Gerhard Fritz

Summary

Affiliation: University of Mainz
Country: Germany

Publications

  1. ncbi Rho GTPases: promising cellular targets for novel anticancer drugs
    Gerhard Fritz
    Department of Toxicology, University of Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Curr Cancer Drug Targets 6:1-14. 2006
  2. ncbi HMG-CoA reductase inhibitors (statins) as anticancer drugs (review)
    Gerhard Fritz
    Department of Toxicology, University of Mainz, D 55131 Mainz, Germany
    Int J Oncol 27:1401-9. 2005
  3. ncbi Targeting the mevalonate pathway for improved anticancer therapy
    G Fritz
    Department of Toxicology, University of Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Curr Cancer Drug Targets 9:626-38. 2009
  4. doi Potential use of HMG-CoA reductase inhibitors (statins) as radioprotective agents
    Gerhard Fritz
    University Medical Center of the Johannes Gutenberg University Mainz, Institute of Toxicology, Germany
    Br Med Bull 97:17-26. 2011
  5. ncbi Ionizing radiation-induced E-selectin gene expression and tumor cell adhesion is inhibited by lovastatin and all-trans retinoic acid
    Tobias Nubel
    University of Mainz, Institute of Toxicology, Division of Applied Toxicology, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Carcinogenesis 25:1335-44. 2004
  6. doi Expression and cytoprotective activity of the small GTPase RhoB induced by the Escherichia coli cytotoxic necrotizing factor 1
    Stefanie C Huelsenbeck
    Institute of Toxicology, Hannover Medical School, D 30625 Hannover, Germany
    Int J Biochem Cell Biol 45:1767-75. 2013
  7. pmc Late activation of stress-activated protein kinases/c-Jun N-terminal kinases triggered by cisplatin-induced DNA damage in repair-defective cells
    Lars Helbig
    Department of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany
    J Biol Chem 286:12991-3001. 2011
  8. doi DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK)
    Julia Damrot
    Department of Toxicology, University of Mainz, Mainz, Germany
    J Mol Biol 385:1409-21. 2009
  9. ncbi The lipid lowering drug lovastatin protects against doxorubicin-induced hepatotoxicity
    Christian Henninger
    Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Toxicol Appl Pharmacol 261:66-73. 2012
  10. ncbi Lovastatin protects human endothelial cells from killing by ionizing radiation without impairing induction and repair of DNA double-strand breaks
    Tobias Nubel
    Department of Toxicology, University of Mainz, Mainz, Germany
    Clin Cancer Res 12:933-9. 2006

