Experts and Doctors on tumor suppressor protein p53 in Germany


Locale: Germany
Topic: tumor suppressor protein p53

Top Publications

  1. Rödicker F, Pützer B. p73 is effective in p53-null pancreatic cancer cells resistant to wild-type TP53 gene replacement. Cancer Res. 2003;63:2737-41 pubmed
    ..Our findings support the use of p73 as an anticancer drug in p53-null pancreatic cancer cells that are resistant to wild-type TP53 gene replacement. ..
  2. Ying S, Seiffert B, Hacker G, Fischer S. Broad degradation of proapoptotic proteins with the conserved Bcl-2 homology domain 3 during infection with Chlamydia trachomatis. Infect Immun. 2005;73:1399-403 pubmed
    ..These results show that chlamydial infection leads to a broad degradation of BH3-only proteins. This loss of proapoptotic factors can explain the almost general protection of infected cells against apoptotic stimuli. ..
  3. Popanda O, Edler L, Waas P, Schattenberg T, Butkiewicz D, Muley T, et al. Elevated risk of squamous-cell carcinoma of the lung in heavy smokers carrying the variant alleles of the TP53 Arg72Pro and p21 Ser31Arg polymorphisms. Lung Cancer. 2007;55:25-34 pubmed
    ..Nevertheless, confirmation by further molecular and epidemiological studies is warranted. ..
  4. Tarasov V, Jung P, Verdoodt B, Lodygin D, Epanchintsev A, Menssen A, et al. Differential regulation of microRNAs by p53 revealed by massively parallel sequencing: miR-34a is a p53 target that induces apoptosis and G1-arrest. Cell Cycle. 2007;6:1586-93 pubmed
    ..siRNAs corresponding to p53-induced miRNAs may have potential as cancer therapeutic agents as RNA interference based therapies are currently emerging. ..
  5. Nambiar S, Mirmohammadsadegh A, Hassan M, Hegemann J, Hengge U. Transcriptional regulation of ASK/Dbf4 in cutaneous melanoma is dependent on E2F1. Exp Dermatol. 2008;17:986-91 pubmed publisher
  6. Reinhardt H, Schumacher B. The p53 network: cellular and systemic DNA damage responses in aging and cancer. Trends Genet. 2012;28:128-36 pubmed publisher
    ..The network of p53 target genes thus functions as an important regulator of cancer prevention and aging. ..
  7. Jackstadt R, Jung P, Hermeking H. AP4 directly downregulates p16 and p21 to suppress senescence and mediate transformation. Cell Death Dis. 2013;4:e775 pubmed publisher
    ..In conclusion, this study identified AP4 as an oncogenic antagonist of cellular senescence. AP4 achieves this effect by direct repression of p16 and p21, and may thereby critically contribute to c-MYC function and tumor progression. ..
  8. Göhring U, Bersch A, Becker M, Neuhaus W, Schondorf T. p21(waf) correlates with DNA replication but not with prognosis in invasive breast cancer. J Clin Pathol. 2001;54:866-70 pubmed
    ..These data confirm the hypothesis of a p53 independent p21(waf) induction and suggest a functional role in the inhibition of PCNA mediated DNA replication. ..
  9. Pohnke Y, Schneider Merck T, Fahnenstich J, Kempf R, Christian M, Milde Langosch K, et al. Wild-type p53 protein is up-regulated upon cyclic adenosine monophosphate-induced differentiation of human endometrial stromal cells. J Clin Endocrinol Metab. 2004;89:5233-44 pubmed
    ..The observation that p53 protein expression is closely associated with decidual transformation indicates a novel role for this tumor suppressor in regulating human endometrial function. ..

More Information

Publications250 found, 100 shown here

  1. Baumann C, Boehden G, Burkle A, Wiesmuller L. Poly(ADP-RIBOSE) polymerase-1 (Parp-1) antagonizes topoisomerase I-dependent recombination stimulation by P53. Nucleic Acids Res. 2006;34:1036-49 pubmed
    ..Our data further indicate that PARP-1, probably through topoisomerase I interactions rather than poly(ADP-ribosyl)ation, prevents p53 from stimulating spontaneous HR on chromosomes via topoisomerase I activity. ..
  2. Knopf A, Plettenberg C, Pickhard A, Bas M, Reifenberger J, Bier H, et al. Analysis of the functional integrity of the p53 tumor-suppressor gene in malignant melanoma. Melanoma Res. 2011;21:380-8 pubmed publisher
    ..Altogether, accumulation of p53 protein is due to posttranslational modification or aberrant expression of p53 modifiers. p53 is functionally disrupted although the p53 upstream signaling pathway remains inducible. ..
  3. Weber A, Langhanki L, Schutz A, Gerstner A, Bootz F, Wittekind C, et al. Expression profiles of p53, p63, and p73 in benign salivary gland tumors. Virchows Arch. 2002;441:428-36 pubmed
    ..The prevalence of p53 mutations and the observation of the expression of DeltaNp63 isoforms only in pleomorphic adenomas, myoepitheliomas, and also basal cell adenomas may reflect their possible malignant potential. ..
