Tomasz Skorski

Summary

Affiliation: Temple University
Country: USA

Publications

  1. ncbi request reprint Oncogenic tyrosine kinases and the DNA-damage response
    Tomasz Skorski
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA
    Nat Rev Cancer 2:351-60. 2002
  2. ncbi request reprint BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability
    Tomasz Skorski
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania, PA 19122, USA
    Oncogene 21:8591-604. 2002
  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. ncbi request reprint Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase
    Shu Yue Ren
    Center for Biotechnology, College of Science and Technology, Temple University, 1900 N 12th St, Philadelphia, PA 19122, USA
    Exp Hematol 33:1222-8. 2005
  6. ncbi request reprint T-antigen of the human polyomavirus JC attenuates faithful DNA repair by forcing nuclear interaction between IRS-1 and Rad51
    Joanna Trojanek
    Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Biology Life Science Building, Philadelphia, Pennsylvania 19122, USA
    J Cell Physiol 206:35-46. 2006
  7. pmc BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance
    Mateusz Koptyra
    Department of Microbiology and Immunology, School of Medicine and the Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19140, USA
    Blood 108:319-27. 2006
  8. 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
  9. 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
  10. pmc Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells
    Elisabeth Bolton-Gillespie
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA
    Blood 121:4175-83. 2013

