Heiko Hermeking

Summary

Country: Germany

Publications

  1. pmc Characterization of the c-MYC-regulated transcriptome by SAGE: identification and analysis of c-MYC target genes
    Antje Menssen
    Max Planck Institute of Biochemistry, Molecular Oncology, Independent Junior Research Group, Am Klopferspitz 18a, D 82152 Martinsried Munich, Germany
    Proc Natl Acad Sci U S A 99:6274-9. 2002
  2. ncbi request reprint The role of epigenetic inactivation of 14-3-3sigma in human cancer
    Dmitri Lodygin
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
    Cell Res 15:237-46. 2005
  3. pmc Inducible microRNA expression by an all-in-one episomal vector system
    Alexey Epanchintsev
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried Munich, Germany
    Nucleic Acids Res 34:e119. 2006
  4. ncbi request reprint p53 enters the microRNA world
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
    Cancer Cell 12:414-8. 2007
  5. ncbi request reprint 14-3-3 proteins in cell cycle regulation
    Heiko Hermeking
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
    Semin Cancer Biol 16:183-92. 2006
  6. ncbi request reprint Serial analysis of gene expression and cancer
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinreid Munich, Germany
    Curr Opin Oncol 15:44-9. 2003
  7. ncbi request reprint The MYC oncogene as a cancer drug target
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Curr Cancer Drug Targets 3:163-75. 2003
  8. ncbi request reprint The 14-3-3 cancer connection
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Nat Rev Cancer 3:931-43. 2003
  9. ncbi request reprint Inactivation of miR-34a by aberrant CpG methylation in multiple types of cancer
    Dmitri Lodygin
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Cell Cycle 7:2591-600. 2008
  10. ncbi request reprint c-MYC delays prometaphase by direct transactivation of MAD2 and BubR1: identification of mechanisms underlying c-MYC-induced DNA damage and chromosomal instability
    Antje Menssen
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Cell Cycle 6:339-52. 2007

