Varda Rotter

Summary

Affiliation: Weizmann Institute of Science
Country: Israel

Publications

  1. pmc The promoters of human cell cycle genes integrate signals from two tumor suppressive pathways during cellular transformation
    Yuval Tabach
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Mol Syst Biol 1:2005.0022. 2005
  2. pmc Modulated expression of WFDC1 during carcinogenesis and cellular senescence
    Shalom Madar
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Carcinogenesis 30:20-7. 2009
  3. pmc A novel translocation breakpoint within the BPTF gene is associated with a pre-malignant phenotype
    Yosef Buganim
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 5:e9657. 2010
  4. pmc p53-Repressed miRNAs are involved with E2F in a feed-forward loop promoting proliferation
    Ran Brosh
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Mol Syst Biol 4:229. 2008
  5. pmc Mutant p53 attenuates the anti-tumorigenic activity of fibroblasts-secreted interferon beta
    Shalom Madar
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 8:e61353. 2013
  6. pmc Mutant p53 facilitates somatic cell reprogramming and augments the malignant potential of reprogrammed cells
    Rachel Sarig
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Exp Med 207:2127-40. 2010
  7. pmc Convergence of logic of cellular regulation in different premalignant cells by an information theoretic approach
    Nataly Kravchenko-Balasha
    Unit of Cellular Signaling, Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel
    BMC Syst Biol 5:42. 2011
  8. pmc Global profiling of histone and DNA methylation reveals epigenetic-based regulation of gene expression during epithelial to mesenchymal transition in prostate cells
    Xi Song Ke
    The Gade Institute, University of Bergen, Laboratory building, 5, etg, Vest, Helse Bergen, NO 5021 Bergen, Norway
    BMC Genomics 11:669. 2010
  9. ncbi request reprint Expression of prolyl-hydroxylase-1 (PHD1/EGLN2) suppresses hypoxia inducible factor-1alpha activation and inhibits tumor growth
    Neta Erez
    Departments of Molecular Cell Biology and Experimental Animals, The Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 63:8777-83. 2003
  10. ncbi request reprint p53-dependent down-regulation of telomerase is mediated by p21waf1
    Igor Shats
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Biol Chem 279:50976-85. 2004

Collaborators

Detail Information

Publications65

  1. pmc The promoters of human cell cycle genes integrate signals from two tumor suppressive pathways during cellular transformation
    Yuval Tabach
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Mol Syst Biol 1:2005.0022. 2005
    ..Our study demonstrates how a well-controlled transformation process allows linking between gene expression, promoter architecture, and activity of upstream signaling molecules...
  2. pmc Modulated expression of WFDC1 during carcinogenesis and cellular senescence
    Shalom Madar
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Carcinogenesis 30:20-7. 2009
    ..Taken together, our data suggest an important role for WFDC1 in inhibiting proliferation of both tumors and senescent cells. Finally, we suggest that the downregulation of WFDC1 might serve as a biomarker for cellular transformation...
  3. pmc A novel translocation breakpoint within the BPTF gene is associated with a pre-malignant phenotype
    Yosef Buganim
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 5:e9657. 2010
    ....
  4. pmc p53-Repressed miRNAs are involved with E2F in a feed-forward loop promoting proliferation
    Ran Brosh
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Mol Syst Biol 4:229. 2008
    ..Taken together, these findings position miRNAs as novel key players in the mammalian cellular proliferation network...
  5. pmc Mutant p53 attenuates the anti-tumorigenic activity of fibroblasts-secreted interferon beta
    Shalom Madar
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 8:e61353. 2013
    ..These data underscore mutant p53 oncogenic properties in the context of the tumor microenvironment and suggest that mutant p53 positive cancer patients might benefit from IFNβ treatment...
  6. pmc Mutant p53 facilitates somatic cell reprogramming and augments the malignant potential of reprogrammed cells
    Rachel Sarig
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Exp Med 207:2127-40. 2010
    ....
  7. pmc Convergence of logic of cellular regulation in different premalignant cells by an information theoretic approach
    Nataly Kravchenko-Balasha
    Unit of Cellular Signaling, Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel
    BMC Syst Biol 5:42. 2011
    ..The constraints identified by the analysis are transcription patterns underlying the process of transformation. Each pattern highlights the role of a group of genes that act coherently to define a transformed phenotype...
