Igor B Roninson

Summary

Affiliation: University of Illinois at Chicago
Country: USA

Publications

  1. ncbi request reprint Tumor cell senescence in cancer treatment
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607 7170, USA
    Cancer Res 63:2705-15. 2003
  2. ncbi request reprint Oncogenic functions of tumour suppressor p21(Waf1/Cip1/Sdi1): association with cell senescence and tumour-promoting activities of stromal fibroblasts
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607 7170, USA
    Cancer Lett 179:1-14. 2002
  3. ncbi request reprint If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells
    I B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago 60607 7170, USA
    Drug Resist Updat 4:303-13. 2001
  4. ncbi request reprint Induction of senescence-associated growth inhibitors in the tumor-suppressive function of retinoids
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    J Cell Biochem 88:83-94. 2003
  5. ncbi request reprint Retinoid-induced growth arrest of breast carcinoma cells involves co-activation of multiple growth-inhibitory genes
    Milos Dokmanovic
    Department of Molecular Genetics, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, Illinois 60607 7170, USA
    Cancer Biol Ther 1:24-7. 2002
  6. ncbi request reprint Identification of potential anticancer drug targets through the selection of growth-inhibitory genetic suppressor elements
    Thomas Primiano
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607, USA
    Cancer Cell 4:41-53. 2003
  7. pmc Molecular determinants of terminal growth arrest induced in tumor cells by a chemotherapeutic agent
    Bey Dih Chang
    Department of Molecular Genetics, University of Illinois, 900 South Ashland Avenue, Chicago, IL 60607 7170, USA
    Proc Natl Acad Sci U S A 99:389-94. 2002
  8. ncbi request reprint Identification of promoter elements responsible for transcriptional inhibition of polo-like kinase 1 and topoisomerase IIalpha genes by p21(WAF1/CIP1/SDI1)
    Hongming Zhu
    Department of Molecular Genetics, University of Illinois at Chicago, 60607 7170, USA
    Cell Cycle 1:59-66. 2002
  9. ncbi request reprint Genetic suppressor elements in the characterization and identification of tumor suppressor genes
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois, Chicago, USA
    Methods Mol Biol 222:413-36. 2003
  10. ncbi request reprint Tumor senescence as a determinant of drug response in vivo
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607 7170, USA
    Drug Resist Updat 5:204-8. 2002