Collaborators

Detail Information

Publications29

  1. pmc Characterization of the c-MYC-regulated transcriptome by SAGE: identification and analysis of c-MYC target genes
    Antje Menssen
    Max Planck Institute of Biochemistry, Molecular Oncology, Independent Junior Research Group, Am Klopferspitz 18a, D 82152 Martinsried Munich, Germany
    Proc Natl Acad Sci U S A 99:6274-9. 2002
    ..The c-MYC-regulated genes/tags identified here will help to define the set of bona fide c-MYC targets and may have potential therapeutic value for inhibition of cancer cell proliferation, tumor-vascularization, and restenosis...
  2. ncbi request reprint The role of epigenetic inactivation of 14-3-3sigma in human cancer
    Dmitri Lodygin
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
    Cell Res 15:237-46. 2005
    ....
  3. pmc Inducible microRNA expression by an all-in-one episomal vector system
    Alexey Epanchintsev
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried Munich, Germany
    Nucleic Acids Res 34:e119. 2006
    ..Furthermore, the vector was adapted for convenient ligation-free transfer of microRNA cassettes from public libraries. This conditional knockdown-system should prove useful for many research and gene therapeutic applications...
  4. ncbi request reprint p53 enters the microRNA world
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
    Cancer Cell 12:414-8. 2007
    ..The initial evidence suggesting that miR-34 genes are central mediators of p53 function is summarized here...
  5. ncbi request reprint 14-3-3 proteins in cell cycle regulation
    Heiko Hermeking
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
    Semin Cancer Biol 16:183-92. 2006
    ..Effects of 14-3-3 proteins on cell cycle progression and the regulation of 14-3-3 activity during the cell cycle are reviewed in this chapter...
  6. ncbi request reprint Serial analysis of gene expression and cancer
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinreid Munich, Germany
    Curr Opin Oncol 15:44-9. 2003
    ..In addition, cancer diagnosis and treatment may benefit from a complementation between serial analysis of gene expression and quantitative proteomics in the future...
  7. ncbi request reprint The MYC oncogene as a cancer drug target
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Curr Cancer Drug Targets 3:163-75. 2003
    ..These and other recent developments, which address the use of myc genes as therapeutic targets for cancer treatment, are discussed in this review...
  8. ncbi request reprint The 14-3-3 cancer connection
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
    Nat Rev Cancer 3:931-43. 2003
  9. ncbi request reprint Inactivation of miR-34a by aberrant CpG methylation in multiple types of cancer
    Dmitri Lodygin
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Cell Cycle 7:2591-600. 2008
    ..These results show that miR-34a represents a tumor suppressor gene which is inactivated by CpG methylation and subsequent transcriptional silencing in a broad range of tumors...
  10. ncbi request reprint c-MYC delays prometaphase by direct transactivation of MAD2 and BubR1: identification of mechanisms underlying c-MYC-induced DNA damage and chromosomal instability
    Antje Menssen
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried, Germany
    Cell Cycle 6:339-52. 2007
    ....
  11. ncbi request reprint Prostate cancer is characterized by epigenetic silencing of 14-3-3sigma expression
    Dimitri Lodygin
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried Munich, Germany
    Oncogene 23:9034-41. 2004
    ....
  12. ncbi request reprint Differential regulation of microRNAs by p53 revealed by massively parallel sequencing: miR-34a is a p53 target that induces apoptosis and G1-arrest
    Valery Tarasov
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
    Cell Cycle 6:1586-93. 2007
    ..siRNAs corresponding to p53-induced miRNAs may have potential as cancer therapeutic agents as RNA interference based therapies are currently emerging...
  13. ncbi request reprint Epigenetic silencing of 14-3-3sigma in cancer
    Dmitri Lodygin
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried, Munich, Germany
    Semin Cancer Biol 16:214-24. 2006
    ..In the future the detection of CpG methylation of 14-3-3sigma may be used for diagnostic and prognostic purposes...
  14. pmc Induction of cullin 7 by DNA damage attenuates p53 function
    Peter Jung
    Molecular Oncology, Max Planck Institute of Biochemistry, D 82152 Martinsried, Germany
    Proc Natl Acad Sci U S A 104:11388-93. 2007
    ..Pharmacological modulation of Cul7 function may allow the sensitization of cancer cells expressing wild-type p53 to genotoxic agents used in cancer therapy...
  15. ncbi request reprint Large-scale identification of c-MYC-associated proteins using a combined TAP/MudPIT approach
    Heike B Koch
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried, Germany
    Cell Cycle 6:205-17. 2007
    ..Furthermore, this first comprehensive description of the c-MYC-associated sub-proteome will facilitate further studies aimed to elucidate the biology of c-MYC...
  16. pmc Induction of the Cdk inhibitor p21 by LY83583 inhibits tumor cell proliferation in a p53-independent manner