Collaborators

Detail Information

Publications36

  1. ncbi Rho GTPases: promising cellular targets for novel anticancer drugs
    Gerhard Fritz
    Department of Toxicology, University of Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Curr Cancer Drug Targets 6:1-14. 2006
    ..Indeed, compounds developed as specific inhibitors of the RhoA-effector molecule Rho-kinase (ROK) have been demonstrated to exert anti-metastatic activity in vivo...
  2. ncbi HMG-CoA reductase inhibitors (statins) as anticancer drugs (review)
    Gerhard Fritz
    Department of Toxicology, University of Mainz, D 55131 Mainz, Germany
    Int J Oncol 27:1401-9. 2005
    ..Here, data available at present arguing for the usefulness of statins in anticancer therapy are summarized and discussed...
  3. ncbi Targeting the mevalonate pathway for improved anticancer therapy
    G Fritz
    Department of Toxicology, University of Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Curr Cancer Drug Targets 9:626-38. 2009
    ..Here, the pros and cons of compounds that interfere with the mevalonate pathway for cancer treatment are summarized and discussed...
  4. doi Potential use of HMG-CoA reductase inhibitors (statins) as radioprotective agents
    Gerhard Fritz
    University Medical Center of the Johannes Gutenberg University Mainz, Institute of Toxicology, Germany
    Br Med Bull 97:17-26. 2011
    ..Furthermore, statins increase the mRNA expression of DNA repair factors in vivo. Thus, although the molecular mechanisms involved are still ambiguous, preclinical data concordantly show a promising radioprotective capacity of statins...
  5. ncbi Ionizing radiation-induced E-selectin gene expression and tumor cell adhesion is inhibited by lovastatin and all-trans retinoic acid
    Tobias Nubel
    University of Mainz, Institute of Toxicology, Division of Applied Toxicology, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Carcinogenesis 25:1335-44. 2004
    ..Therefore, application of statins and at-RA might have clinical impact in protecting against E-selectin-promoted metastasis, which might arise as an unwanted side effect from radiation treatment...
  6. doi Expression and cytoprotective activity of the small GTPase RhoB induced by the Escherichia coli cytotoxic necrotizing factor 1
    Stefanie C Huelsenbeck
    Institute of Toxicology, Hannover Medical School, D 30625 Hannover, Germany
    Int J Biochem Cell Biol 45:1767-75. 2013
    ..In conclusion, the cytoprotective RhoB response is not only evoked by bacterial protein toxins inactivating Rho/Ras proteins but also by the Rac1-activating toxin CNF1. ..
  7. pmc Late activation of stress-activated protein kinases/c-Jun N-terminal kinases triggered by cisplatin-induced DNA damage in repair-defective cells
    Lars Helbig
    Department of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany
    J Biol Chem 286:12991-3001. 2011
    ....
  8. doi DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK)
    Julia Damrot
    Department of Toxicology, University of Mainz, Mainz, Germany
    J Mol Biol 385:1409-21. 2009
    ..Based on these data, we suggest that DNA replication blockage caused by genotoxin-induced DNA damage contributes to early activation of SAPK/JNK...
  9. ncbi The lipid lowering drug lovastatin protects against doxorubicin-induced hepatotoxicity
    Christian Henninger
    Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Toxicol Appl Pharmacol 261:66-73. 2012
    ..Based on the data, we hypothesize that statins might be suitable to lower hepatic injury following anthracycline-based anticancer therapy...
  10. ncbi Lovastatin protects human endothelial cells from killing by ionizing radiation without impairing induction and repair of DNA double-strand breaks
    Tobias Nubel
    Department of Toxicology, University of Mainz, Mainz, Germany
    Clin Cancer Res 12:933-9. 2006
    ..Whether statins affect the sensitivity of primary human cells to ionizing radiation (IR) is still unknown. The present study aims at answering this question...
  11. pmc Rac1 protein signaling is required for DNA damage response stimulated by topoisomerase II poisons
    Stefanie C Huelsenbeck
    Institute of Toxicology, Heinrich Heine University Dusseldorf, Moorenstrasse 5, D 40225 Dusseldorf, Germany
    J Biol Chem 287:38590-9. 2012
    ..Based on the data we suggest that Rac1-regulated mechanisms are required for DNA damage induction and subsequent activation of the DDR following treatment with topo II but not topo I poisons...
  12. ncbi Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response
    Anamaria Brozovic
    Institute of Toxicology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany
    Mutat Res 670:32-41. 2009
    ..Rather, the accuracy of DNA damage processing and late checkpoint control mechanisms determine the extent of cell death triggered by cisplatin-induced DNA lesions...
  13. doi Cytoprotective effect of the small GTPase RhoB expressed upon treatment of fibroblasts with the Ras-glucosylating Clostridium sordellii lethal toxin
