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Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells.

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Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells. / Brassat, Ute; Balabanov, Stefan; Bali, Daniel; Dierlamm, Judith; Balabanov, Melanie; Hartmann, Ulrike; Sirma, Hüseyin; Günes, Cagatay; Wege, Henning; Fehse, Boris; Gontarewicz, Artur; Dikomey, Ekkehard; Borgmann, Kerstin; Brümmendorf, Tim.

In: EXP HEMATOL, Vol. 39, No. 1, 1, 2011, p. 62-66.

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

Harvard

Brassat, U, Balabanov, S, Bali, D, Dierlamm, J, Balabanov, M, Hartmann, U, Sirma, H, Günes, C, Wege, H, Fehse, B, Gontarewicz, A, Dikomey, E, Borgmann, K & Brümmendorf, T 2011, 'Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells.', EXP HEMATOL, vol. 39, no. 1, 1, pp. 62-66. <http://www.ncbi.nlm.nih.gov/pubmed/20940029?dopt=Citation>

APA

Brassat, U., Balabanov, S., Bali, D., Dierlamm, J., Balabanov, M., Hartmann, U., Sirma, H., Günes, C., Wege, H., Fehse, B., Gontarewicz, A., Dikomey, E., Borgmann, K., & Brümmendorf, T. (2011). Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells. EXP HEMATOL, 39(1), 62-66. [1]. http://www.ncbi.nlm.nih.gov/pubmed/20940029?dopt=Citation

Vancouver

Brassat U, Balabanov S, Bali D, Dierlamm J, Balabanov M, Hartmann U et al. Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells. EXP HEMATOL. 2011;39(1):62-66. 1.

Bibtex

@article{fbb291b4e89e45c5abaf30e9286ce3f9,
title = "Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells.",
abstract = "In chronic myeloid leukemia (CML), increased cellular turnover of hematopoietic cells driven by the oncogene BCR-ABL leads to accelerated telomere shortening despite increased telomerase activity. It has been postulated that shortened telomeres, particularly in the context of increased telomerase activity, might facilitate accumulation of genetic aberrations and, consequently, disease progression from chronic phase to accelerated phase and blast crisis. Therefore, inhibition of telomerase might be a promising approach in CML therapy.",
keywords = "Humans, inhibitors, Apoptosis, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Blotting, Western, Genes, abl, Genomic Instability, K562 Cells, Leukemia, Myelogenous, Chronic, BCR-ABL Positive enzymology, Telomerase antagonists, Telomere, Tumor Suppressor Protein p53 physiology, Humans, inhibitors, Apoptosis, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Blotting, Western, Genes, abl, Genomic Instability, K562 Cells, Leukemia, Myelogenous, Chronic, BCR-ABL Positive enzymology, Telomerase antagonists, Telomere, Tumor Suppressor Protein p53 physiology",
author = "Ute Brassat and Stefan Balabanov and Daniel Bali and Judith Dierlamm and Melanie Balabanov and Ulrike Hartmann and H{\"u}seyin Sirma and Cagatay G{\"u}nes and Henning Wege and Boris Fehse and Artur Gontarewicz and Ekkehard Dikomey and Kerstin Borgmann and Tim Br{\"u}mmendorf",
year = "2011",
language = "English",
volume = "39",
pages = "62--66",
journal = "EXP HEMATOL",
issn = "0301-472X",
publisher = "Elsevier Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Functional p53 is required for effective execution of telomerase inhibition in BCR-ABL-positive CML cells.

AU - Brassat, Ute

AU - Balabanov, Stefan

AU - Bali, Daniel

AU - Dierlamm, Judith

AU - Balabanov, Melanie

AU - Hartmann, Ulrike

AU - Sirma, Hüseyin

AU - Günes, Cagatay

AU - Wege, Henning

AU - Fehse, Boris

AU - Gontarewicz, Artur

AU - Dikomey, Ekkehard

AU - Borgmann, Kerstin

AU - Brümmendorf, Tim

PY - 2011

Y1 - 2011

N2 - In chronic myeloid leukemia (CML), increased cellular turnover of hematopoietic cells driven by the oncogene BCR-ABL leads to accelerated telomere shortening despite increased telomerase activity. It has been postulated that shortened telomeres, particularly in the context of increased telomerase activity, might facilitate accumulation of genetic aberrations and, consequently, disease progression from chronic phase to accelerated phase and blast crisis. Therefore, inhibition of telomerase might be a promising approach in CML therapy.

AB - In chronic myeloid leukemia (CML), increased cellular turnover of hematopoietic cells driven by the oncogene BCR-ABL leads to accelerated telomere shortening despite increased telomerase activity. It has been postulated that shortened telomeres, particularly in the context of increased telomerase activity, might facilitate accumulation of genetic aberrations and, consequently, disease progression from chronic phase to accelerated phase and blast crisis. Therefore, inhibition of telomerase might be a promising approach in CML therapy.

KW - Humans

KW - inhibitors

KW - Apoptosis

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Oligonucleotide Array Sequence Analysis

KW - Blotting, Western

KW - Genes, abl

KW - Genomic Instability

KW - K562 Cells

KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive enzymology

KW - Telomerase antagonists

KW - Telomere

KW - Tumor Suppressor Protein p53 physiology

KW - Humans

KW - inhibitors

KW - Apoptosis

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Oligonucleotide Array Sequence Analysis

KW - Blotting, Western

KW - Genes, abl

KW - Genomic Instability

KW - K562 Cells

KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive enzymology

KW - Telomerase antagonists

KW - Telomere

KW - Tumor Suppressor Protein p53 physiology

M3 - SCORING: Journal article

VL - 39

SP - 62

EP - 66

JO - EXP HEMATOL

JF - EXP HEMATOL

SN - 0301-472X

IS - 1

M1 - 1

ER -