Artur Slupianek

Summary

Affiliation: Temple University
Country: USA

Publications

  1. ncbi request reprint NPM/ALK downregulates p27Kip1 in a PI-3K-dependent manner
    Artur Slupianek
    College of Science and Technology, Center for Biotechnology, Temple University, Philadelphia, PA 19008, USA
    Exp Hematol 32:1265-71. 2004
  2. pmc BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability
    A Slupianek
    Department of Microbiology and Immunology, Temple University, Philadelphia, PA, USA
    Leukemia 27:629-34. 2013
  3. ncbi request reprint ATR-Chk1 axis protects BCR/ABL leukemia cells from the lethal effect of DNA double-strand breaks
    Margaret Nieborowska-Skorska
    Department of Microbiology and Immunology, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cell Cycle 5:994-1000. 2006
  4. pmc Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells
    Lori Rink
    Department of Microbiology and Immunology, Temple University, Philadelphia, PA 19140, USA
    Blood 110:651-60. 2007
  5. doi request reprint BCR/ABL inhibits mismatch repair to protect from apoptosis and induce point mutations
    Tomasz Stoklosa
    Department of Microbiology and Immunology, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cancer Res 68:2576-80. 2008
  6. ncbi request reprint BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks
    Michal O Nowicki
    Center for Biotechnology, College of Science and Technology, Temple University, Bio Life Sciences Bldg, Rm 419, 1900 N 12th St, Philadelphia, PA 19122, USA
    Blood 104:3746-53. 2004
  7. pmc BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells
    Artur Slupianek
    Center for Biotechnology, College of Science and Technology, Temple University, Bio Life Sciences Building, Room 419, 1900 N 12th Street, Philadelphia, PA 19122, USA
    DNA Repair (Amst) 5:243-50. 2006
  8. ncbi request reprint BLM helicase is activated in BCR/ABL leukemia cells to modulate responses to cisplatin
    Artur Slupianek
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
    Oncogene 24:3914-22. 2005
  9. ncbi request reprint BCR/ABL recruits p53 tumor suppressor protein to induce drug resistance
    Tomasz Stoklosa
    Molecular Carcinogenesis Section, Center of Biotechnology, College of Science and Technology, Temple University, 1900 N 12th Street, Philadelphia, Pennsylvania 19122, USA
    Cell Cycle 3:1463-72. 2004
  10. pmc BCR/ABL stimulates WRN to promote survival and genomic instability
    Artur Slupianek
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cancer Res 71:842-51. 2011