  8. pmc Global profiling of histone and DNA methylation reveals epigenetic-based regulation of gene expression during epithelial to mesenchymal transition in prostate cells
    Xi Song Ke
    The Gade Institute, University of Bergen, Laboratory building, 5, etg, Vest, Helse Bergen, NO 5021 Bergen, Norway
    BMC Genomics 11:669. 2010
    ..Here we investigated the hypothesis that specific histone and DNA methylations are involved in coordination of gene expression during EMT...
  9. ncbi request reprint Expression of prolyl-hydroxylase-1 (PHD1/EGLN2) suppresses hypoxia inducible factor-1alpha activation and inhibits tumor growth
    Neta Erez
    Departments of Molecular Cell Biology and Experimental Animals, The Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 63:8777-83. 2003
    ....
  10. ncbi request reprint p53-dependent down-regulation of telomerase is mediated by p21waf1
    Igor Shats
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Biol Chem 279:50976-85. 2004
    ..Inhibition of histone deacetylases also interfered with the repression of hTERT by p53. Therefore, our results suggest that repression of hTERT by endogenous p53 is mediated by p21 and E2F...
  11. ncbi request reprint Transcriptional programs following genetic alterations in p53, INK4A, and H-Ras genes along defined stages of malignant transformation
    Michael Milyavsky
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 65:4530-43. 2005
    ....
  12. ncbi request reprint Activated p53 suppresses the histone methyltransferase EZH2 gene
    Xiaohu Tang
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Oncogene 23:5759-69. 2004
    ..Suppression of EZH2 expression in tumors by p53 may lead to novel approaches to control cancer progression...
  13. ncbi request reprint Inactivation of myocardin and p16 during malignant transformation contributes to a differentiation defect
    Michael Milyavsky
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Cell 11:133-46. 2007
    ..Myocardin expression is reduced in multiple types of human tumors. Collectively, our results demonstrate that myocardin is an important suppressive modifier of the malignant transformation process...
  14. doi request reprint Prostate stromal cells produce CXCL-1, CXCL-2, CXCL-3 and IL-8 in response to epithelia-secreted IL-1
    Ira Kogan-Sakin
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Carcinogenesis 30:698-705. 2009
    ..Such interactions might contribute to prostatic inflammation and progression at early stages of prostate cancer formation...
  15. doi request reprint Differential influence of normal and cancer-associated fibroblasts on the growth of human epithelial cells in an in vitro cocultivation model of prostate cancer
    Nicole Paland
    Department of Molecular Cell Biology, Weizmann Institute of Science, Herzl, 1, Rehovot 76303, Israel
    Mol Cancer Res 7:1212-23. 2009
    ....
  16. pmc Mutant p53 attenuates the SMAD-dependent transforming growth factor beta1 (TGF-beta1) signaling pathway by repressing the expression of TGF-beta receptor type II
    Eyal Kalo
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell Biol 27:8228-42. 2007
    ..These data provide important insights into the molecular mechanisms that underlie mutant p53 "gain of function" pertaining to the TGF-beta signaling pathway...
  17. ncbi request reprint Hypoxia-dependent regulation of PHD1: cloning and characterization of the human PHD1/EGLN2 gene promoter
    Neta Erez
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    FEBS Lett 567:311-5. 2004
    ..Taken together, our findings suggest a hypoxia-induced regulatory loop of PHD1 expression, mediated by ARNT...
  18. ncbi request reprint Prolonged culture of telomerase-immortalized human fibroblasts leads to a premalignant phenotype
    Michael Milyavsky
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Res 63:7147-57. 2003
    ....
  19. ncbi request reprint Transactivation of the EGR1 gene contributes to mutant p53 gain of function
    Lilach Weisz
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 64:8318-27. 2004
    ..Functional assays indicate that induction of EGR1 by mutant p53 contributes to enhanced transformed properties and resistance to apoptosis. We propose that EGR1 is a significant contributor to mutant p53 gain of function...
  20. doi request reprint Mutant p53R273H attenuates the expression of phase 2 detoxifying enzymes and promotes the survival of cells with high levels of reactive oxygen species
    Eyal Kalo
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Cell Sci 125:5578-86. 2012
    ..These activities are attributable to mutant p53(R273H) gain of function and might underlie its well-documented oncogenic nature in human cancer...
  21. doi request reprint p53 Regulates the Ras circuit to inhibit the expression of a cancer-related gene signature by various molecular pathways
    Yosef Buganim
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 70:2274-84. 2010
    ..This study further elucidates the molecular loop between p53 and Ras in the transformation process...
  22. pmc SPATA18, a spermatogenesis-associated gene, is a novel transcriptional target of p53 and p63
    Chamutal Bornstein
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell Biol 31:1679-89. 2011
    ..Our data not only enrich the known collection of p53 targets but may also provide insights on spermatogenesis defects that are associated with p53 deficiency...
