@misc{Steinberg2018, author = {Steinberg, Pablo}, title = {Only one Component of a holistic Nutrition Policy}, series = {Fleischwirtschaft}, volume = {98}, journal = {Fleischwirtschaft}, number = {11}, publisher = {Deutscher Fachverlag GmbH}, address = {Frankfurt am Main}, issn = {0015-363X}, pages = {8 -- 9}, year = {2018}, language = {de} } @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} } @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{ThierbachBlumeWolfrumetal.2010, author = {Thierbach, Ren{\´e} and Blume, Urte and Wolfrum, K. and Drewes, Gunnar and Voigt, Anja and Ristow, Michael and Steinberg, Pablo}, title = {Altered carbohydrate metabolism in a tumour developing knock-out mice model}, issn = {0028-1298}, doi = {10.1007/s00210-010-0508-7}, year = {2010}, language = {en} } @misc{ScholtkaSchneiderMelcheretal.2009, author = {Scholtka, Bettina and Schneider, Mandy and Melcher, Ralph and Katzenberger, Tiemo and Friedrich, Daniela and Berghof-J{\"a}ger, Kornelia and Scheppach, Wolfgang and Steinberg, Pablo}, title = {A gene marker panel covering the Wnt and the Ras-Raf-MEK-MAPK signalling pathways allows to detect gene mutations in 80\% of early (UICC I) colon cancer stages in humans}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-44587}, year = {2009}, abstract = {Background: Very recently a gene marker panel that allows the mutational analysis of APC, CTNNB1, B-RAF and K-RAS was conceived. The aim of the present study was to use the 4-gene marker panel covering the Wnt and Ras-Raf-MEK-MAPK signalling pathways to determine the percentage of sporadic colorectal carcinomas (CRC) carrying at least one of the four above-mentioned genes in a mutated form alone and/or in combination with microsatellite instability (MSI) and to compare the sensitivity of the gene marker panel used in this study with that of gene marker panels previously reported in the scientific literature. Methods: CTNNB1 and B-RAF were screened by PCR-single-strand conformation polymorphism analysis and K-RAS gene mutations by restriction fragment length polymorphism analysis. For the mutational analysis of the APC gene mutation cluster region (codons 1243-1567) direct DNA sequencing was performed. The U.S. National Cancer Institute microsatellite panel (BAT25, BAT26, D2S123, D5S346 and D17S250) was used for MSI analysis. Results: It could be shown that about 80\% of early stage CRC (UICC stages I and II) and over 90\% of CRC in the UICC stage IV carried at least one mutated gene and/or showed MSI. No significant increase in the gene mutation frequencies could be determined when comparing tumours in the UICC stage I with those in UICC stage IV. Conclusions: When compared with previously published gene marker panels the 4-gene marker panel used in the present study shows an excellent performance, allowing to detect genetic alterations in 80-90\% of human sporadic CRC samples analyzed.}, language = {en} } @article{ThierbachDrewesFusseretal.2009, author = {Thierbach, Ren{\´e} and Drewes, Gunnar and Fusser, Markus and Wolfrum, Kathrin and Epe, Bernd and Ristow, Michael and Steinberg, Pablo}, title = {A role for iron-sulfur cluster proteins in DNA repair}, issn = {0028-1298}, doi = {10.1007/s00210-009-0404-1}, year = {2009}, language = {en} } @misc{ScholtkaKuehnelTaugneretal.2009, author = {Scholtka, Bettina and K{\"u}hnel, Dana and Taugner, Felicitas and Steinberg, Pablo}, title = {Inflammation does not precede or accompany the induction of perneoplastic lesions in the colon of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-fed rats}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-44570}, year = {2009}, abstract = {Heterocyclic aromatic amines (HCAs) are formed in meat cooked at high temperatures for a long time or over an open flame. In this context 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), the most abundant HCA in cooked meat, has been suggested to be involved in colon and prostate carcinogenesis. In the latter case it has been reported that: (1) roughly 50\% of Fischer F344 male rats treated with PhIP develop carcinomas in the ventral prostate lobe at 1 year of age; (2) inflammation precedes prostatic intraepithelial neoplasia in PhIP-fed rats; (3) inflammation specifically occurs in the ventral prostate lobe of PhIP-fed rats. To test whether PhIP by itself leads to inflammation in the colon and whether a human-relevant concentration of PhIP is able to induce preneoplastic lesions in the colon, male F344 rats were fed 0.1 or 100 ppm PhIP for up to 10 months and thereafter the colon tissue was analyzed histochemically. In none of the experimental groups signs of acute or chronic colonic inflammation were observed. 