  4. Herzog K, Schulz A, Buerkle C, Gromoll C, Braun J. Radiation-induced apoptosis in retinal progenitor cells is p53-dependent with caspase-independent DNA fragmentation. Eur J Neurosci. 2007;25:1349-56 pubmed
  5. Ecke T. Focus on urinary bladder cancer markers: a review. Minerva Urol Nefrol. 2008;60:237-46 pubmed
    ..Molecular staging of urological tumors will allow selecting cases that will require systemic treatment. It is necessary and important to integrate under the same objectives basic and clinical research. ..
  6. Tedeschi A, Nguyen T, Steele S, Feil S, Naumann U, Feil R, et al. The tumor suppressor p53 transcriptionally regulates cGKI expression during neuronal maturation and is required for cGMP-dependent growth cone collapse. J Neurosci. 2009;29:15155-60 pubmed publisher
    ..In conclusion, this study identifies p53 as a transcription factor that regulates the expression of cGKI during neuronal maturation and cGMP-dependent inhibition of growth cone collapse. ..
  7. Strebhardt K. Multifaceted polo-like kinases: drug targets and antitargets for cancer therapy. Nat Rev Drug Discov. 2010;9:643-60 pubmed publisher
    ..In this article, recent insights into the biology of PLKs will be reviewed, with an emphasis on their role in malignant transformation, and progress in the development of small-molecule PLK1 inhibitors will be examined. ..
  8. Nilsson S, Huelsenbeck J, Fritz G. Mevalonate pathway inhibitors affect anticancer drug-induced cell death and DNA damage response of human sarcoma cells. Cancer Lett. 2011;304:60-9 pubmed publisher
    ..In this regard, lovastatin and metformin turned out as the most effective inhibitory drugs. The data show that MP inhibitors can affect the anti-tumor efficacy of anticancer drugs and impact the DDR of human sarcoma cells. ..
  9. Felthaus O, Oliver F, Viale Bouroncle S, Driemel O, Reichert T, Schmalz G, et al. Transcription factors TP53 and SP1 and the osteogenic differentiation of dental stem cells. Differentiation. 2012;83:10-6 pubmed publisher
    ..In conclusion, our study demonstrates that SP1 and TP53 influence cell proliferation and differentiation and similar biological processes in both SHED and DFCs. ..
  10. Mayr D, Pannekamp U, Baretton G, Gropp M, Meier W, Flens M, et al. Immunohistochemical analysis of drug resistance-associated proteins in ovarian carcinomas. Pathol Res Pract. 2000;196:469-75 pubmed
    ..Our observations confirm the prognostic significance of p53 accumulation in ovarian carcinomas. Only GSTpi immunoreactivity was significantly correlated with drug resistance...
  11. Kruse Losler B, Diallo R, Gaertner C, Mischke K, Joos U, Kleinheinz J. Central giant cell granuloma of the jaws: a clinical, radiologic, and histopathologic study of 26 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;101:346-54 pubmed
    ..This should be accounted for to improve the individual planning of the treatment and follow-up...
  12. Rother K, Dengl M, Lorenz J, Tschop K, Kirschner R, Mossner J, et al. Gene expression of cyclin-dependent kinase subunit Cks2 is repressed by the tumor suppressor p53 but not by the related proteins p63 or p73. FEBS Lett. 2007;581:1166-72 pubmed
    ..Thus p53, rather than its homologues p63 and p73, may contribute to control of the first metaphase/anaphase transition of mammalian meiosis by downregulation of Cks2 expression. ..
  13. Peifer M, Fernandez Cuesta L, Sos M, George J, Seidel D, Kasper L, et al. Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer. Nat Genet. 2012;44:1104-10 pubmed publisher
  14. Yeghiazaryan K, Schild H, Golubnitschaja O. Chromium-picolinate therapy in diabetes care: individual outcomes require new guidelines and navigation by predictive diagnostics. Infect Disord Drug Targets. 2012;12:332-9 pubmed
    ..Consequently, a multimodal approach of integrative medicine by predictive diagnostics, targeted prevention and individually created treatment algorithms is highly desirable. ..
  15. Sarin N, Engel F, Kalayda G, Mannewitz M, Cinatl J, Rothweiler F, et al. Cisplatin resistance in non-small cell lung cancer cells is associated with an abrogation of cisplatin-induced G2/M cell cycle arrest. PLoS ONE. 2017;12:e0181081 pubmed publisher
    ..In conclusion, these findings suggest that acquired resistance of NSCLC cells against cisplatin is the consequence of altered signaling leading to reduced G2/M cell cycle arrest and apoptosis. ..
  16. Janz C, Wiesmuller L. Wild-type p53 inhibits replication-associated homologous recombination. Oncogene. 2002;21:5929-33 pubmed
    ..Consequently, we propose that p53 is a surveillance factor of homologous recombination at replication forks, when they stall as a consequence of endogenous or of exogenously introduced damage. ..
