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Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib

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Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib. / Hartmann, Ulrike; Balabanov, Stefan; Ziegler, Patrick; Fellenberg, Jörg; van der Kuip, Heiko; Duyster, Justus; Lipp, Hans-Peter; Bokemeyer, Carsten; Kanz, Lothar; Brümmendorf, Tim H.

In: EXP HEMATOL, Vol. 33, No. 5, 05.2005, p. 542-9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hartmann, U, Balabanov, S, Ziegler, P, Fellenberg, J, van der Kuip, H, Duyster, J, Lipp, H-P, Bokemeyer, C, Kanz, L & Brümmendorf, TH 2005, 'Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib', EXP HEMATOL, vol. 33, no. 5, pp. 542-9. https://doi.org/10.1016/j.exphem.2005.02.002

APA

Hartmann, U., Balabanov, S., Ziegler, P., Fellenberg, J., van der Kuip, H., Duyster, J., Lipp, H-P., Bokemeyer, C., Kanz, L., & Brümmendorf, T. H. (2005). Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib. EXP HEMATOL, 33(5), 542-9. https://doi.org/10.1016/j.exphem.2005.02.002

Vancouver

Hartmann U, Balabanov S, Ziegler P, Fellenberg J, van der Kuip H, Duyster J et al. Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib. EXP HEMATOL. 2005 May;33(5):542-9. https://doi.org/10.1016/j.exphem.2005.02.002

Bibtex

@article{2df8aca90dbb4d50b4921c8ef551cecb,
title = "Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib",
abstract = "OBJECTIVE: Imatinib mesylate is a novel tyrosine kinase inhibitor used for the treatment of Philadelphia chromosome positive (Ph+) leukemia and other malignancies. In previous studies, we found significant telomere shortening in Ph+ cells from patients with chronic myeloid leukemia (CML). Interestingly, imatinib treatment was found to lead to a normalization of previously shortened telomere length in CML patients. Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others. Such an effect could be of potential importance for telomere maintenance in Ph+ cells by facilitating clonal selection and progression of the disease to blast crisis.METHODS: We investigated the impact of imatinib on telomere length and telomerase activity of the interleukin-3 (IL-3)-dependent murine pro-B cell line BaF3 and the BCR-ABL-positive, IL-3-independent transfectant BaF3p185 in vitro.RESULTS: When BaF3 and BaF3p185 cells were treated with imatinib (the latter being rescued with IL-3), no effect on either telomerase activity or telomere length was observed. These findings can be explained by the cytoplasmatic localization of BCR-ABL found in BaF3p185 as compared to the nuclear localization of telomerase (and c-ABL).CONCLUSION: As opposed to recent reports for c-ABL, we do not see evidence for a functional interaction between BCR-ABL and hTERT in this model system arguing against imatinib-mediated upregulation of hTERT as a crucial factor for clonal selection and disease progression of CML.",
keywords = "Animals, B-Lymphocytes, Benzamides, Cell Division, Cell Line, Transformed, Culture Media, Fluorescent Antibody Technique, Fusion Proteins, bcr-abl, In Situ Hybridization, Fluorescence, Interleukin-3, Mice, Piperazines, Pyrimidines, Telomerase, Telomere",
author = "Ulrike Hartmann and Stefan Balabanov and Patrick Ziegler and J{\"o}rg Fellenberg and {van der Kuip}, Heiko and Justus Duyster and Hans-Peter Lipp and Carsten Bokemeyer and Lothar Kanz and Br{\"u}mmendorf, {Tim H}",
year = "2005",
month = may,
doi = "10.1016/j.exphem.2005.02.002",
language = "English",
volume = "33",
pages = "542--9",
journal = "EXP HEMATOL",
issn = "0301-472X",
publisher = "Elsevier Inc.",
number = "5",

}

RIS

TY - JOUR

T1 - Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib

AU - Hartmann, Ulrike

AU - Balabanov, Stefan

AU - Ziegler, Patrick

AU - Fellenberg, Jörg

AU - van der Kuip, Heiko

AU - Duyster, Justus

AU - Lipp, Hans-Peter

AU - Bokemeyer, Carsten

AU - Kanz, Lothar

AU - Brümmendorf, Tim H

PY - 2005/5

Y1 - 2005/5

N2 - OBJECTIVE: Imatinib mesylate is a novel tyrosine kinase inhibitor used for the treatment of Philadelphia chromosome positive (Ph+) leukemia and other malignancies. In previous studies, we found significant telomere shortening in Ph+ cells from patients with chronic myeloid leukemia (CML). Interestingly, imatinib treatment was found to lead to a normalization of previously shortened telomere length in CML patients. Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others. Such an effect could be of potential importance for telomere maintenance in Ph+ cells by facilitating clonal selection and progression of the disease to blast crisis.METHODS: We investigated the impact of imatinib on telomere length and telomerase activity of the interleukin-3 (IL-3)-dependent murine pro-B cell line BaF3 and the BCR-ABL-positive, IL-3-independent transfectant BaF3p185 in vitro.RESULTS: When BaF3 and BaF3p185 cells were treated with imatinib (the latter being rescued with IL-3), no effect on either telomerase activity or telomere length was observed. These findings can be explained by the cytoplasmatic localization of BCR-ABL found in BaF3p185 as compared to the nuclear localization of telomerase (and c-ABL).CONCLUSION: As opposed to recent reports for c-ABL, we do not see evidence for a functional interaction between BCR-ABL and hTERT in this model system arguing against imatinib-mediated upregulation of hTERT as a crucial factor for clonal selection and disease progression of CML.

AB - OBJECTIVE: Imatinib mesylate is a novel tyrosine kinase inhibitor used for the treatment of Philadelphia chromosome positive (Ph+) leukemia and other malignancies. In previous studies, we found significant telomere shortening in Ph+ cells from patients with chronic myeloid leukemia (CML). Interestingly, imatinib treatment was found to lead to a normalization of previously shortened telomere length in CML patients. Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others. Such an effect could be of potential importance for telomere maintenance in Ph+ cells by facilitating clonal selection and progression of the disease to blast crisis.METHODS: We investigated the impact of imatinib on telomere length and telomerase activity of the interleukin-3 (IL-3)-dependent murine pro-B cell line BaF3 and the BCR-ABL-positive, IL-3-independent transfectant BaF3p185 in vitro.RESULTS: When BaF3 and BaF3p185 cells were treated with imatinib (the latter being rescued with IL-3), no effect on either telomerase activity or telomere length was observed. These findings can be explained by the cytoplasmatic localization of BCR-ABL found in BaF3p185 as compared to the nuclear localization of telomerase (and c-ABL).CONCLUSION: As opposed to recent reports for c-ABL, we do not see evidence for a functional interaction between BCR-ABL and hTERT in this model system arguing against imatinib-mediated upregulation of hTERT as a crucial factor for clonal selection and disease progression of CML.

KW - Animals

KW - B-Lymphocytes

KW - Benzamides

KW - Cell Division

KW - Cell Line, Transformed

KW - Culture Media

KW - Fluorescent Antibody Technique

KW - Fusion Proteins, bcr-abl

KW - In Situ Hybridization, Fluorescence

KW - Interleukin-3

KW - Mice

KW - Piperazines

KW - Pyrimidines

KW - Telomerase

KW - Telomere

U2 - 10.1016/j.exphem.2005.02.002

DO - 10.1016/j.exphem.2005.02.002

M3 - SCORING: Journal article

C2 - 15850831

VL - 33

SP - 542

EP - 549

JO - EXP HEMATOL

JF - EXP HEMATOL

SN - 0301-472X

IS - 5

ER -