0.1 ppm PhIP leads to the development of hyperplastic and dysplastic lesions in the colon of single animals, but the incidence of these lesions does not reach a statistical significance. In contrast, in rats fed 100 ppm PhIP for 10 months hyperplastic and dysplastic colonic lesions were induced in a statistically significant number of animals. It is concluded that: (1) the induction of preneoplastic lesions in rat colon by PhIP is not preceded or accompanied by an inflammatory process; (2) a human-relevant concentration of PhIP alone is not sufficient to initiate colon carcinogenesis in rats.}, language = {en} } @article{MuellerUllmannWilkensetal.2009, author = {Mueller, Carsten and Ullmann, Kristina and Wilkens, Andrea and Winterhalter, Peter and Toyokuni, Shinya and Steinberg, Pablo}, title = {Potent antioxidative activity of vineatrol (R) 30 grapevine-shoot extract}, issn = {0916-8451}, doi = {10.1271/Bbb.90213}, year = {2009}, abstract = {The health promoting effects of a grapevine-shoot extract named Vineatrol (R) 30, which contains resveratrol (Resv) as well as considerable amounts of Resv oligomers, have recently been investigated. In the present study, we analyzed the free radical scavenging capacity, the ability to inhibit lipid peroxidation, and the capacity to enhance the human glutathione peroxidase 1 (GPx) and the human superoxide dismutase 1 (SOD) gene promoter activities of Vineatrol (R) 30. Vineatrol (R) 30 was able to scavenge the 2,2'-azinobis-3-ethylbenzothiazoline-6-sulfonic acid radical cation and led to concentration-dependent inhibition of lipid peroxidation, Vineatrol (R) 30 not being superior to Resv alone in both cases. Vineatrol (R) 30 also enhanced the gene promoter activities of human GPx and SOD expressed in V79 cells, whereas this effect could not be demonstrated for Resv. In summary, the results presented in this study show that the Vineatrol (R) 30 grapevine-shoot extract is a free radical scavenger and potent antioxidant at non- eytotoxic concentrations.}, language = {en} } @article{SinghDaniSharmaetal.2006, author = {Singh, Jasbir and Dani, Harinder M. and Sharma, Reeta and Steinberg, Pablo}, title = {Inhibition of the biosynthesis of SRP polypeptides and secretory proteins by aflatoxin B-1 can disrupt protein targeting}, series = {Cell biochemistry and function}, volume = {24}, journal = {Cell biochemistry and function}, publisher = {Wiley}, address = {Chichester}, issn = {0263-6484}, doi = {10.1027/cbf.1285}, pages = {507 -- 510}, year = {2006}, abstract = {Cell culture and western blotting studies revealed that aflatoxin B-1 (AFB(1)) inhibits the biosynthesis of two of the constituent polypeptides of signal recognition particle (SRP) (SRP54 and 72). SRP escorts polyribosomes carrying signal peptides from free form in the cytosol to the bound form on endoplasmic reticulum (ER) membrane during protein targeting. These effects of AFB(1) on SRP biosynthesis may inhibit the formation of functional SRP Our experiments have further shown that AFB(1) also inhibits the biosynthesis/translocation of a secretory protein, preprolactin, which fails to appear in the lumen of ER consequent to the treatment with this hepatocarcinogen. The results of the experiments presented in this article therefore enable us to infer for the first time that aflatoxin B-1 may inhibit the functioning of SRP as an escort and deplete the ER of polyribosomes for secretory protein synthesis. As these secretory proteins are important components of the plasma membrane, gap junctions and intercellular matrix, their absence from these locations could disturb cell to cell communication leading to tumorigenesis.