  17. Uhle S, Medalia O, Waldron R, Dumdey R, Henklein P, Bech Otschir D, et al. Protein kinase CK2 and protein kinase D are associated with the COP9 signalosome. EMBO J. 2003;22:1302-12 pubmed
    ..Curcumin treatment results in elevated amounts of c-Jun-Ub conjugates. We conclude that CK2 and PKD are recruited by CSN in order to regulate Ub conjugate formation. ..
  18. Bhonde M, Hanski M, Notter M, Gillissen B, Daniel P, Zeitz M, et al. Equivalent effect of DNA damage-induced apoptotic cell death or long-term cell cycle arrest on colon carcinoma cell proliferation and tumour growth. Oncogene. 2006;25:165-75 pubmed
    ..In conclusion, cell cycle arrest as well as apoptosis may be equipotent mechanisms mediating the chemotherapeutic effects of irinotecan. ..
  19. Epanchintsev A, Jung P, Menssen A, Hermeking H. Inducible microRNA expression by an all-in-one episomal vector system. Nucleic Acids Res. 2006;34:e119 pubmed
    ..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. ..
  20. Fuchs D, Berges C, Opelz G, Daniel V, Naujokat C. Increased expression and altered subunit composition of proteasomes induced by continuous proteasome inhibition establish apoptosis resistance and hyperproliferation of Burkitt lymphoma cells. J Cell Biochem. 2008;103:270-83 pubmed
  21. Sauer M, Bretz A, Beinoraviciute Kellner R, Beitzinger M, Burek C, Rosenwald A, et al. C-terminal diversity within the p53 family accounts for differences in DNA binding and transcriptional activity. Nucleic Acids Res. 2008;36:1900-12 pubmed publisher
    ..The different DNA-binding characteristics of the p53 family members could therefore reflect their predominant role in the cellular stress response (p53) or developmental processes (p73). ..
  22. Meulmeester E, Jochemsen A. p53: a guide to apoptosis. Curr Cancer Drug Targets. 2008;8:87-97 pubmed
    ..The continually increasing understanding of the mechanisms of regulation of p53 may provide the basis for new drug designs that could eventually lead to therapeutics to reactivate p53 in cancers. ..
  23. Eltze E, Wild P, Wulfing C, Zwarthoff E, Burger M, Stoehr R, et al. Expression of the endothelin axis in noninvasive and superficially invasive bladder cancer: relation to clinicopathologic and molecular prognostic parameters. Eur Urol. 2009;56:837-45 pubmed publisher
    ..Lack of ET(A)R expression may be an independent negative marker for recurrence-free survival. ..
  24. Berges C, Fuchs D, Opelz G, Daniel V, Naujokat C. Helenalin suppresses essential immune functions of activated CD4+ T cells by multiple mechanisms. Mol Immunol. 2009;46:2892-901 pubmed publisher
    ..Thus, helenalin can be defined as a new immunosuppressive compound suited for the treatment of deregulated and unwanted T cell-mediated immune responses. ..
  25. Burger K, Mühl B, Harasim T, Rohrmoser M, Malamoussi A, Orban M, et al. Chemotherapeutic drugs inhibit ribosome biogenesis at various levels. J Biol Chem. 2010;285:12416-25 pubmed publisher
    ..We conclude that inhibition of ribosome biogenesis by chemotherapeutic drugs potentially may contribute to the efficacy of therapeutic regimens. ..
  26. Kreis N, Sanhaji M, Kramer A, Sommer K, Rodel F, Strebhardt K, et al. Restoration of the tumor suppressor p53 by downregulating cyclin B1 in human papillomavirus 16/18-infected cancer cells. Oncogene. 2010;29:5591-603 pubmed publisher
    ..Taken together, targeting cyclin B1 might be an attractive strategy for preventing and treating papillomavirus-associated cancer by reactivating p53 and by reducing the Cdk1 activity. ..
  27. Vieth M, Kushima R, Mukaisho K, Sakai R, Kasami T, Hattori T. Immunohistochemical analysis of pyloric gland adenomas using a series of Mucin 2, Mucin 5AC, Mucin 6, CD10, Ki67 and p53. Virchows Arch. 2010;457:529-36 pubmed publisher
    ..The high frequency of malignant transformation of PGA underlines its high potential for invasive malignancy. ..
  28. Timofeev O, Schlereth K, Wanzel M, Braun A, Nieswandt B, Pagenstecher A, et al. p53 DNA binding cooperativity is essential for apoptosis and tumor suppression in vivo. Cell Rep. 2013;3:1512-25 pubmed publisher
  29. El Khatib M, Bozko P, Palagani V, Malek N, Wilkens L, Plentz R. Activation of Notch signaling is required for cholangiocarcinoma progression and is enhanced by inactivation of p53 in vivo. PLoS ONE. 2013;8:e77433 pubmed publisher
    ..Our study highlights the importance of Notch signaling in the tumorigenesis of CC and demonstrates that additional inactivation of p53 in vivo. ..