  23. doi request reprint Transcriptional activity of ATF3 in the stromal compartment of tumors promotes cancer progression
    Yosef Buganim
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Carcinogenesis 32:1749-57. 2011
    ..In sum, our findings implicate ATF3 as a novel stromal tumor promoter and suggest that targeting ATF3 pathway might be beneficial for anticancer therapy...
  24. ncbi request reprint Various p53 mutant proteins differently regulate the Ras circuit to induce a cancer-related gene signature
    Hilla Solomon
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    J Cell Sci 125:3144-52. 2012
    ..Our findings were further corroborated in human tumor-derived cell lines expressing Ras and the aforementioned mutated p53 proteins. These data might assist in future tailor-made therapy targeting the mutant p53-Ras axis in cancer...
  25. ncbi request reprint Myocardin in tumor suppression and myofibroblast differentiation
    Igor Shats
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cell Cycle 6:1141-6. 2007
    ..Here we discuss the emerging role of myocardin in tumor suppression as well as novel aspects of its regulation in normal and malignant conditions...
  26. pmc Modulation of the vitamin D3 response by cancer-associated mutant p53
    Perry Stambolsky
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Cell 17:273-85. 2010
    ..Furthermore, mutp53 increases the nuclear accumulation of VDR. Importantly, mutp53 converts vitamin D into an antiapoptotic agent. Thus, p53 status can determine the biological impact of vitamin D on tumor cells...
  27. doi request reprint Structural basis of restoring sequence-specific DNA binding and transactivation to mutant p53 by suppressor mutations
    Oded Suad
    Department of Structural Biology, Weizmann Institute of Science, Rehovot, Israel
    J Mol Biol 385:249-65. 2009
    ....
  28. ncbi request reprint Falkor, a novel cell growth regulator isolated by a functional genetic screen
    Neta Erez
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel 76100
    Oncogene 21:6713-21. 2002
    ..elegans protein EGL-9, recently shown to modify the Hypoxia Inducible Factor-1alpha. The homology suggests that these proteins share a functional domain that is conserved among a family of growth regulation proteins...
  29. ncbi request reprint hTERT-immortalized prostate epithelial and stromal-derived cells: an authentic in vitro model for differentiation and carcinogenesis
    Ira Kogan
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Res 66:3531-40. 2006
    ....
  30. doi request reprint The C-terminal domain of the Arabidopsis AtMBD7 protein confers strong chromatin binding activity
    Assaf Zemach
    Department of Plant Sciences, The Weizmann Institute of Science, Rehovot 76100, Israel
    Exp Cell Res 315:3554-62. 2009
    ..It may be possible to utilize this motif for fastening nuclear proteins to their chromosomal sites both in plant and animal cells for research and gene therapy applications...
  31. doi request reprint p53, a novel regulator of lipid metabolism pathways
    Ido Goldstein
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel
    J Hepatol 56:656-62. 2012
    ..In this study we aimed at characterizing the regulation of hepatic metabolic pathways by the p53 transcription factor...
  32. pmc Coupling transcriptional and post-transcriptional miRNA regulation in the control of cell fate
    Reut Shalgi
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Aging (Albany NY) 1:762-70. 2009
    ..We propose that examining miRNAs in the context of the regulatory transcriptional and post-transcriptional networks they are embedded in may provide a broader view of their role in controlling cell fate...
  33. doi request reprint p53-dependent transcriptional regulation of EDA2R and its involvement in chemotherapy-induced hair loss
    Ran Brosh
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel
    FEBS Lett 584:2473-7. 2010
    ..Moreover, we show that EDA2R is transactivated by p53 during chemotherapy-induced hair-loss, although its presence is not necessary for this process. These data shed new light on the role of EDA2R in exerting p53 function...
  34. ncbi request reprint Mutant p53 enhances nuclear factor kappaB activation by tumor necrosis factor alpha in cancer cells
    Lilach Weisz
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 67:2396-401. 2007
    ..Together, these findings suggest that p53 mutations may promote cancer progression by augmenting NFkappaB activation in the context of chronic inflammation...
  35. ncbi request reprint Mutant p53 protects cells from 12-O-tetradecanoylphorbol-13-acetate-induced death by attenuating activating transcription factor 3 induction
    Yosef Buganim
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 66:10750-9. 2006
    ..These data provide important insights into the molecular mechanisms that underlie mutant p53 gain of function...
