin/1995/volume_16/issue_8/101093carcin1681693/authorship/3
http://hub.abes.fr/oup/periodical/carcin/1998/volume_19/issue_10/101093carcin19101743/authorship/1
http://hub.abes.fr/oup/periodical/carcin/1998/volume_19/issue_2/101093carcin192299/authorship/1
http://hub.abes.fr/acs/periodical/jnprdf/2008/volume_71/issue_3/101021np070477p/authorship/4
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The rodent non-genotoxic hepatocarcinogen nafenopin suppresses apoptosis preferentially in non-cycling hepatocytes but also elevates CDK4, a cell cycle progression factor.
The non-genotoxic hepatocarcinogen nafenopin suppresses rodent hepatocyte apoptosis induced by TGFbeta1, DNA damage and Fas.
Non-genotoxic hepatocarcinogenesis stimulate DNA synthesis and their withdrawal induces apoptosis, but in different hepatocyte populations
Sodium Pancratistatin 3,4-O-Cyclic Phosphate, a Water-Soluble Synthetic Derivative of Pancratistatin, Is Highly Effective in a Human Colon Tumor Model
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