  30. Messmer U, Ankarcrona M, Nicotera P, Brune B. p53 expression in nitric oxide-induced apoptosis. FEBS Lett. 1994;355:23-6 pubmed
  31. Contente A, Dittmer A, Koch M, Roth J, Dobbelstein M. A polymorphic microsatellite that mediates induction of PIG3 by p53. Nat Genet. 2002;30:315-20 pubmed
    ..Moreover, this sequence of PIG3 is the first p53-responsive element found to be polymorphic. Inheritance of this microsatellite may affect an individual's susceptibility to cancer. ..
  32. Langheinrich U, Hennen E, Stott G, Vacun G. Zebrafish as a model organism for the identification and characterization of drugs and genes affecting p53 signaling. Curr Biol. 2002;12:2023-8 pubmed
    ..We conclude that zebrafish represents a promising model organism for future compound-based and genetic screens and believe that it will help to identify and characterize new anticancer drugs and new targets for cancer treatment. ..
  33. Wölcke J, Reimann M, Klumpp M, Gohler T, Kim E, Deppert W. Analysis of p53 "latency" and "activation" by fluorescence correlation spectroscopy. Evidence for different modes of high affinity DNA binding. J Biol Chem. 2003;278:32587-95 pubmed
    ..Because high affinity nonspecific DNA binding of latent p53 is restricted to wild type p53, we propose that it relates to its tumor suppressor functions. ..
  34. Dunkern T, Roos W, Kaina B. Apoptosis induced by MNNG in human TK6 lymphoblastoid cells is p53 and Fas/CD95/Apo-1 related. Mutat Res. 2003;544:167-72 pubmed
    ..This is in contrast to CHO fibroblasts in which, in response to O(6)MeG, the mitochondrial damage pathway becomes activated. ..
  35. Weinmann L, Wischhusen J, Demma M, Naumann U, Roth P, Dasmahapatra B, et al. A novel p53 rescue compound induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis. Cell Death Differ. 2008;15:718-29 pubmed publisher
    ..0 are sensitive to siRNA-mediated downregulation of p53. Thus this new p53 rescue compound may open up novel perspectives for the treatment of cancers currently considered resistant to the therapeutic induction of apoptosis. ..
  36. Busch C, Jacob C, Anwar A, Burkholz T, Aicha Ba L, Cerella C, et al. Diallylpolysulfides induce growth arrest and apoptosis. Int J Oncol. 2010;36:743-9 pubmed
    ..These results support the therapeutic potential of polysulfides and allow insight into the mechanisms based on the polysulfide biochemistry. ..
  37. Fahrer J, Schweitzer B, Fiedler K, Langer T, Gierschik P, Barth H. C2-streptavidin mediates the delivery of biotin-conjugated tumor suppressor protein p53 into tumor cells. Bioconjug Chem. 2013;24:595-603 pubmed publisher
    ..In conclusion, our results demonstrate the successful conjugation of biotin-p53 to C2-streptavidin and its subsequent receptor-mediated endocytosis into different human tumor cell lines. ..
  38. Quintanilla Martinez L, Kremer M, Keller G, Nathrath M, Gamboa Dominguez A, Meneses A, et al. p53 Mutations in nasal natural killer/T-cell lymphoma from Mexico: association with large cell morphology and advanced disease. Am J Pathol. 2001;159:2095-105 pubmed
    ..The overexpression of p53 and p21, independent of p53 mutations, although as yet not clear, might be the result of Epstein-Barr virus infection, and warrants further investigation. ..
  39. Peiro G, Diebold J, Löhrs U. CAS (cellular apoptosis susceptibility) gene expression in ovarian carcinoma: Correlation with 20q13.2 copy number and cyclin D1, p53, and Rb protein expression. Am J Clin Pathol. 2002;118:922-9 pubmed
    ..05). In OC, alteration of CAS and ZNF217 genes, both located at 20q13, is frequent and relevant prognostically. Cyclin D1, Rb, and p53 seem to have a secondary role. ..
  40. Wilhelm J, Pingoud A, Hahn M. Real-time PCR-based method for the estimation of genome sizes. Nucleic Acids Res. 2003;31:e56 pubmed
    ..The method was evaluated on three different eukaryotic species, Saccharomyces cerevisiae (12.1 Mb), Xiphophorus maculatus (550 Mb) and Homo sapiens sapiens (2.9 Gb), and found to be fast, highly accurate and reliable. ..
  41. Stürzenhofecker B, Schlott T, Quentin T, Kube D, Jung W, Trumper L. Abundant expression of spliced HDM2 in Hodgkin lymphoma cells does not interfere with p14(ARF) and p53 binding. Leuk Lymphoma. 2003;44:1587-96 pubmed
    ..Co-localization of the potential binding partners HDM2/p14(ARF) and HDM2/p53 was found in HL cell lines. We suggest that HDM2-sv have no significant disturbing influence on the interaction of these proteins. ..