Collaborators

Detail Information

Publications22

  1. ncbi request reprint Tumor cell senescence in cancer treatment
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607 7170, USA
    Cancer Res 63:2705-15. 2003
    ....
  2. ncbi request reprint Oncogenic functions of tumour suppressor p21(Waf1/Cip1/Sdi1): association with cell senescence and tumour-promoting activities of stromal fibroblasts
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607 7170, USA
    Cancer Lett 179:1-14. 2002
    ..Therapeutic strategies targeting the oncogenic consequences of p21 expression may provide a new approach to chemoprevention and treatment of cancer...
  3. ncbi request reprint If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells
    I B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago 60607 7170, USA
    Drug Resist Updat 4:303-13. 2001
    ..Elucidation of the factors that regulate different aspects of treatment-induced senescence and mitotic catastrophe should assist in improving the efficacy and decreasing side effects of cancer therapy...
  4. ncbi request reprint Induction of senescence-associated growth inhibitors in the tumor-suppressive function of retinoids
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    J Cell Biochem 88:83-94. 2003
    ..Elucidation of the mechanisms responsible for the induction of growth-inhibitory genes in retinoid-treated cells should help in developing agents that would mimic the antiproliferative effect of retinoids in retinoid-insensitive cancers...
  5. ncbi request reprint Retinoid-induced growth arrest of breast carcinoma cells involves co-activation of multiple growth-inhibitory genes
    Milos Dokmanovic
    Department of Molecular Genetics, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, Illinois 60607 7170, USA
    Cancer Biol Ther 1:24-7. 2002
    ..Elucidation of the mechanisms that mediate co-induction of growth-inhibitory genes in retinoid-treated cells may suggest an approach to reproducing the growth-inhibitory effect of retinoids in retinoid-insensitive human cancers...
  6. ncbi request reprint Identification of potential anticancer drug targets through the selection of growth-inhibitory genetic suppressor elements
    Thomas Primiano
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607, USA
    Cancer Cell 4:41-53. 2003
    ..Hence, selection for growth-inhibitory GSEs allows one to find potential targets for new anticancer drugs...
  7. pmc Molecular determinants of terminal growth arrest induced in tumor cells by a chemotherapeutic agent
    Bey Dih Chang
    Department of Molecular Genetics, University of Illinois, 900 South Ashland Avenue, Chicago, IL 60607 7170, USA
    Proc Natl Acad Sci U S A 99:389-94. 2002
    ..Elucidation of molecular changes in tumor cells that undergo drug-induced senescence suggests potential strategies for diagnostics and therapeutic modulation of this antiproliferative response in cancer treatment...
  8. ncbi request reprint Identification of promoter elements responsible for transcriptional inhibition of polo-like kinase 1 and topoisomerase IIalpha genes by p21(WAF1/CIP1/SDI1)
    Hongming Zhu
    Department of Molecular Genetics, University of Illinois at Chicago, 60607 7170, USA
    Cell Cycle 1:59-66. 2002
    ..These results indicate that inhibition of cell division-associated genes by p21 is mediated by different but overlapping mechanisms, which are not a general con-sequence of cell cycle arrest...
  9. ncbi request reprint Genetic suppressor elements in the characterization and identification of tumor suppressor genes
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois, Chicago, USA
    Methods Mol Biol 222:413-36. 2003
  10. ncbi request reprint Tumor senescence as a determinant of drug response in vivo
    Igor B Roninson
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607 7170, USA
    Drug Resist Updat 5:204-8. 2002
    ..This review discusses the results of the latter study, as well as the differences between the genetic determinants of treatment-induced senescence in murine lymphoma and in human solid tumor cells...
  11. ncbi request reprint Induction of transcription by p21Waf1/Cip1/Sdi1: role of NFkappaB and effect of non-steroidal anti-inflammatory drugs
    Jason C Poole
    Department of Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois, USA
    Cell Cycle 3:931-40. 2004
    ..These findings suggest the feasibility of developing agents that will counteract p21-mediated induction of disease-associated genes...
  12. ncbi request reprint Agonist and antagonist of retinoic acid receptors cause similar changes in gene expression and induce senescence-like growth arrest in MCF-7 breast carcinoma cells
    Yuhong Chen
    Cancer Center, Ordway Research Institute, Albany, NY 12208, USA
    Cancer Res 66:8749-61. 2006
    ..These results indicate that RARE-independent transcriptional effects of RAR ligands lead to senescence-like growth arrest and paracrine growth-inhibitory activity in MCF-7 breast carcinoma cells...
  13. ncbi request reprint Hallmarks of senescence in carcinogenesis and cancer therapy
    Jerry W Shay
    The University of Texas Southwestern Medical Center, Department of Cell Biology, 5323 Harry Hines Boulevard, Dallas, TX 75390 9039, USA
    Oncogene 23:2919-33. 2004
    ..The emerging knowledge about the pathways that lead to senescence and determine the pattern of gene expression in senescent cells may lead to more effective treatments for cancer...
  14. ncbi request reprint Tumor suppressor maspin is up-regulated during keratinocyte senescence, exerting a paracrine antiangiogenic activity
    Brian J Nickoloff
    Department of Pathology, Loyola University Medical Center, Maywood, Illinois 60153, USA
    Cancer Res 64:2956-61. 2004
    ..These findings indicate that senescent KCs exert a paracrine antiangiogenic activity, and maspin is the principal contributor to this potentially tumor-suppressive effect of cellular senescence...
  15. ncbi request reprint p21 (CDKN1A) is a negative regulator of p53 stability
    Eugenia V Broude
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 6:1468-71. 2007
    ..These results indicate that p21 acts as a negative regulator of p53 stability in different cell types. p53 regulation by p21 may provide a negative regulatory loop that limits p53 induction...
  16. ncbi request reprint Cell adhesion molecule L1 disrupts E-cadherin-containing adherens junctions and increases scattering and motility of MCF7 breast carcinoma cells
    Michael Shtutman
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cancer Res 66:11370-80. 2006
    ..Based on these results, we propose a model for the role of L1 as a trigger of EMT-like events in transformed epithelial cells...
  17. ncbi request reprint The STAT3 oncogene as a predictive marker of drug resistance
    Benjamin Barré
    School of Life Sciences, Division of Gene Regulation and Expression, Dundee, DD1 5EH, Scotland, UK
    Trends Mol Med 13:4-11. 2007
    ..Furthermore, interfering with the STAT3 oncogenic pathway might restore the sensitivity to anticancer drugs...
  18. ncbi request reprint Cell cycle arrest drastically extends the duration of gene silencing after transient expression of short hairpin RNA
    Anil Maliyekkel
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 5:2390-5. 2006
    ..These results indicate that gene silencing by transiently expressed shRNA is extremely stable in nondividing cells, and that this effect is not merely a consequence of siRNA stability...
  19. ncbi request reprint Induction of transcription through the p300 CRD1 motif by p21WAF1/CIP1 is core promoter specific and cyclin dependent kinase independent
    David J Gregory
    School of Life Sciences, Division of Gene Regulation and Expression, MSI WTB complex, University of Dundee, Dundee, Scotland, UK
    Cell Cycle 1:343-50. 2002
    ..These results give further insight into how regulators of cell growth and tumorigenesis, such as p21, can specifically target and induce the expression of select groups of genes...
  20. ncbi request reprint Src inhibits adriamycin-induced senescence and G2 checkpoint arrest by blocking the induction of p21waf1
    Arnaud Vigneron
    Institut National de la Sante et de la Recherche Medicale U564, Cancer Center Paul Papin, Angers, France
    Cancer Res 65:8927-35. 2005
    ..These results reveal a complex effect of Src on cellular drug responses and provide an explanation for the effect of this oncogene on cellular drug resistance...
  21. ncbi request reprint Seeking favors from nature
    Igor B Roninson
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cancer Biol Ther 4:794-9. 2005
  22. pmc Repression of the SUMO-specific protease Senp1 induces p53-dependent premature senescence in normal human fibroblasts
    Kristin E Yates
    Department of Genetics, Yale University School of Medicine, New Haven, CT 06520 8005, USA
    Aging Cell 7:609-21. 2008
    ..These data indicate that Senp1 repression induces p53-mediated premature senescence and that SUMO proteases may thus be required for proliferation of normal human cells...