}, language = {en} } @article{SchulzThierbachVoigtetal.2006, author = {Schulz, Tim Julius and Thierbach, Ren{\`e} and Voigt, Anja and Drewes, Gunnar and Mietzner, Brun and Steinberg, Pablo and Pfeiffer, Andreas F. H. and Ristow, Michael}, title = {Induction of oxidative metabolism by mitochondrial frataxin inhibits cancer growth : Otto Warburg revisited}, doi = {10.1074/jbc.M511064200}, year = {2006}, abstract = {More than 80 years ago Otto Warburg suggested that cancer might be caused by a decrease in mitochondrial energy metabolism paralleled by an increase in glycolytic flux. In later years, it was shown that cancer cells exhibit multiple alterations in mitochondrial content, structure, function, and activity. We have stably overexpressed the Friedreich ataxia-associated protein frataxin in several colon cancer cell lines. These cells have increased oxidative metabolism, as shown by concurrent increases in aconitase activity, mitochondrial membrane potential, cellular respiration, and ATP content. Consistent with Warburg's hypothesis, we found that frataxin-overexpressing cells also have decreased growth rates and increased population doubling times, show inhibited colony formation capacity in soft agar assays, and exhibit a reduced capacity for tumor formation when injected into nude mice. Furthermore, overexpression of frataxin leads to an increased phosphorylation of the tumor suppressor p38 mitogen-activated protein kinase, as well as decreased phosphorylation of extracellular signal-regulated kinase. Taken together, these results support the view that an increase in oxidative metabolism induced by mitochondrial frataxin may inhibit cancer growth in mammals}, language = {en} } @article{HerbstFuchsTeubneretal.2006, author = {Herbst, Uta and Fuchs, Iris Judith and Teubner, Wera and Steinberg, Pablo}, title = {Malignant transformation of human colon epithelial cells by benzo[c]phenanthrene dihydrodiolepoxides as well as 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine}, issn = {0041-008X}, doi = {10.1016/j.taap.2005.07.016}, year = {2006}, abstract = {Polycyclic aromatic hydrocarbons (PAHs) and heterocyclic aromatic amines (HCAs) ingested with food have repeatedly been suggested to be involved in the malignant transformation of colon epithelial cells. In order to test this hypothesis, HCEC cells (SV40 large T antigen-immortalized human colon epithelial cells) were incubated with a racemic mixture of benzo[c]phenanthrene dihydrodiol epoxides (B[c]PhDE), extremely potent carcinogenic PAH metabolites in vivo, or with 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OH-PhIP), the N-hydroxylated metabolite of the most abundant HCA in cooked meat. First, it was shown that HCEC cells express sulfotransferase 1A1, which is needed to metabolize N-OH-PhIP to the corresponding N-sulfonyloxy derivative, the direct precursor molecule of genotoxic nitrenium ions. Thereafter, exponentially growing HCEC cells were exposed five times to 0.1 mu g (0.37 nmol) B[c]PhDE/ml for 30 min or 0.72 mu g (3 mnol) N-OH-PhTP/ml for 24 h. Chemically treated HCEC cells showed an enhanced saturation density and grew faster than the corresponding solvent-treated cell cultures. After five treatment cycles, HCECB[c]PhDE as well as HCECN-OH-PhIP cells lost cell-cell contact inhibition and started piling up and forming foci in the culture flasks. Furthermore, HCECB[c]phDE and HCECN-OH-PhIP cells were injected i.m. into SCID mice. Within 6 weeks after injection, eight animals out of eight injected with HCECB[c]phDE or HCECN-OH-PhIP cells developed tumors at the site of injection, thus demonstrating the high tumorigenic potential of the HCECB[c]PhDE and HCECN-OH-PhIP cell cultures. Taken together, we show for the first time that the abovementioned active PAH metabolites as well as N-OH-PhIP are indeed able to malignantly transform human colon epithelial cells in vitro.