    Johannes Huelsenbeck
    Institute of Toxicology, Hannover Medical School, D 30625 Hannover, Germany
    FEBS Lett 586:3665-73. 2012
    ..The finding on the cytoprotective activity of RhoB in TcsL-treated cells re-enforces the concept that RhoB exhibits cytoprotective rather than pro-apoptotic activity in a cellular background of inactive Ras...
  14. ncbi Long-term activation of SAPK/JNK, p38 kinase and fas-L expression by cisplatin is attenuated in human carcinoma cells that acquired drug resistance
    Anamaria Brozovic
    Division of Applied Toxicology, Institute of Toxicology, Mainz, Germany
    Int J Cancer 112:974-85. 2004
    ..ACR cells displayed a reduced level of DNA damage, indicating long-term stimulation of SAPK/JNK and p38 kinase is triggered by nonrepaired cDDP-induced DNA lesions...
  15. doi Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo
    Christian Ostrau
    Department of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Germany
    Radiother Oncol 92:492-9. 2009
    ..Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo...
  16. pmc Late activation of stress kinases (SAPK/JNK) by genotoxins requires the DNA repair proteins DNA-PKcs and CSB
    Gerhard Fritz
    Department of Toxicology, University of Mainz, D 55131 Mainz, Germany
    Mol Biol Cell 17:851-61. 2006
    ..The data show that sensing of DNA damage by DNA-PK(cs) and CSB causes a delayed SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK...
  17. doi DNA damage response (DDR) induced by topoisomerase II poisons requires nuclear function of the small GTPase Rac
    Friedrich Wartlick
    Institute of Toxicology, Heinrich Heine University Dusseldorf, Moorenstrasse 5, D 40225 Dusseldorf, Germany
    Biochim Biophys Acta 1833:3093-103. 2013
    ..We suggest that multiple kinase-dependent but p53- and heat shock protein-independent Rac-regulated nuclear mechanisms are required for activation of the DDR following treatment with topo II poisons. ..
  18. ncbi Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells
    Tobias Nubel
    Department of Toxicology, University of Mainz, Mainz, Germany
    Int J Mol Med 16:1139-45. 2005
    ..Based on the data, we suggest that statins have impact on endothelial responses to inflammatory stress by modulation of the expression of cytokine receptors...
  19. pmc Rac1-regulated endothelial radiation response stimulates extravasation and metastasis that can be blocked by HMG-CoA reductase inhibitors
    Melanie Hamalukic
    Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany
    PLoS ONE 6:e26413. 2011
    ..The data support the concern that radiation exposure might increase the extravasation of circulating tumor cells and recommend co-administration of lipid-lowering drugs to avoid this adverse effect of ionizing radiation...
  20. ncbi Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion
    Tobias Nubel
    University of Mainz, Institute of Toxicology, Division of Applied Toxicology, Mainz, Germany
    FASEB J 18:140-2. 2004
    ..e., < or =1 microM) attenuated TNF-alpha induced tumor cell invasion in vitro. The data support the view that statins might be clinically useful in protection against E-selectin mediated metastasis...
  21. ncbi Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses
    Gerhard Fritz
    Department of Toxicology, University of Mainz, D 55131 Mainz, Germany
    Int J Oncol 35:1151-7. 2009
    ..In contrast to resorufin, TBB protected cells from cisplatin-induced cell killing. Furthermore, the inhibition of endogenous CK2 activity was cell type-dependent as endogenous CK2 was inhibited to different degrees in the cell lines...
  22. doi Comparative analysis of stress responses of H9c2 rat cardiomyoblasts following treatment with doxorubicin and tBOOH
    Mareike Döhrmann
    University Medical Center of the Johannes Gutenberg University Mainz, Institute of Toxicology, Mainz, Germany
    Exp Cell Res 318:779-88. 2012
    ....
  23. doi Intrinsic anticancer drug resistance of malignant melanoma cells is abrogated by IFN-β and valproic acid
    Wynand P Roos
    Institute of Toxicology, Medical Center of the University Mainz, Mainz, Germany
    Cancer Res 71:4150-60. 2011
    ....
  24. ncbi Ultraviolet light-induced apoptotic death is impaired by the HMG-CoA reductase inhibitor lovastatin
    Renate v Bardeleben
    Division of Applied Toxicology, Institute of Toxicology, University of Mainz, Germany
    Biochem Biophys Res Commun 307:401-7. 2003
    ....
  25. pmc Azathioprine suppresses ezrin-radixin-moesin-dependent T cell-APC conjugation through inhibition of Vav guanosine exchange activity on Rac proteins
    Daniela Poppe
    Laboratory of Immunology, I Department of Medicine, University of Mainz, Mainz, Germany
    J Immunol 176:640-51. 2006
    ..These findings provide novel insights into the immunosuppressive effects of azathioprine and suggest that antagonists of the Vav-Rac signaling pathway may be useful for suppression of T cell-dependent pathogenic immune responses...