  42. Roos W, Baumgartner M, Kaina B. Apoptosis triggered by DNA damage O6-methylguanine in human lymphocytes requires DNA replication and is mediated by p53 and Fas/CD95/Apo-1. Oncogene. 2004;23:359-67 pubmed
  43. Steinbach J, Eisenmann C, Klumpp A, Weller M. Co-inhibition of epidermal growth factor receptor and type 1 insulin-like growth factor receptor synergistically sensitizes human malignant glioma cells to CD95L-induced apoptosis. Biochem Biophys Res Commun. 2004;321:524-30 pubmed
    ..These findings suggest that adding inhibitors of IGF-1R may be a strategy to overcome escape from the anti-apoptotic effects of EGFR inhibition in malignant gliomas. ..
  44. Fischer S, Vier J, Kirschnek S, Klos A, Hess S, Ying S, et al. Chlamydia inhibit host cell apoptosis by degradation of proapoptotic BH3-only proteins. J Exp Med. 2004;200:905-16 pubmed
    ..These results reveal a novel way by which microbes can interfere with the host cell's apoptotic machinery, and provide a molecular explanation of the cellular resistance to apoptosis during infection with Chlamydia. ..
  45. Schlott T, Taubert H, Fayyazi A, Schweyer S, Bartel F, Korabiowska M, et al. Analysis of central regulatory pathways in p53-deficient primary cultures of malignant fibrous histiocytoma exposed to ifosfamide. Anticancer Res. 2004;24:3819-29 pubmed
    ..Further experiments are necessary to test whether the novel candidate genes favor development of chemoresistance and whether MDM2 mRNA splicing variants contribute to this process in vivo. ..
  46. Derouet Hümbert E, Roemer K, Bureik M. Adrenodoxin (Adx) and CYP11A1 (P450scc) induce apoptosis by the generation of reactive oxygen species in mitochondria. Biol Chem. 2005;386:453-61 pubmed
    ..We conclude that mitochondrial cytochrome P450 systems are a source of mitochondrial ROS production and can play a role in the induction of mitochondrial apoptosis. ..
  47. Wild P, Kunz Schughart L, Stoehr R, Burger M, Blaszyk H, Simon R, et al. High-throughput tissue microarray analysis of COX2 expression in urinary bladder cancer. Int J Oncol. 2005;27:385-91 pubmed
    ..Expression of COX2 is common in advanced BC with poor prognostic characteristics, supporting efforts to initiate clinical trials on the efficacy of COX2 inhibitors in the adjuvant treatment of high-risk urinary BC. ..
  48. Materna V, Surowiak P, Markwitz E, Spaczynski M, Drag Zalesinska M, Zabel M, et al. Expression of factors involved in regulation of DNA mismatch repair- and apoptosis pathways in ovarian cancer patients. Oncol Rep. 2007;17:505-16 pubmed
    ..In conclusion, these data indicate that analysis of proteins involved in DNA mismatch repair and apoptosis can be useful for prediction of clinical outcome in ovarian carcinoma patients. ..
  49. Koster F, Schröer A, Fischer D, Horn A, Diedrich K, Friedrich M. Immunohistochemistry of proteins for DNA mismatch repair in correlation to prognostic factors of mammarian cancer. Oncol Rep. 2007;17:1223-7 pubmed
    ..No correlation was detected between hMLH1 or PMS2 and any of the investigated factors. The expression of hMSH2 seems to be related with predictors of an unfavorable course of disease in breast cancer. ..
  50. Bartel F, Jung J, Böhnke A, Gradhand E, Zeng K, Thomssen C, et al. Both germ line and somatic genetics of the p53 pathway affect ovarian cancer incidence and survival. Clin Cancer Res. 2008;14:89-96 pubmed publisher
  51. Hemmati P, Normand G, Gillissen B, Wendt J, Dorken B, Daniel P. Cooperative effect of p21Cip1/WAF-1 and 14-3-3sigma on cell cycle arrest and apoptosis induction by p14ARF. Oncogene. 2008;27:6707-19 pubmed publisher
    ..Furthermore, our data delineate that the disruption of G2/M cell cycle checkpoint control critically determines the sensitivity of the cell toward p14(ARF)-induced mitochondrial apoptosis. ..
  52. Nollen M, Ebert F, Moser J, Mullenders L, Hartwig A, Schwerdtle T. Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression. Mol Nutr Food Res. 2009;53:572-82 pubmed publisher
    ..In summary, our data demonstrate that in human skin fibroblasts arsenite and even more pronounced MMA(III) interact with XPC expression, resulting in decreased XPC protein level and diminished assembly of the NER machinery. ..
  53. Greten F, Weber C, Greten T, Schneider G, Wagner M, Adler G, et al. Stat3 and NF-kappaB activation prevents apoptosis in pancreatic carcinogenesis. Gastroenterology. 2002;123:2052-63 pubmed
    ..These findings indicate that apoptosis resistance precedes formation of invasive pancreatic cancer. Therefore, combined inhibition of Stat3 and NF-kappaB might represent a novel strategy for tumor prevention and therapy. ..
  54. Hiller T, Poppelreuther S, Stubenrauch F, Iftner T. Comparative analysis of 19 genital human papillomavirus types with regard to p53 degradation, immortalization, phylogeny, and epidemiologic risk classification. Cancer Epidemiol Biomarkers Prev. 2006;15:1262-7 pubmed
    ..This could imply that other important functional differences exist between phylogenetically highly related viruses displaying similar biological properties in tissue culture that may affect their carcinogenicity in vivo. ..
