@article{SchlegerHeckSteinberg2000,
  author    = {Schleger, C. and Heck, R. and Steinberg, Pablo},
  title     = {The role of wild-type and mutated N-ras in the malignant transformation of liver cells},
  year      = {2000},
  language  = {en}
}
@article{StarkPoratVolohonskyetal.2003,
  author    = {Stark, Avishay abraham and Porat, Noga and Volohonsky, Gloria and Konlosh, A. and Bluvshtein, Evgenia and Tubi, C. and Steinberg, Pablo},
  title     = {The role of gamma-glutamyl transpeptidase in the biosynthesis of glutathione},
  year      = {2003},
  language  = {en}
}
@article{FuchsTeubnerSteinberg2004,
  author    = {Fuchs, J. and Teubner, Wera and Steinberg, Pablo},
  title     = {The resistance of intestinal epithelial cells towards the transforming activity of 2-hydroxyamino-1-methyl-6- phenylimidazo[4,5-B]pyridine is accompanied by glutathione S-transferase induction},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{SteinbergZschalerThometal.2001,
  author    = {Steinberg, Pablo and Zschaler, Ingrid and Thom, Elke and Kuna, Manuela and W{\"u}st, G{\"u}nter and Sch{\"a}fer-Schwebel, Angelika and M{\"u}ller, Rolf and Kramer, Peter-J{\"u}rgen and Weiße, G{\"u}nter},
  title     = {The polycyclic musk 7-acetyl-1,1,3,4,4,6-hexamethyl-1,2,3,4-tetrahydronaphthaline lacks liver tumor initiating and promoting activity in rats exposed to human-relevant doses},
  issn      = {0340-5761},
  doi       = {10.1007/s002040100274},
  year      = {2001},
  language  = {en}
}
@article{SchlegerBeckerOeschetal.1999,
  author    = {Schleger, C. and Becker, Rolf and Oesch, Franz and Steinberg, Pablo},
  title     = {The human p53 gene mutated at position 249 per se is not sufficient to immortalize human liver cells},
  year      = {1999},
  language  = {en}
}
@article{MuellerUllmannSteinberg2011,
  author    = {M{\"u}ller, Carsten and Ullmann, Kristina and Steinberg, Pablo},
  title     = {The grapevine-shoot extract Vineatrol30 Inhibits the chemically induced malignant transformation of BALB/c-3T3 Cells},
  series = {Journal of medicinal food},
  volume    = {14},
  journal   = {Journal of medicinal food},
  number    = {1-2},
  publisher = {Liebert},
  address   = {New Rochelle},
  issn      = {1096-620X},
  doi       = {10.1089/jmf.2010.0022},
  pages     = {34 -- 39},
  year      = {2011},
  abstract  = {Vineatrol (R) 30 (developed and produced jointly by Breko GmbH [Bremen, Germany] and Actichem [Montauban, France]) is a grapevine-shoot extract that contains resveratrol as well as considerable amounts of resveratrol oligomers. In the present study it is shown that Vineatrol30 at a noncytotoxic concentration of 2.3 mu g/mL significantly reduced the number of malignantly transformed foci induced by a sequential treatment of BALB/c-3T3 cells with 3-methylcholanthrene and 12-O-tetradecanoylphorbol 13-acetate in the so-called BALB/c-3T3 cell transformation assay. At a higher concentration Vineatrol30 drastically decreased the relative plating efficiency of the cells. Furthermore, the results suggest that the resveratrol oligomers present in Vineatrol30, independently from resveratrol itself, were indeed able to inhibit the formation of malignantly transformed BALB/c-3T3 foci.},
  language  = {en}
}
@article{ThierbachDrewesFusseretal.2010,
  author    = {Thierbach, Ren{\´e} and Drewes, Gunnar and Fusser, Markus and Voigt, Anja and Kuhlow, Doreen and Blume, Urte and Schulz, Tim Julius and Reiche, Carina and Glatt, Hansruedi and Epe, Bernd and Steinberg, Pablo and Ristow, Michael},
  title     = {The Friedreich's ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals},
  issn      = {0264-6021},
  doi       = {10.1042/Bj20101116},
  year      = {2010},
  abstract  = {DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron-sulfur clusters). The nuclear-encoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte- specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frataxin deficiency in murine liver is associated with increased basal levels of oxidative DNA base damage. Accordingly, eukaryotic V79 fibroblasts overexpressing human frataxin show decreased basal levels of these modifications, while prokaryotic Salmonella enterica serotype Typhimurium TA 104 strains transformed with human frataxin show decreased mutation rates. The repair rates of oxidative DNA base modifications in V79 cells overexpressing frataxin were significantly higher than in control cells. Lastly, cleavage activity related to the ISC-independent repair enzyme 8-oxoguanine glycosylase was found to be unaltered by frataxin overexpression. These findings indicate that frataxin modulates DNA-repair mechanisms probably due to its impact on ISC-dependent repair proteins, linking mitochondrial dysfunction to DNA repair and tumour initiation.},
