Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia
Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shorte...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Brümmendorf, Tim Henrik - 1966- [verfasserIn] Ersöz, Inci [verfasserIn] Hartmann, Ulrike [verfasserIn] Balabanov, Stefan [verfasserIn] Wolke, Holger [verfasserIn] Paschka, Peter - 1970- [verfasserIn] Lahaye, Tanja [verfasserIn] Berner, Birgit [verfasserIn] Bartolovic, Kerol [verfasserIn] Kreil, Sebastian - 1972- [verfasserIn] Berger, Ute [verfasserIn] Gschaidmeier, Harald - 1965- [verfasserIn] Bokemeyer, Carsten [verfasserIn] Hehlmann, Rüdiger - 1941- [verfasserIn] Dietz, Klaus [verfasserIn] Lansdorp, Peter M. [verfasserIn] Kanz, Lothar [verfasserIn] Hochhaus, Andreas - 1959- [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2003 |
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| Schlagwörter: |
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| Anmerkung: |
Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 |
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| Umfang: |
13 |
| Übergeordnetes Werk: |
Enthalten in: Annals of the New York Academy of Sciences - New York Academy of Sciences, Oxford [u.a.] : Wiley-Blackwell, 1877, 996(2003), 1, Seite 26-38 |
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| Übergeordnetes Werk: |
volume:996 ; year:2003 ; number:1 ; pages:26-38 ; extent:13 |
| Links: |
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| DOI / URN: |
10.1111/j.1749-6632.2003.tb03229.x |
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| Katalog-ID: |
1801719640 |
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| 245 | 1 | 0 | |a Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia |c Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus |
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| 500 | |a Elektronische Reproduktion der Druckausgabe | ||
| 500 | |a Gesehen am 13.05.2022 | ||
| 520 | |a Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. | ||
| 650 | 4 | |a chronic myeloid leukemia | |
| 650 | 4 | |a hematopoietic stem cells | |
| 650 | 4 | |a imatinib mesylate (Gleevec) | |
| 650 | 4 | |a prognosis | |
| 650 | 4 | |a reponse | |
| 650 | 4 | |a telomeres | |
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| 700 | 1 | |a Hartmann, Ulrike |e verfasserin |4 aut | |
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| 700 | 1 | |a Wolke, Holger |e verfasserin |4 aut | |
| 700 | 1 | |a Paschka, Peter |d 1970- |e verfasserin |0 (DE-588)123089840 |0 (DE-627)706156870 |0 (DE-576)293550832 |4 aut | |
| 700 | 1 | |a Lahaye, Tanja |e verfasserin |4 aut | |
| 700 | 1 | |a Berner, Birgit |e verfasserin |4 aut | |
| 700 | 1 | |a Bartolovic, Kerol |e verfasserin |4 aut | |
| 700 | 1 | |a Kreil, Sebastian |d 1972- |e verfasserin |0 (DE-588)1072240564 |0 (DE-627)827077742 |0 (DE-576)433714093 |4 aut | |
| 700 | 1 | |a Berger, Ute |e verfasserin |0 (DE-588)1255399929 |0 (DE-627)1799635341 |4 aut | |
| 700 | 1 | |a Gschaidmeier, Harald |d 1965- |e verfasserin |0 (DE-588)172811074 |0 (DE-627)697741354 |0 (DE-576)133667324 |4 aut | |
| 700 | 1 | |a Bokemeyer, Carsten |e verfasserin |4 aut | |
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| 700 | 1 | |a Dietz, Klaus |e verfasserin |4 aut | |
| 700 | 1 | |a Lansdorp, Peter M. |e verfasserin |4 aut | |
| 700 | 1 | |a Kanz, Lothar |e verfasserin |4 aut | |
| 700 | 1 | |a Hochhaus, Andreas |d 1959- |e verfasserin |0 (DE-588)1107039339 |0 (DE-627)863321976 |0 (DE-576)474976130 |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |a New York Academy of Sciences |t Annals of the New York Academy of Sciences |d Oxford [u.a.] : Wiley-Blackwell, 1877 |g 996(2003), 1, Seite 26-38 |h Online-Ressource |w (DE-627)342320122 |w (DE-600)2071584-5 |w (DE-576)098305034 |x 1749-6632 |7 nnns |
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| 856 | 4 | 0 | |u https://doi.org/10.1111/j.1749-6632.2003.tb03229.x |x Verlag |x Resolving-System |z lizenzpflichtig |3 Volltext |