  55. Nold M, Nold Petry C, Fischer D, Richter B, Blaheta R, Pfeilschifter J, et al. Activated protein C downregulates p38 mitogen-activated protein kinase and improves clinical parameters in an in-vivo model of septic shock. Thromb Haemost. 2007;98:1118-26 pubmed
    ..APC's clinical success may, in part, be due to p38MAPK inhibition. ..
  56. Leuschner I, Langhans I, Schmitz R, Harms D, Mattke A, Treuner J. p53 and mdm-2 expression in Rhabdomyosarcoma of childhood and adolescence: clinicopathologic study by the Kiel Pediatric Tumor Registry and the German Cooperative Soft Tissue Sarcoma Study. Pediatr Dev Pathol. 2003;6:128-36 pubmed
    ..In conclusion, we could not demonstrate that any of the investigated parameters had an influence on prognosis of RMS. p53 protein overexpression might be a crucial step in metastatic disease for patients with embryonal RMS. ..
  57. Gasser M, Gerstlauer C, Grimm M, Bueter M, Lebedeva T, Lutz J, et al. Comparative analysis of predictive biomarkers for therapeutical strategies in colorectal cancer. Ann Surg Oncol. 2007;14:1272-84 pubmed
    ..Overall increased p53, CEA, and CA 19-9 serum levels and their marker expression in the tumor may be used at the time of primary tumor removal for defining patients at risk for tumor recurrence. ..
  58. Stubenrauch F, Straub E, Fertey J, Iftner T. The E8 repression domain can replace the E2 transactivation domain for growth inhibition of HeLa cells by papillomavirus E2 proteins. Int J Cancer. 2007;121:2284-92 pubmed
    ..In summary, our results demonstrate that the small E8 repression domain can functionally replace the large E2 transactivation domain for growth inhibition of HeLa cervical cancer cells. ..
  59. Schmidt F, Knobbe C, Frank B, Wolburg H, Weller M. The topoisomerase II inhibitor, genistein, induces G2/M arrest and apoptosis in human malignant glioma cell lines. Oncol Rep. 2008;19:1061-6 pubmed
    ..Thus, genistein-like protein kinase inhibitors are promising agents for the experimental treatment of malignant gliomas. ..
  60. Kreis N, Sommer K, Sanhaji M, Kramer A, Matthess Y, Kaufmann M, et al. Long-term downregulation of Polo-like kinase 1 increases the cyclin-dependent kinase inhibitor p21(WAF1/CIP1). Cell Cycle. 2009;8:460-72 pubmed
    ..Importantly, HeLa cells with reduced level of Plk1, which induces an increase of p21, p73 and Bax, are more sensitive to some chemotherapeutic agents, such as cisplatin. ..
  61. Hermeking H. MicroRNAs in the p53 network: micromanagement of tumour suppression. Nat Rev Cancer. 2012;12:613-26 pubmed publisher
    ..In the future, knowledge about the p53-miRNA network may be able to be exploited for diagnostic and therapeutic approaches in cancer prevention and treatment. ..
  62. Schaefer I, Sahlmann C, Overbeck T, Schweyer S, Menke J. Blastomatoid pulmonary carcinosarcoma: report of a case with a review of the literature. BMC Cancer. 2012;12:424 pubmed publisher
    ..The observed molecular and cytogenetic findings may provide additional tools for the differential diagnosis of biphasic pulmonary neoplasms. Furthermore, TP53, MDM2, CDK4, and PTPN1 may be involved in tumourigenesis. ..
  63. Othman E, Kreissl M, Kaiser F, Arias Loza P, Stopper H. Insulin-mediated oxidative stress and DNA damage in LLC-PK1 pig kidney cell line, female rat primary kidney cells, and male ZDF rat kidneys in vivo. Endocrinology. 2013;154:1434-43 pubmed publisher
  64. Heering J, Jonker H, Löhr F, Schwalbe H, Dötsch V. Structural investigations of the p53/p73 homologs from the tunicate species Ciona intestinalis reveal the sequence requirements for the formation of a tetramerization domain. Protein Sci. 2016;25:410-22 pubmed publisher
    ..By mutational analysis, we identify a proline as well as large hydrophobic residues in the hinge region between both helices as the crucial determinant for the formation of a second helix. ..
  65. Fukami S, Riemenschneider M, Kohno M, Steiger H. Expression and gene doses changes of the p53-regulator PPM1D in meningiomas: a role in meningioma progression?. Brain Tumor Pathol. 2016;33:191-9 pubmed publisher
    ..Thus, PPM1D in the chromosomal location 17q22-24 might be the most relevant candidate gene with respect to a potential functional implication in meningioma progression. ..
  66. Klein C, Georges G, Kunkele K, Huber R, Engh R, Hansen S. High thermostability and lack of cooperative DNA binding distinguish the p63 core domain from the homologous tumor suppressor p53. J Biol Chem. 2001;276:37390-401 pubmed
    ..The model also shows differences in the electrostatic and hydrophobic potentials of the domains relevant to folding stability. ..