    Dimitri Lodygin
    Max Planck Institute of Biochemistry, Molecular Oncology, Munich, Germany
    J Clin Invest 110:1717-27. 2002
    ..These results suggest that LY, or derivatives, may be useful therapeutic agents for the treatment of tumors...
  17. ncbi request reprint Digital karyotyping reveals frequent inactivation of the dystrophin/DMD gene in malignant melanoma
    Henrike Körner
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried, Germany
    Cell Cycle 6:189-98. 2007
    ..Therefore, loss of DMD may critically change the migratory and proliferative capacity of melanocytes. Taken together, our results suggest that inactivation of DMD is involved in the pathogenesis of malignant melanoma...
  18. ncbi request reprint Targeted proteomic analysis of 14-3-3 sigma, a p53 effector commonly silenced in cancer
    Anne Benzinger
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried Munich, Germany
    Mol Cell Proteomics 4:785-95. 2005
    ..The data suggest that the cancer-specific loss of 14-3-3 sigma expression by epigenetic silencing or p53 mutations contributes to cancer formation by multiple routes...
  19. ncbi request reprint Characterization of epithelial senescence by serial analysis of gene expression: identification of genes potentially involved in prostate cancer
    Gerold Untergasser
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18 A, D 82152 Martinsried Munich, Germany
    Cancer Res 62:6255-62. 2002
    ....
  20. ncbi request reprint Extracellular 14-3-3sigma protein: a potential mediator of epithelial-mesenchymal interactions
    Heiko Hermeking
    Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
    J Invest Dermatol 124:ix-x. 2005
  21. ncbi request reprint Characterization of 14-3-3sigma dimerization determinants: requirement of homodimerization for inhibition of cell proliferation
    Berlinda Verdoodt
    Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Munich, Germany
    Cell Cycle 5:2920-6. 2006
    ..As inactivation of 14-3-3sigma sensitizes to DNA-damaging drugs, substances designed to interfere with 14-3-3sigma homodimerization may be used to inactivate 14-3-3sigma function for cancer therapeutic purposes...
  22. ncbi request reprint Analysis of 14-3-3sigma expression in hyperproliferative skin diseases reveals selective loss associated with CpG-methylation in basal cell carcinoma
    Dimitri Lodygin
    Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried near Munich, Germany
    Oncogene 22:5519-24. 2003
    ..As experimental removal of 14-3-3sigma sensitizes to DNA damage, silencing of 14-3-3sigma may explain the high efficacy of radiation therapy in the treatment of BCC...
  23. ncbi request reprint 14-3-3 proteins and cancer biology
    Heiko Hermeking
    Semin Cancer Biol 16:161. 2006
  24. pmc AP4 encodes a c-MYC-inducible repressor of p21
    Peter Jung
    Molecular Tumorpathology, Institute of Pathology, Ruhr University Bochum, D 44789 Bochum, Germany
    Proc Natl Acad Sci U S A 105:15046-51. 2008
    ..Notably, AP4 is specifically expressed in colonic progenitor and colorectal carcinoma cells. In conclusion, our results indicate that c-MYC employs AP4 to maintain cells in a proliferative, progenitor-like state...
  25. ncbi request reprint Downregulation of 14-3-3sigma in ovary, prostate and endometrial carcinomas is associated with CpG island methylation
    Paulette Mhawech
    Department of Clinical Pathology, Geneva University Hospital, Geneva, Switzerland
    Mod Pathol 18:340-8. 2005
    ..Loss of 14-3-3sigma expression due to promoter hypermethylation may represent the most frequent molecular aberration in ovarian, endometrial and prostate adenocarcinomas...
  26. ncbi request reprint Evidence for a cancer-specific switch at the CDK4 promoter with loss of control by both USF and c-Myc
    Snehalata A Pawar
    Department of Molecular Genetics, The University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA
    Oncogene 23:6125-35. 2004
    ..These results suggest that a major switch in the transcriptional control of CDK4 occurs during breast carcinogenesis, with likely alteration of cell cycle regulation...
  27. ncbi request reprint The crystal structure of the non-liganded 14-3-3sigma protein: insights into determinants of isoform specific ligand binding and dimerization
    Anne Benzinger
    Molecular Oncology Group, Max Planck Institute for Biochemistry, Martinsried, Germany
    Cell Res 15:219-27. 2005
    ..The structural differences among the 14-3-3 isoforms described here presumably contribute to isoform-specific interactions and functions...
  28. doi request reprint Human Proteinpedia enables sharing of human protein data
    Suresh Mathivanan
    Nat Biotechnol 26:164-7. 2008
  29. ncbi request reprint Functional epigenomics identifies genes frequently silenced in prostate cancer
    Dimitri Lodygin
    Molecular Oncology Group, Max Planck Institutes of Biochemistry, Martinsried and Institute of Pathology, Ludwig Maximilians University, Munich, Germany
    Cancer Res 65:4218-27. 2005
    ..The high frequency of CpG methylation detected in the promoters of the identified genes suggests a potential causal involvement in prostate cancer and may prove useful for diagnostic purposes...