}, language = {en} } @article{SinghSinghDanietal.2005, author = {Singh, Jasbir and Singh, S. and Dani, H. M. and Sharma, Reeta and Steinberg, Pablo}, title = {Interactions of aflatoxin B-1 with SRP components can disrupt protein targeting}, issn = {0263-6484}, year = {2005}, abstract = {Spectrofluorimetric studies have revealed that aflatoxin B-1 (AFB(1)) interacts with signal recognition particle (SRP), which acts as an escort for polyribosomes with signal peptides to be transported and bound to the cytoplasmic face of the endoplasmic reticulum (ER). We further report that the binding of AFB(1) to SRP is selective as it only binds to two (SRP9 and 14) out of its three constituent polypeptides studied. Binding of AFB(1) to proteins is known to alter their conformations. Interactions of AFB(1) with SRP polypeptides may generate structural and functional alterations in this particle and hinder secretory protein synthesis. Copyright (C) 2004 John Wiley Sons, Ltd}, 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{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{TeubnerLangheinrichSeideletal.2004, author = {Teubner, Wera and Langheinrich, C. and Seidel, Albrecht and Steinberg, Pablo}, title = {Inhibition of p53 transactivation activity does not promote mutagen-induced transformation of IEC-18}, issn = {0028-1298}, year = {2004}, language = {en} } @article{KuehnelSteinbergScholtka2004, author = {K{\"u}hnel, Dana and Steinberg, Pablo and Scholtka, Bettina}, title = {A human-relevant dose of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PHIP) can induce precancerous lesions in rat intestine after 6 months of exposure}, issn = {0028-1298}, year = {2004}, 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{HerbstFuchsTeubneretal.2004, author = {Herbst, Uta and Fuchs, Iris Judith and Teubner, Wera and Seidel, Albrecht and Frank, Heinz and Steinberg, Pablo}, title = {Malignant transformation of human colon epithelial cells by polycyclic aromatic hydrocarbons and heterocyclic aromatic amines}, issn = {0028-1298}, year = {2004}, 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{OkanoShiotaMatsumotoetal.2003, author = {Okano, J. and Shiota, G. and Matsumoto, K. and Yasui, S. and Kurimasa, A. and Hisatome, I. and Steinberg, Pablo and Murawaki, Y.}, title = {Hepatocyte growth factor exerts a proliferative effect on oval cells through the PI3K/AKT signaling pathway}, year = {2003}, language = {en} } @article{BartschZschalerHaseloffetal.2003, author = {Bartsch, Ingrid and Zschaler, Ingrid and Haseloff, Monika and Steinberg, Pablo}, title = {Establishment of a long-term culture system for rat colon epithelial cells}, issn = {1071-2690}, doi = {10.1290/0404035.1}, year = {2003}, abstract = {The aim of this study was to establish a long-term culture. system for rat colon epithelia isolaled by incubating a 4-cm-long rat colon segment cut longitudinally with all ethylenediaminetetraacetic acid [disodium salt]- containing buffer, taken up in conditioned medium from the normal rat kidney fibroblast cell line NRK (i.e., the supernatant Of pure NRK cultures), directly plated on mitomycin C-treated NRK cells and subcultured with conditioned medium from NRK cells. Cells started to migrate out of the crypts shortly after plating them on NRK feeder layers. Some of the crypts fell apart during the isolation procedure. whereas the vast majority of them did it within I to 2 Ill after plating. The cells proliferated extremely slowly but continuously over a period of 4 mo and were epithelial because they expressed cytokeratin 19 and were stained by crystal violet at pH 2.8. In conclusion, the experimental system described ill this study allows to maintain rat colon epithelial cells for up to 4 mo in culture and can be used to Study the effects of a variety of tumor-modulating factors on growth and gene expression of normal colon epithelial cells in vitro}, language = {en} } @article{BarlowGreigBridgesetal.2002, author = {Barlow, S. M. and Greig, J. B. and Bridges, J. W. and Carere, A. and Carpy, A. J. and Galli, Corrado L. and Kleiner, J. and Knudsen, I. and Koeter, H. B. and Levy, L. S. and Madsen, C. and Mayer, S. and Narbonne, J. F. and Pfannkuch, F. and Prodanchuk, M. G. and Smith, Mason R. and Steinberg, Pablo}, title = {Hazard identification by methods of animal-based toxicology}, year = {2002}, language = {en} } @article{DybingDoeGrotenetal.2002, author = {Dybing, E. and Doe, J. and Groten, J. and Kleiner, J. and O'Brien, J. and Renwick, A. G. and Schlatter, J. and Steinberg, Pablo and Tritschler, A. and Walker, R. and Younes, M.