Collaborators

Detail Information

Publications42

  1. ncbi request reprint Oncogenic tyrosine kinases and the DNA-damage response
    Tomasz Skorski
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA
    Nat Rev Cancer 2:351-60. 2002
    ..So, what are the mechanisms involved, and what is the potential for overcoming OTK-mediated resistance in the clinic?..
  2. ncbi request reprint BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability
    Tomasz Skorski
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania, PA 19122, USA
    Oncogene 21:8591-604. 2002
    ..Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect...
  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. ncbi request reprint Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase
    Shu Yue Ren
    Center for Biotechnology, College of Science and Technology, Temple University, 1900 N 12th St, Philadelphia, PA 19122, USA
    Exp Hematol 33:1222-8. 2005
    ..Therefore, we made an attempt to better characterize p85alpha-BCR/ABL interactions...
  6. ncbi request reprint T-antigen of the human polyomavirus JC attenuates faithful DNA repair by forcing nuclear interaction between IRS-1 and Rad51
    Joanna Trojanek
    Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Biology Life Science Building, Philadelphia, Pennsylvania 19122, USA
    J Cell Physiol 206:35-46. 2006
    ..Our observations define a new mechanism by which viral protein utilizes cytosolic molecule to inhibit faithful DNA repair, and suggest how polyomaviruses could compromise stability of the genome. (c) 2005 Wiley-Liss, Inc...
  7. pmc BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance
    Mateusz Koptyra
    Department of Microbiology and Immunology, School of Medicine and the Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19140, USA
    Blood 108:319-27. 2006
    ..Simultaneous administration of IM and an antioxidant exerted better antimutagenic effect than an antioxidant alone. Therefore, inhibition of ROS should diminish mutagenesis and enhance the effectiveness of IM...
  8. 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...
  9. 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...
  10. pmc Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells
    Elisabeth Bolton-Gillespie
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA
    Blood 121:4175-83. 2013
    ..Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients...
  11. 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...
  12. 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...
  13. ncbi request reprint Impaired homologous recombination DNA repair and enhanced sensitivity to DNA damage in prostate cancer cells exposed to anchorage-independence
    Jin Ying Wang
    1Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, 1900 North 12th Street, Biology Life Science Building, Philadelphia, PA 19122, USA
    Oncogene 24:3748-58. 2005
    ..This temporal attenuation of HRR may contribute to the accumulation mutations after DNA damage, and possibly the selection of new adaptations in cells, which survived genotoxic treatment...
  14. 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...
  15. 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...
  16. pmc Rac2-MRC-cIII-generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors
    Margaret Nieborowska-Skorska
    Department of Microbiology and Immunology, Temple University School of Medicine, 3400 N Broad Street, Philadelphia, PA 19140, USA
    Blood 119:4253-63. 2012
    ..We postulate that the Rac2-MRC-cIII pathway triggers ROS-mediated genomic instability in LSCs and primitive LPCs, which could be targeted to prevent the relapse and malignant progression of CML...
  17. ncbi request reprint HIV-1 Tat increases cell survival in response to cisplatin by stimulating Rad51 gene expression
    Galina Chipitsyna
    Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, 1900 North 12th Street, 015 96, Philadelphia, PA 19122, USA
    Oncogene 23:2664-71. 2004
    ..These observations ascribe a new role for Tat in host genomic integrity, perhaps by affecting the expression of genes involved in DNA repair...
  18. 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...
  19. doi request reprint Genomic instability: The cause and effect of BCR/ABL tyrosine kinase
    Tomasz Skorski
    Department of Microbiology and Immunology, School of Medicine, Temple University, MRB 548A, 3400 N Broad Street, Philadelphia, PA 19140, USA
    Curr Hematol Malig Rep 2:69-74. 2007
    ..Therefore, chronic myelogenous leukemia cells display mutator phenotype...
  20. 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...
  21. doi request reprint Chronic myeloid leukemia stem cells display alterations in expression of genes involved in oxidative phosphorylation
    Krzysztof Flis
    Department of Microbiology and Immunology, Temple University, School of Medicine, Philadelphia, PA 19140, USA
    Leuk Lymphoma 53:2474-8. 2012
    ..Therefore we postulate that abnormal expression of MRC genes may facilitate electron "leakage" to promote the production of ROS and accumulation of genomic instability in LSCs in imatinib-naive and imatinib-treated patients...
  22. pmc BCR-ABL1 kinase facilitates localization of acetylated histones 3 and 4 on DNA double-strand breaks
    Rafal Falinski
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA 19140, USA
    Leuk Res 36:241-4. 2012
    ....
  23. 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...
  24. 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...
  25. ncbi request reprint Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells
    Margaret Nieborowska-Skorska
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania 19140, USA
    Cancer Res 66:4108-16. 2006
    ..These data suggest that BCR/ABL-STAT5-Id1-MMP9 pathway may play a critical role in BCR/ABL-mediated leukemogenesis by enhancing invasiveness of leukemia cells...
  26. doi request reprint Genetic mechanisms of chronic myeloid leukemia blastic transformation
    Tomasz Skorski
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA 19140, USA
    Curr Hematol Malig Rep 7:87-93. 2012
    ..CML-BP responds poorly to treatment and is usually fatal. This review discusses the role of genomic instability leading to blastic transformation of CML and proposes some novel therapeutic approaches...
  27. pmc Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences
    Shu Yue Ren
    Molecular Carcinogenesis Section, Center for Biotechnology, College of Science and Technology, Temple University, BLSB 419, 1900 N 12th Street, Philadelphia, PA 19122, USA
    Mol Cell Biol 25:8001-8. 2005
    ..In conclusion, we have identified the domains of p85alpha responsible for the interaction with the FTK protein network and transduction of leukemogenic signaling...
  28. doi request reprint Chronic myeloid leukemia cells refractory/resistant to tyrosine kinase inhibitors are genetically unstable and may cause relapse and malignant progression to the terminal disease state
    Tomasz Skorski
    Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania 19140, USA
    Leuk Lymphoma 52:23-9. 2011
    ....
  29. 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...
  30. doi request reprint BCR/ABL, DNA damage and DNA repair: implications for new treatment concepts
    Tomasz Skorski
    Department of Microbiology and Immunology, Temple University, Philadelphia, PA 19140, USA
    Leuk Lymphoma 49:610-4. 2008
    ..Possible benefits of anti-mutagenic therapy used in pursuing the cure of BCR/ABL-positive leukemias are discussed...
  31. pmc Role of the insulin-like growth factor I/insulin receptor substrate 1 axis in Rad51 trafficking and DNA repair by homologous recombination
    Joanna Trojanek
    Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA
    Mol Cell Biol 23:7510-24. 2003
    ..These results point to a direct role of IRS-1 in HRR and suggest a novel role for the IGF-IR/IRS-1 axis in supporting the stability of the genome...
  32. ncbi request reprint Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis
    Malgorzata Nieborowska-Skorska
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
    Blood 99:4531-9. 2002
    ..These data indicate that induction of A1 and pim-1 expression may play a critical role in the BCR/ABL-dependent transformation...
  33. ncbi request reprint Chronic myelogenous leukemia molecular signature
    Michal Oskar Nowicki
    Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
    Oncogene 22:3952-63. 2003
    ..Altogether, this work provides a large body of information regarding gene expression profiles associated with CML and also represents a source of potential targets for CML therapeutics...
  34. ncbi request reprint [Uracil-DNA glycosylases]
    Dariusz Pytel
    Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, USA
    Postepy Biochem 54:362-70. 2008
    ..UNG2, MBD4 and TDG glycosylases may cooperate with mismatch repair proteins and TDG can be involved in nucleotide excision repair system...
  35. 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...
  36. ncbi request reprint Multilevel dysregulation of STAT3 activation in anaplastic lymphoma kinase-positive T/null-cell lymphoma
    Qian Zhang
    Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Immunol 168:466-74. 2002
    ..These results also suggest that activated STAT3, which is known to display oncogenic properties, as well as its regulatory molecules may represent attractive targets for novel therapies in ALK+ TCL...
  37. 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...
  38. 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...
  39. ncbi request reprint TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine
    Ewa Gloc
    Department of Molecular Genetics, University of Lodz, Poland
    Acta Biochim Pol 49:121-8. 2002
    ..Moreover, TEL/JAK2 tyrosine kinase might be involved in cellular response to DNA damage. Amifostine could promote apoptosis or lower the threshold for apoptosis induction dependent on TEL/JAK2 activation...
  40. ncbi request reprint p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to UV radiation
    Yvan Canitrot
    Genetic Instability and Cancer, Institut de Pharmacologie et Biologie Structurale, Toulouse, France
    Blood 102:2632-7. 2003
    ..In contrast, p210 BCR/ABL expression in myeloid cells facilitated NER and induced resistance to UV...
  41. ncbi request reprint The role of focal adhesion kinase in the emigration of cells from confluent cultures
    Halina Trembacz
    Department of Cell Biology, Cancer Center, M Skłodowska Curie Institute of Oncology, W K Roentgen 5, 02 781Warsaw, Poland
    Cell Mol Biol Lett 7:1047-57. 2002
    ..In conclusion, it can be postulated that FAK plays an important role in the mechanism of contact inhibition...
  42. doi request reprint STI571 reduces NER activity in BCR/ABL-expressing cells
    Tomasz Sliwinski
    Department of Molecular Genetics, University of Lodz, Banacha 12 16, 90 237 Lodz, Poland
    Mutat Res 654:162-7. 2008
    ..Therefore, STI571 may overcome the drug resistance associated with increased DNA repair in BCR/ABL-positive leukemias...