  26. ncbi Resistance of p53 knockout cells to doxorubicin is related to reduced formation of DNA strand breaks rather than impaired apoptotic signaling
    Torsten R Dunkern
    Division of Applied Toxicology, Institute of Toxicology, University of Mainz, Obere Zahlbacher Strasse 67, D 55131 Mainz, Germany
    DNA Repair (Amst) 2:49-60. 2003
    ..Since human tumors are frequently mutated in p53 the findings bear clinical implications...
  27. ncbi Premature senescence is a primary fail-safe mechanism of ERBB2-driven tumorigenesis in breast carcinoma cells
    Tatjana M Trost
    Children s Hospital, University of Mainz, Obere Zahlbacher Strasse 63, 55131 Mainz, Germany
    Cancer Res 65:840-9. 2005
    ..We propose a multistep model for the process of malignant transformation by ERBB2 wherein secondary lesions either target P21 or downstream effectors of senescence to bypass this primary fail-safe mechanism...
  28. ncbi APE/Ref-1 and the mammalian response to genotoxic stress
    Gerhard Fritz
    Division of Applied Toxicology, Institute of Toxicology, University of Mainz, Obere Zahlbacher Str 67, D 55131 Mainz, Germany
    Toxicology 193:67-78. 2003
    ..Because of its involvement in DNA repair and apoptosis-related signaling mechanisms, APE/Ref-1 is also being discussed as a novel target for tumor-therapeutic approaches...
  29. ncbi Nuclear expression of apurinic/apyrimidinic endonuclease increases with progression of ovarian carcinomas
    Berno Tanner
    Department of Gynecology and Obstetrics, University of Mainz, Mainz, Germany
    Gynecol Oncol 92:568-77. 2004
    ..Because of the importance of APE in maintaining genomic stability and gene regulation, we examined whether APE expression is associated with survival and histopathological parameters of patients with ovarian cancer...
  30. ncbi Cytolethal distending toxin (CDT) is a radiomimetic agent and induces persistent levels of DNA double-strand breaks in human fibroblasts
    Jörg Fahrer
    Department of Toxicology, University Medical Center Mainz, Germany
    DNA Repair (Amst) 18:31-43. 2014
    ..In conclusion, the findings suggest that CDT functions as a radiomimetic agent and, therefore, is an attractive tool for selectively inducing persistent levels of DSBs and unveiling the associated cellular responses...
  31. ncbi Clostridium difficile toxin A induces expression of the stress-induced early gene product RhoB
    Ralf Gerhard
    Institute of Toxicology, Hannover Medical School, Carl Neuberg Strasse 1, 30625 Hannover, Germany
    J Biol Chem 280:1499-505. 2005
    ....
  32. ncbi The HMG-CoA reductase inhibitor lovastatin protects cells from the antineoplastic drugs doxorubicin and etoposide
    Renate v Bardeleben
    Division of Applied Toxicology, Institute of Toxicology, University of Mainz, D 55131 Mainz, Germany
    Int J Mol Med 10:473-9. 2002
    ..The finding that lovastatin renders cells resistant to doxorubicin and etoposide by reducing their genotoxic and cytotoxic effects might have clinical implications for cancer therapy...
  33. pmc CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes
    Imke Tiede
    Laboratory of Immunology, Department of Medicine, University of Mainz, Langenbeckstrasse 1, 55101 Mainz, Germany
    J Clin Invest 111:1133-45. 2003
    ..These findings explain the immunosuppressive effects of azathioprine and suggest that 6-Thio-GTP derivates may be useful as potent immunosuppressive agents in autoimmune diseases and organ transplantation...
  34. ncbi alpha(v)beta(3) Integrin-mediated drug resistance in human laryngeal carcinoma cells is caused by glutathione-dependent elimination of drug-induced reactive oxidative species
    Anamaria Brozovic
    Division of Molecular Biology, Ruder Boskovic Institute, Bijenicka 54, 10000 Zagreb, Croatia
    Mol Pharmacol 74:298-306. 2008
    ..Since this increased elimination of ROS could be reverted by GSH depletion, we concluded that multidrug resistance is the consequence of GSH-dependent increased ability of alpha(v)beta(3)-expressing cells to eliminate drug-induced ROS...
  35. ncbi Inhibition of Rho modulates cytokine-induced prostaglandin E2 formation in renal mesangial cells
    Claudia Petry
    Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe Universitat, Theodor Stern Kai 7, D 60590, Frankfurt am Main, Germany
    Biochim Biophys Acta 1636:108-18. 2004
    ..ii) In the presence of inflammatory cytokines it potentiates sPLA2-IIA expression and subsequent PGE2 formation. In addition, we identified lovastatin and Y27632 as direct inhibitors of sPLA2-IIA in a cell-free system...
  36. pmc Proteasomal degradation of cytotoxic necrotizing factor 1-activated rac
    Maria Lerm
    Institut fur Experimentelle und Klinische Pharmakologie und Toxikologie, Albert Ludwigs Universitat Freiburg, Germany
    Infect Immun 70:4053-8. 2002
    ..Schmidt, Infect. Immun. 67:496-503, 1998). Here we show that CNF1-induced JNK activation is stabilized in the presence of lactacystin. The data indicate that Rac is degraded by a proteasome-dependent pathway in CNF1-treated cells...