  67. Stiewe T, Stanelle J, Theseling C, Pollmeier B, Beitzinger M, Pützer B. Inactivation of retinoblastoma (RB) tumor suppressor by oncogenic isoforms of the p53 family member p73. J Biol Chem. 2003;278:14230-6 pubmed
    ..These findings provide an explanation for the fundamentally different functions of p53 and p73 in tumorigenesis. ..
  68. Linares L, Hengstermann A, Ciechanover A, Muller S, Scheffner M. HdmX stimulates Hdm2-mediated ubiquitination and degradation of p53. Proc Natl Acad Sci U S A. 2003;100:12009-14 pubmed
  69. Marchini A, Marttila T, Winter A, Caldeira S, Malanchi I, Blaschke R, et al. The short stature homeodomain protein SHOX induces cellular growth arrest and apoptosis and is expressed in human growth plate chondrocytes. J Biol Chem. 2004;279:37103-14 pubmed
    ..This study provides the first insight into the biological function of SHOX as regulator of cellular proliferation and viability and relates these cellular events to the phenotypic consequences of SHOX deficiency. ..
  70. Speidel D, Helmbold H, Deppert W. Dissection of transcriptional and non-transcriptional p53 activities in the response to genotoxic stress. Oncogene. 2006;25:940-53 pubmed
    ..Our results demonstrate the impact and in vivo relevance of non-transcriptional mechanisms for wild-type and mutant p53-mediated apoptosis. ..
  71. Wanka C, Brucker D, Bähr O, Ronellenfitsch M, Weller M, Steinbach J, et al. Synthesis of cytochrome C oxidase 2: a p53-dependent metabolic regulator that promotes respiratory function and protects glioma and colon cancer cells from hypoxia-induced cell death. Oncogene. 2012;31:3764-76 pubmed publisher
    ..Targeting SCO2 may therefore represent a valuable strategy to enhance sensitivity towards hypoxia and may complement strategies targeting glucose metabolism. ..
  72. Sanhaji M, Kreis N, Zimmer B, Berg T, Louwen F, Yuan J.  p53 is not directly relevant to the response of Polo-like kinase 1 inhibitors. Cell Cycle. 2012;11:543-53 pubmed publisher
  73. Süsse S, Janz C, Janus F, Deppert W, Wiesmuller L. Role of heteroduplex joints in the functional interactions between human Rad51 and wild-type p53. Oncogene. 2000;19:4500-12 pubmed
    ..Oncogene (2000) 19, 4500 - 4512. ..
  74. Fricke E, Keller G, Becker I, Rosivatz E, Schott C, Plaschke S, et al. Relationship between E-cadherin gene mutation and p53 gene mutation, p53 accumulation, Bcl-2 expression and Ki-67 staining in diffuse-type gastric carcinoma. Int J Cancer. 2003;104:60-5 pubmed
    ..00). These data suggest that the presence of E-cadherin mutations can significantly alter the accumulation of the apoptosis-regulating p53 protein, whereas no correlation with the p53 mutation status or with Ki-67 staining was observed. ..
  75. Schick B, Veldung B, Wemmert S, Jung V, Montenarh M, Meese E, et al. p53 and Her-2/neu in juvenile angiofibromas. Oncol Rep. 2005;13:453-7 pubmed
    ..However, comparison of p53 and Her-2/neu mRNA levels in laser microdissected endothelial and stromal cells were not conclusive to answer the question of the tumour cell of origin in JA. ..
  76. Hassan I, Wunderlich A, Slater E, Hoffmann S, Celik I, Zielke A. Antisense p53 decreases production of VEGF in follicular thyroid cancer cells. Endocrine. 2006;29:409-12 pubmed
    ..03). These results suggest that transient MTp53 knockout with ODNs complementary to p53 nucleotide sequences impair secretion of VEGF in the undifferentiated thyroid cancer cell line FTC-133. ..
  77. Kahl P, Gullotti L, Heukamp L, Wolf S, Friedrichs N, Vorreuther R, et al. Androgen receptor coactivators lysine-specific histone demethylase 1 and four and a half LIM domain protein 2 predict risk of prostate cancer recurrence. Cancer Res. 2006;66:11341-7 pubmed
    ..Our present study suggests that LSD1 and nuclear FHL2 may serve as novel biomarkers predictive for prostate cancer with aggressive biology and point to a role of LSD1 and FHL2 in constitutive activation of AR-mediated growth signals. ..
  78. Wassmann S, Wassmann K, Jung A, Velten M, Knuefermann P, Petoumenos V, et al. Induction of p53 by GKLF is essential for inhibition of proliferation of vascular smooth muscle cells. J Mol Cell Cardiol. 2007;43:301-7 pubmed
    ..The transcription factor GKLF induces inhibition of proliferation of VSMC which is mechanistically linked to a GKLF-induced enhancement of the expression of the tumor suppressor gene p53. ..