  36. pmc Amplification of the 20q chromosomal arm occurs early in tumorigenic transformation and may initiate cancer
    Yuval Tabach
    Department of Physics of Complex Systems, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 6:e14632. 2011
    ....
  37. pmc Wide-scale analysis of human functional transcription factor binding reveals a strong bias towards the transcription start site
    Yuval Tabach
    Department of Physics of Complex Systems, Weizmann Institute of Science, Rehovot, Israel Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 2:e807. 2007
    ..Understanding how these parameters control functionality of different TFs in different biological contexts is a must for identifying functional TF binding sites and for understanding regulation of transcription...
  38. ncbi request reprint Inactivation of the p53 tumor suppressor gene and activation of the Ras oncogene: cooperative events in tumorigenesis
    Hilla Solomon
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Discov Med 9:448-54. 2010
    ..Here we review recent studies on the cooperative molecular mechanisms by which p53 inactivation and oncogenic Ras converge to enhance tumorigenesis...
  39. doi request reprint p53 is balancing development, differentiation and de-differentiation to assure cancer prevention
    Alina Molchadsky
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Carcinogenesis 31:1501-8. 2010
    ..This conclusion is further supporting the notion that aberrant differentiation is associated with malignant transformation...
  40. pmc p53 plays a role in mesenchymal differentiation programs, in a cell fate dependent manner
    Alina Molchadsky
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 3:e3707. 2008
    ..Therefore, it is critical to evaluate whether this inconsistency represents an authentic differential p53 activity manifested in the various differentiation programs...
  41. pmc Mutant p53 gain-of-function in cancer
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute, Rehovot 76100, Israel
    Cold Spring Harb Perspect Biol 2:a001107. 2010
    ..This article addresses the biological manifestations of mutant p53 gain-of-function, the underlying molecular mechanisms, and their possible clinical implications...
  42. doi request reprint Chemotherapeutic agents induce the expression and activity of their clearing enzyme CYP3A4 by activating p53
    Ido Goldstein
    The Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, 76100 Israel
    Carcinogenesis 34:190-8. 2013
    ..Importantly, this study reveals a novel pathway for the induction of CYP3As by their substrates through p53, warranting the need for careful consideration when designing systemically administered chemotherapeutic regimens...
  43. doi request reprint Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues
    Gilad Landan
    Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot, Israel
    Nat Genet 44:1207-14. 2012
    ..Characterizing epigenomic polymorphism within cell populations is therefore critical to understanding methylation dynamics in normal and cancer cells...
  44. doi request reprint p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes
    Ariel Rinon
    Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel
    Development 138:1827-38. 2011
    ....
  45. pmc Discovery of novel proteasome inhibitors using a high-content cell-based screening system
    Irena Lavelin
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 4:e8503. 2009
    ..The special features of the current screen, compared to those of other approaches are discussed...
  46. pmc Rescue of embryonic stem cells from cellular transformation by proteomic stabilization of mutant p53 and conversion into WT conformation
    Noa Rivlin
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel and
    Proc Natl Acad Sci U S A 111:7006-11. 2014
    ..Harnessing the ability of these protein interactors to transform the oncogenic mutant p53 to the tumor suppressor WT form can be the basis for future development of p53-targeted cancer therapy. ..
  47. doi request reprint The human 1-8D gene (IFITM2) is a novel p53 independent pro-apoptotic gene
    Vered Daniel-Carmi
    Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel
    Int J Cancer 125:2810-9. 2009
    ..Our data suggest a role for the 1-8D gene as a novel pro-apoptotic gene that will provide new insights into the regulated cellular pathways to death...
  48. ncbi request reprint The paradigm of mutant p53-expressing cancer stem cells and drug resistance
    Yoav Shetzer
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Carcinogenesis 35:1196-208. 2014
    ....
  49. doi request reprint 'Cancer associated fibroblasts'--more than meets the eye
    Shalom Madar
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100, Israel
    Trends Mol Med 19:447-53. 2013
    ..We hope this conceptualization can resolve the ongoing discrepancies revolving around CAF research and aid in designing better anti-cancer treatment strategies. ..
  50. ncbi request reprint The murine telomerase catalytic subunit shares the PAb-240 mutant specific epitope of the p53 protein
    Igor Shats
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    FEBS Lett 546:321-4. 2003
    ..The existence of a shared epitope between mutant p53 and telomerase may suggest that the two proteins contribute to malignant transformation through a common pathway...
  51. ncbi request reprint The onset of p53-dependent DNA repair or apoptosis is determined by the level of accumulated damaged DNA
    Hagai Offer
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Carcinogenesis 23:1025-32. 2002
    ..Taken together, this suggests that the decision of cells to induce a p53-dependent DNA repair or apoptosis is most probably controlled by the level of genotoxic agent introduced to cells...