}, title = {Hazard characterisation of chemicals in food and diet : dose response, mechanisms and extrapolation issues}, year = {2002}, language = {en} } @article{VolohonskyTubyPoratetal.2002, author = {Volohonsky, Gloria and Tuby, Chen N. Y. H. and Porat, Noga and Wellman-Rousseau, Maria and Visvikis, Athanase and Leroy, Pierre and Rashi, Sharon and Steinberg, Pablo and Stark, Avishay Abraham}, title = {A spectrophotometric assay of gamma-glutamylcysteine synthetase and glutathione synthetase in crude extracts from tissues and cultured mammalian cells}, year = {2002}, 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{KomloshVolohonskyPoratetal.2001, author = {Komlosh, A. and Volohonsky, Gloria and Porat, Noga and Tuby, chen n. y. h. and Bluvshtein, Evgenia and Steinberg, Pablo and Oesch, Franz and Stark, Avishay Abraham}, title = {Gamma-glutamyl transpeptidase and glutathione biosynthesis in non-tumorigenic and tumorigenic rat liver oval cell lines}, year = {2001}, language = {en} } @article{HengstlerUteschSteinberg2000, author = {Hengstler, Jan Georg and Utesch, D. and Steinberg, Pablo}, title = {Cryopreserved primary hepatocytes as a constantly available in vitro model for the evaluation of human and animal drug metabolism and enzyme induction}, year = {2000}, language = {en} } @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{HengstlerRingelBiefangetal.2000, author = {Hengstler, Jan Georg and Ringel, M. and Biefang, Katja and Hammel, S. and Milbert, U. and Gerl, M. and Klebach, M. and Diener, B. and Platt, Karl-Ludwig and B{\"o}ttger, Thomas and Steinberg, Pablo and Oesch, Franz}, title = {Cultures with cryopreserved hepatocytes : applicability for studies of enzyme induction}, year = {2000}, language = {en} } @article{SteinbergKlingelhoefferSchaeferetal.1999, author = {Steinberg, Pablo and Klingelh{\"o}ffer, Alexandra and Sch{\"a}fer, Angelika and W{\"u}st, G{\"u}nter and Weiße, G{\"u}nter and Oesch, Franz and Eigenbrodt, Erich}, title = {Expression of pyruvate kinase M2 in preneoplastic hepatic foci of N-nitrosomorpholine-treated rats}, year = {1999}, language = {en} } @article{MazurekEigenbrodtFailingetal.1999, author = {Mazurek, Sybille and Eigenbrodt, Erich and Failing, Klaus and Steinberg, Pablo}, title = {Alterations in the glycolytic and glutaminolytic pathways after malignant transformation of rat liver oval cells}, year = {1999}, language = {en} } @article{SteinbergFischerArandetal.1999, author = {Steinberg, Pablo and Fischer, Thomas M. and Arand, Michael and Park, Eunju and Elmadfa, Ibrahim and Rimkus, Gerhard and Brunn, Hubertus and Dienes, Hans-Peter}, title = {Acute hepatotoxicity of the polycyclic musk 7-acetyl-1,1,3,4,4,6-hexamethyl-1,2,3,4-tetrahydronaphthaline (AHTN)}, year = {1999}, language = {en} } @article{BluvshteinGlassVolohonskyetal.1999, author = {Bluvshtein, Evgenia and Glass, George and Volohonsky, Gloria and Yaakubowitz, Margalit and Harness, Ella and Smorodinsky, Nechama and Seidel, Albrecht and Frank, Heinz and Stark, Avishay Abraham and Steinberg, Pablo}, title = {Inhibition of the hydrolytic and transpeptidatic activities of rat kidney gamma-glutamyltranspeptidase by specific monoclonal antibodies}, year = {1999}, 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{HengstlerVanDerBurgSteinbergetal.1999, author = {Hengstler, Jan Georg and VanDerBurg, Bart and Steinberg, Pablo and Oesch, Franz}, title = {Interspecies differences in cancer susceptibility and toxicity}, year = {1999}, language = {en} } @article{SteinbergFischerKiuliesetal.1999, author = {Steinberg, Pablo and Fischer, Thomas M. and Kiulies, Sandra and Biefang, Katja and Platt, Karl-Ludwig and Oesch, Franz and B{\"o}ttger, Thomas and Bulitta, Clemens and Kempf, Peter and Hengstler, Jan Georg}, title = {Drug metabolizing capacity of cryopreserved human, rat and mouse liver parenchymal cells in suspension}, year = {1999}, language = {en} } @article{HackerSteinbergBannasch1998, author = {Hacker, Hans-J{\"o}rg and Steinberg, Pablo and Bannasch, Peter}, title = {Pyruvate kinase isoenzyme shift from L-type to M2-type is a late event in hepatocarcinogenesis induced in rats by a choline-deficient/DL-ethionine supplemented diet}, year = {1998}, language = {en} }