  language  = {en}
}
@article{ThierbachSchulzIskenetal.2005,
  author    = {Thierbach, Ren{\`e} and Schulz, Tim Julius and Isken, Frank and Voigt, Aanja and Mietzner, Brun and Drewes, Gunnar and von Kleist-Retzow, J{\"u}rgen-Christoph and Wiesner, Rudolf J. and Magnuson, Mark A. and Puccio, Helene and Pfeiffer, Andreas F. H. and Steinberg, Pablo and Ristow, Michael},
  title     = {Targeted disruption of hepatic frataxin expression causes impaired mitochondrial function, decreased life span and tumor growth in mice},
  year      = {2005},
  abstract  = {We have disrupted expression of the mitochondrial Friedreich ataxia protein frataxin specifically in murine hepatocytes to generate mice with impaired mitochondrial function and decreased oxidative phosphorylation. These animals have a reduced life span and develop multiple hepatic tumors. Livers also show increased oxidative stress, impaired respiration and reduced ATP levels paralleled by reduced activity of iron-sulfur cluster (Fe/S) containing proteins (ISP), which all leads to increased hepatocyte turnover by promoting both apoptosis and proliferation. Accordingly, phosphorylation of the stress-inducible p38 MAP kinase was found to be specifically impaired following disruption of frataxin. Taken together, these findings indicate that frataxin may act as a mitochondrial tumor suppressor protein in mammals},
  language  = {en}
}
@article{ThierbachSchulzVoigtetal.2004,
  author    = {Thierbach, Rene and Schulz, Tim Julius and Voigt, Aanja and Drewes, Gunnar and Isken, F. and Pfeiffer, Andreas F. H. and Ristow, Michael and Steinberg, Pablo},
  title     = {Targeted disruption of frataxin in hepatocytes causes spontaneous neoplasia accompanied by increased ROS formation},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{ThierbachFlorianWolfrumetal.2012,
  author    = {Thierbach, Rene and Florian, Simone and Wolfrum, Katharina and Voigt, Anja and Drewes, Gunnar and Blume, Urte and Bannasch, Peter and Ristow, Michael and Steinberg, Pablo},
  title     = {Specific alterations of carbohydrate metabolism are associated with hepatocarcinogenesis in mitochondrially impaired mice},
  series = {Human molecular genetics},
  volume    = {21},
  journal   = {Human molecular genetics},
  number    = {3},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0964-6906},
  doi       = {10.1093/hmg/ddr499},
  pages     = {656 -- 663},
  year      = {2012},
  abstract  = {Friedreich's ataxia is an inherited neurodegenerative disease caused by the reduced expression of the mitochondrially active protein frataxin. We have previously shown that mice with a hepatocyte-specific frataxin knockout (AlbFxn(-/-)) develop multiple hepatic tumors in later life. In the present study, hepatic carbohydrate metabolism in AlbFxn(-/-) mice at an early and late life stage was analyzed. In young (5-week-old) AlbFxn(-/-) mice hepatic ATP, glucose-6-phosphate and glycogen levels were found to be reduced by similar to 74, 80 and 88\%, respectively, when compared with control animals. This pronounced ATP, G6P and glycogen depletion in the livers of young mice reverted in older animals: while half of the mice die before 30 weeks of age, the other half reaches 17 months of age and exhibits glycogen, G6P and ATP levels similar to those in age-matched controls. A key event in this respect seems to be the up-regulation of GLUT1, the predominant glucose transporter in fetal liver parenchyma, which became evident in AlbFxn(-/-) mice being 5-12 weeks of age. The most significant histological findings in animals being 17 or 22 months of age were the appearance of multiple clear cell, mixed cell and basophilic foci throughout the liver parenchyma as well as the development of hepatocellular adenomas and carcinomas. The hepatocarcinogenic process in AlbFxn 2/2 mice shows remarkable differences regarding carbohydrate metabolism alterations when compared with all other chemically and virally driven liver cancer models described up to now.},
  language  = {en}
}