Collaborators

Detail Information

Publications22

  1. ncbi request reprint NPM/ALK downregulates p27Kip1 in a PI-3K-dependent manner
    Artur Slupianek
    College of Science and Technology, Center for Biotechnology, Temple University, Philadelphia, PA 19008, USA
    Exp Hematol 32:1265-71. 2004
    ..It was reported that p27Kip1 function is impaired in many tumors. In this study we investigated the role of PI-3K/AKT in NPM/ALK-dependent downregulation of p27Kip1 protein...
  2. pmc BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability
    A Slupianek
    Department of Microbiology and Immunology, Temple University, Philadelphia, PA, USA
    Leukemia 27:629-34. 2013
    ....
  3. ncbi request reprint ATR-Chk1 axis protects BCR/ABL leukemia cells from the lethal effect of DNA double-strand breaks
    Margaret Nieborowska-Skorska
    Department of Microbiology and Immunology, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cell Cycle 5:994-1000. 2006
    ..In conclusion, ATR-Chk1 axis was strongly activated in BCR/ABL-positive cells and contributed to the resistance to DNA cross-linking agents causing numerous replication-dependent DSBs...
  4. pmc Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells
    Lori Rink
    Department of Microbiology and Immunology, Temple University, Philadelphia, PA 19140, USA
    Blood 110:651-60. 2007
    ..Interestingly, inhibition of Nbs1 phosphorylation by S343A mutant enhanced the antileukemia effect of the combination of imatinib and genotoxic agent...
  5. doi request reprint BCR/ABL inhibits mismatch repair to protect from apoptosis and induce point mutations
    Tomasz Stoklosa
    Department of Microbiology and Immunology, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cancer Res 68:2576-80. 2008
    ..In conclusion, these results suggest that BCR/ABL kinase abrogates MMR activity to inhibit apoptosis and induce mutator phenotype...
  6. ncbi request reprint BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks
    Michal O Nowicki
    Center for Biotechnology, College of Science and Technology, Temple University, Bio Life Sciences Bldg, Rm 419, 1900 N 12th St, Philadelphia, PA 19122, USA
    Blood 104:3746-53. 2004
    ..We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair...
  7. pmc BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells
    Artur Slupianek
    Center for Biotechnology, College of Science and Technology, Temple University, Bio Life Sciences Building, Room 419, 1900 N 12th Street, Philadelphia, PA 19122, USA
    DNA Repair (Amst) 5:243-50. 2006
    ..We propose that unfaithful repair of DSBs may contribute to genomic instability in the Philadelphia chromosome-positive leukemias...
  8. ncbi request reprint BLM helicase is activated in BCR/ABL leukemia cells to modulate responses to cisplatin
    Artur Slupianek
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
    Oncogene 24:3914-22. 2005
    ..These data suggest that BLM collaborates with RAD51 to facilitate HRR and promotes the resistance of BCR/ABL-positive leukemia cells to DNA-damaging agents...
  9. ncbi request reprint BCR/ABL recruits p53 tumor suppressor protein to induce drug resistance
    Tomasz Stoklosa
    Molecular Carcinogenesis Section, Center of Biotechnology, College of Science and Technology, Temple University, 1900 N 12th Street, Philadelphia, Pennsylvania 19122, USA
    Cell Cycle 3:1463-72. 2004
    ..In conclusion, accumulation of the p53 protein contributed to prolonged G(2)/M checkpoint activation and drug resistance in myeloid cells expressing the BCR/ABL oncoproteins...
  10. pmc BCR/ABL stimulates WRN to promote survival and genomic instability
    Artur Slupianek
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cancer Res 71:842-51. 2011
    ..In summary, we postulate that BCR/ABL-mediated stimulation of WRN modulates the efficiency and fidelity of major DSB repair mechanisms to protect leukemia cells from apoptosis and to facilitate genomic instability...
  11. pmc BCR/ABL and other kinases from chronic myeloproliferative disorders stimulate single-strand annealing, an unfaithful DNA double-strand break repair
    Kimberly Cramer
    Department of Microbiology and Immunology, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cancer Res 68:6884-8. 2008
    ..Taken together, these findings suggest a role of FTKs in causing disease progression in MPDs by inducing chromosomal instability through the production of DSBs and stimulation of SSA repair...
  12. pmc Targeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia
    Artur Slupianek
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA, USA
    Blood 118:1062-8. 2011
    ..In conclusion, we postulate that BCR-ABL1 kinase-mediated RAD51(pY315) promotes unfaithful HomeoRR in leukemia cells, which may contribute to accumulation of secondary chromosomal aberrations responsible for CML relapse and progression...
  13. pmc The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells
    Agata Klejman
    Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
    EMBO J 21:5766-74. 2002
    ..These data identify a novel BCR/ABL-Hck-STAT5 signaling pathway, which plays an important role in BCR/ABL-mediated transformation of myeloid cells...
  14. ncbi request reprint Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571
    Agata Klejman
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA
    Oncogene 21:5868-76. 2002
    ..In conclusion, combination of STI571+WT or STI571+LY may represent a novel approach against the Ph(1)-positive leukemias...
  15. doi request reprint The chromatin remodeling factor SRCAP modulates expression of prostate specific antigen and cellular proliferation in prostate cancer cells
    Artur Slupianek
    Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA
    J Cell Physiol 224:369-75. 2010
    ..These data identify SRCAP as a physiologically relevant mediator of PSA expression, and demonstrate that SRCAP plays a role in prostate cancer cell proliferation...
  16. pmc Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile
    Kimberly Cramer-Morales
    Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Blood 122:1293-304. 2013
    ..We believe this work may initiate a personalized therapeutic approach in numerous patients with tumors displaying encoded and functional BRCA deficiency. ..
  17. pmc Fusion tyrosine kinases induce drug resistance by stimulation of homology-dependent recombination repair, prolongation of G(2)/M phase, and protection from apoptosis
    Artur Slupianek
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA
    Mol Cell Biol 22:4189-201. 2002
    ..Thus, we postulate that RAD51-dependent facilitation of DSB repair, antiapoptotic activity of Bcl-xL, and delay in progression through the G(2)/M phase work in concert to induce drug resistance in FTK-positive leukemias and lymphomas...
  18. ncbi request reprint Activation of mammalian target of rapamycin in transformed B lymphocytes is nutrient dependent but independent of Akt, mitogen-activated protein kinase/extracellular signal-regulated kinase kinase, insulin growth factor-I, and serum
    Pawel Wlodarski
    Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104, USA
    Cancer Res 65:7800-8. 2005
    ..They also suggest that inhibition of mTOR signaling might be effective in therapy of the large spectrum of B-cell lymphomas...
  19. ncbi request reprint Brain tumor formation in tuberous sclerosis depends on Erk activation
    Jaroslaw Jozwiak
    Department of Histology and Embryology, Center for Biostructure Research, Medical University of Warsaw, and Department of Pathology, The Children s Memorial Health Institute, Warsaw, Poland
    Neuromolecular Med 9:117-27. 2007
    ..Importantly, Erk inhibition leads to the decrease of proliferation potential of such lines. These results show that Erk is specifically implicated in the pathogenesis of hamartomas...
  20. ncbi request reprint TEL-fusion oncogenic tyrosine kinases determine leukemic cells response to idarubicin
    Ireneusz Majsterek
    Department of Molecular Genetics University of Lodz, Poland
    Anticancer Drugs 14:625-31. 2003
    ..The results obtained suggest that TEL-related FTKs may stimulate the repair of DNA damaged by idarubicin and be relevant to the resistance of the leukemic cells to this drug...
  21. ncbi request reprint Fusion oncogenic tyrosine kinases alter DNA damage and repair after genotoxic treatment: role in drug resistance?
    Grazyna Hoser
    Department of Clinical Cytobiology, Medical Center for Postgraduate Education, 01 813 Warszawa, Marymoncka 99, Poland
    Leuk Res 27:267-73. 2003
    ..We hypothesize that facilitation of the DNA repair in FTK-positive cells may contribute to their resistance to genotoxic treatment...
  22. ncbi request reprint Imatinib mesylate (STI571) abrogates the resistance to doxorubicin in human K562 chronic myeloid leukemia cells by inhibition of BCR/ABL kinase-mediated DNA repair
    Ireneusz Majsterek
    Department of Molecular Genetics, University of Lodz, Banacha 12 16 Street, 90 237 Lodz, Poland
    Mutat Res 603:74-82. 2006
    ..The results suggest that STI571-mediated inhibition of BCR/ABL kinase activity can affect the effectiveness of the DNA-repair pathways, which in turn may enhance drug sensitivity of leukemia cells...