  52. doi request reprint When mutants gain new powers: news from the mutant p53 field
    Ran Brosh
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Nat Rev Cancer 9:701-13. 2009
    ..Here, we review recent studies on mutant p53 regulation, gain-of-function mechanisms, transcriptional effects and prognostic association, with a focus on the clinical implications of these findings...
  53. doi request reprint Regulation of lipid metabolism by p53 - fighting two villains with one sword
    Ido Goldstein
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100 Israel
    Trends Endocrinol Metab 23:567-75. 2012
    ..Thus, by regulating lipid metabolism, p53 fights the two major causes of death worldwide - atherosclerosis and cancer...
  54. doi request reprint p53: balancing tumour suppression and implications for the clinic
    Yosef Buganim
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Eur J Cancer 45:217-34. 2009
    ....
  55. doi request reprint Cancer research, a field on the verge of a paradigm shift?
    Ido Goldstein
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Trends Mol Med 18:299-303. 2012
    ....
  56. pmc Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis
    Noa Rivlin
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Genes Cancer 2:466-74. 2011
    ..Here, the authors review the different studies on the involvement of p53 inactivation at various stages of tumorigenesis and highlight the specific contribution of p53 mutations at each phase of cancer progression...
  57. pmc Mutant p53 prolongs NF-κB activation and promotes chronic inflammation and inflammation-associated colorectal cancer
    Tomer Cooks
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Cell 23:634-46. 2013
    ..These findings might explain the early appearance of p53 mutations in human CAC...
  58. doi request reprint Transcriptional control of the proliferation cluster by the tumor suppressor p53
    Ran Brosh
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100, Israel
    Mol Biosyst 6:17-29. 2010
    ..Moreover, a complex regulatory network, which links p53 with the transcription factors that govern the expression of the proliferation cluster genes, is being gradually elucidated...
  59. ncbi request reprint The role of p53 in base excision repair following genotoxic stress
    Irit Zurer
    Department of Molecular Cell Biology, Weizmann Institute of Science, 76100 Rehovot, Israel
    Carcinogenesis 25:11-9. 2004
    ..When p53 is present, it down regulates the transcription of 3-MeAde DNA glycosylase. This provides a new model by which p53 prevents the creation of a mutator phenotype...
  60. doi request reprint Mutant p53 gain of function is interwoven into the hallmarks of cancer
    Hilla Solomon
    The Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    J Pathol 225:475-8. 2011
    ..Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd...
  61. ncbi request reprint DNA binding and 3'-5' exonuclease activity in the murine alternatively-spliced p53 protein
    Zippora Shakked
    Department of Structural Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Oncogene 21:5117-26. 2002
    ..The implications of these findings to a specific cellular role of AS-p53 are discussed...
  62. pmc DNA vaccination with CD25 protects rats from adjuvant arthritis and induces an antiergotypic response
    Avishai Mimran
    Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel
    J Clin Invest 113:924-32. 2004
    ..Thus, CD25 DNA vaccination may induce protection from autoimmunity by inducing a cytokine shift in both the antiergotypic response and the response to the antigens targeted in the disease...
  63. pmc Nitric oxide-induced cellular stress and p53 activation in chronic inflammation
    Lorne J Hofseth
    Laboratories of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 100:143-8. 2003
    ..Our study highlights a pivotal role of NO in the induction of cellular stress and the activation of a p53 response pathway during chronic inflammation...
  64. ncbi request reprint Conditional RNA interference in vivo to study mutant p53 oncogenic gain of function on tumor malignancy
    Gianluca Bossi
    Department of Experimental Oncology, Regina Elena Cancer Institute, Rome, Italy
    Cell Cycle 7:1870-9. 2008
    ..Results are confirmatory that depletion of mutant p53 protein impacts on tumor malignancy and validated the inducible lentiviral-based system as an efficient tool to study the gain of function activity of human tumor derived p53 mutants...
  65. ncbi request reprint Monoclonal antibody to a DNA-binding domain of p53 mimics charge structure of DNA: anti-idiotypes to the anti-p53 antibody are anti-DNA
    Johannes Herkel
    Department of Medicine, Johannes Gutenberg University, Mainz, Germany
    Eur J Immunol 34:3623-32. 2004
    ..Thus, a protein molecule may mimic the structure of DNA and the elusive generation of anti-DNA antibodies could be explained by idiotypic immunity to a DNA-binding protein, like p53...