  79. Bettendorf O, Schmidt H, Staebler A, Grobholz R, Heinecke A, Boecker W, et al. Chromosomal imbalances, loss of heterozygosity, and immunohistochemical expression of TP53, RB1, and PTEN in intraductal cancer, intraepithelial neoplasia, and invasive adenocarcinoma of the prostate. Genes Chromosomes Cancer. 2008;47:565-72 pubmed publisher
    ..Our results indicate that IDC-P in general follows the genetic pathway from normal epithelium over PIN lesion. IDC-P represents a separate prostatic lesion and should be graded as a poorly differentiated carcinoma. ..
  80. Bollmann D, Bollmann M, Bankfalvi A, Heller H, Bollmann R, Pajor G, et al. Quantitative molecular grading of bladder tumours: a tool for objective assessment of the biological potential of urothelial neoplasias. Oncol Rep. 2009;21:39-47 pubmed
    ..Our preliminary data strongly suggest that the combination of quantitative biomarkers provides superior and objective prognostic tools in bladder urothelial neoplasias compared to classic clinicopathological features and indices. ..
  81. Brazdova M, Quante T, Tögel L, Walter K, Loscher C, Tichý V, et al. Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences. Nucleic Acids Res. 2009;37:1486-500 pubmed publisher
    ..We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. ..
  82. Guthoff R, Marx A, Stroebel P. No evidence for a pathogenic role of human papillomavirus infection in ocular surface squamous neoplasia in Germany. Curr Eye Res. 2009;34:666-71 pubmed
    ..TP53 mutations were also rare but may play a role in the progression from conjunctival intraepithelial neoplasia to invasive carcinoma in a subset of cases. ..
  83. Krastev D, Slabicki M, Paszkowski Rogacz M, Hubner N, Junqueira M, Shevchenko A, et al. A systematic RNAi synthetic interaction screen reveals a link between p53 and snoRNP assembly. Nat Cell Biol. 2011;13:809-18 pubmed publisher
    ..This unanticipated function of TP53 in snoRNP assembly highlights the potential of RNAi-mediated synthetic interaction screens to dissect molecular pathways of tumour suppressor genes. ..
  84. Ehrhardt H, Wachter F, Maurer M, Stahnke K, Jeremias I. Important role of caspase-8 for chemosensitivity of ALL cells. Clin Cancer Res. 2011;17:7605-13 pubmed publisher
    ..Reexpression of epigenetically downregulated caspase-8 represents a promising approach to increase efficiency of antileukemic therapy. ..
  85. Keim A, Rössler O, Rothhaar T, Thiel G. Arsenite-induced apoptosis of human neuroblastoma cells requires p53 but occurs independently of c-Jun. Neuroscience. 2012;206:25-38 pubmed publisher
    ..Together, these data show that the upregulation of p53 is causally linked with arsenite-induced cell death in neuroblastoma cells, whereas the upregulation of c-Jun is not part of this apoptotic signaling cascade...
  86. Yentrapalli R, Azimzadeh O, Barjaktarovic Z, Sarioglu H, Wojcik A, Harms Ringdahl M, et al. Quantitative proteomic analysis reveals induction of premature senescence in human umbilical vein endothelial cells exposed to chronic low-dose rate gamma radiation. Proteomics. 2013;13:1096-107 pubmed publisher
    ..This study contributes to the understanding of the increased risk of cardiovascular diseases seen in populations exposed to chronic low-dose irradiation. ..
  87. Schlereth K, Heyl C, Krampitz A, Mernberger M, Finkernagel F, Scharfe M, et al. Characterization of the p53 cistrome--DNA binding cooperativity dissects p53's tumor suppressor functions. PLoS Genet. 2013;9:e1003726 pubmed publisher
  88. Siemens H, Jackstadt R, Kaller M, Hermeking H. Repression of c-Kit by p53 is mediated by miR-34 and is associated with reduced chemoresistance, migration and stemness. Oncotarget. 2013;4:1399-415 pubmed
    ..Therefore, this regulation may be potentially relevant for future diagnostic and therapeutic approaches. ..
  89. Gottlieb A, Althoff K, Grunewald L, Thor T, Odersky A, Schulte M, et al. RITA displays anti-tumor activity in medulloblastomas independent of TP53 status. Oncotarget. 2017;8:27882-27891 pubmed publisher
  90. Laudato S, Patil N, Abba M, Leupold J, Benner A, Gaiser T, et al. P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1. Int J Cancer. 2017;141:1879-1890 pubmed publisher
    ..Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. ..
  91. Hobom U, Dobbelstein M. E1B-55-kilodalton protein is not required to block p53-induced transcription during adenovirus infection. J Virol. 2004;78:7685-97 pubmed
    ..In conclusion, adenovirus does not need direct binding of E1B-55-kDa to inactivate p53, and forced p53 activity with consecutive apoptosis does not severely impair virus replication. ..
  92. Gockel I, Kammerer P, Brieger J, Heinrich U, Mann W, Bittinger F, et al. Image cytometric DNA analysis of mucosal biopsies in patients with primary achalasia. World J Gastroenterol. 2006;12:3020-5 pubmed