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10.1111/j.1749-6632.2003.tb03229.x doi (DE-627)1801719640 (DE-599)KXP1801719640 (OCoLC)1341459895 DE-627 ger DE-627 rda eng Brümmendorf, Tim Henrik 1966- verfasserin (DE-588)115060219 (DE-627)47758148X (DE-576)289817625 aut Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus 2003 13 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. chronic myeloid leukemia hematopoietic stem cells imatinib mesylate (Gleevec) prognosis reponse telomeres Ersöz, Inci verfasserin aut Hartmann, Ulrike verfasserin aut Balabanov, Stefan verfasserin aut Wolke, Holger verfasserin aut Paschka, Peter 1970- verfasserin (DE-588)123089840 (DE-627)706156870 (DE-576)293550832 aut Lahaye, Tanja verfasserin aut Berner, Birgit verfasserin aut Bartolovic, Kerol verfasserin aut Kreil, Sebastian 1972- verfasserin (DE-588)1072240564 (DE-627)827077742 (DE-576)433714093 aut Berger, Ute verfasserin (DE-588)1255399929 (DE-627)1799635341 aut Gschaidmeier, Harald 1965- verfasserin (DE-588)172811074 (DE-627)697741354 (DE-576)133667324 aut Bokemeyer, Carsten verfasserin aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Dietz, Klaus verfasserin aut Lansdorp, Peter M. verfasserin aut Kanz, Lothar verfasserin aut Hochhaus, Andreas 1959- verfasserin (DE-588)1107039339 (DE-627)863321976 (DE-576)474976130 aut Enthalten in New York Academy of Sciences Annals of the New York Academy of Sciences Oxford [u.a.] : Wiley-Blackwell, 1877 996(2003), 1, Seite 26-38 Online-Ressource (DE-627)342320122 (DE-600)2071584-5 (DE-576)098305034 1749-6632 nnns volume:996 year:2003 number:1 pages:26-38 extent:13 https://doi.org/10.1111/j.1749-6632.2003.tb03229.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.2003.tb03229.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2897 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 996 2003 1 26-38 13 2013 01 DE-16-250 4133911741 00 --%%-- --%%-- --%%-- --%%-- l01 13-05-22 2013 01 DE-16-250 00 s hd2003 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_13 2013 01 DE-16-250 04 p (DE-627)1799509028 Paschka, Peter 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_6 2013 01 DE-16-250 05 p (DE-627)150371442X Kreil, Sebastian 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_10 2013 01 DE-16-250 06 p (DE-627)1799635562 Berger, Ute 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_11 2013 01 DE-16-250 07 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 07 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_14 2013 01 DE-16-250 08 p (DE-627)1544976704 Hochhaus, Andreas 2013 01 DE-16-250 08 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_18 |
| spelling |
10.1111/j.1749-6632.2003.tb03229.x doi (DE-627)1801719640 (DE-599)KXP1801719640 (OCoLC)1341459895 DE-627 ger DE-627 rda eng Brümmendorf, Tim Henrik 1966- verfasserin (DE-588)115060219 (DE-627)47758148X (DE-576)289817625 aut Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus 2003 13 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. chronic myeloid leukemia hematopoietic stem cells imatinib mesylate (Gleevec) prognosis reponse telomeres Ersöz, Inci verfasserin aut Hartmann, Ulrike verfasserin aut Balabanov, Stefan verfasserin aut Wolke, Holger verfasserin aut Paschka, Peter 1970- verfasserin (DE-588)123089840 (DE-627)706156870 (DE-576)293550832 aut Lahaye, Tanja verfasserin aut Berner, Birgit verfasserin aut Bartolovic, Kerol verfasserin aut Kreil, Sebastian 1972- verfasserin (DE-588)1072240564 (DE-627)827077742 (DE-576)433714093 aut Berger, Ute verfasserin (DE-588)1255399929 (DE-627)1799635341 aut Gschaidmeier, Harald 1965- verfasserin (DE-588)172811074 (DE-627)697741354 (DE-576)133667324 aut Bokemeyer, Carsten verfasserin aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Dietz, Klaus verfasserin aut Lansdorp, Peter M. verfasserin aut Kanz, Lothar verfasserin aut Hochhaus, Andreas 1959- verfasserin (DE-588)1107039339 (DE-627)863321976 (DE-576)474976130 aut Enthalten in New York Academy of Sciences Annals of the New York Academy of Sciences Oxford [u.a.] : Wiley-Blackwell, 1877 996(2003), 1, Seite 26-38 Online-Ressource (DE-627)342320122 (DE-600)2071584-5 (DE-576)098305034 1749-6632 nnns volume:996 year:2003 number:1 pages:26-38 extent:13 https://doi.org/10.1111/j.1749-6632.2003.tb03229.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.2003.tb03229.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2897 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 996 2003 1 26-38 13 2013 01 DE-16-250 4133911741 00 --%%-- --%%-- --%%-- --%%-- l01 13-05-22 2013 01 DE-16-250 00 s hd2003 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_13 2013 01 DE-16-250 04 p (DE-627)1799509028 Paschka, Peter 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_6 2013 01 DE-16-250 05 p (DE-627)150371442X Kreil, Sebastian 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_10 2013 01 DE-16-250 06 p (DE-627)1799635562 Berger, Ute 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_11 2013 01 DE-16-250 07 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 07 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_14 2013 01 DE-16-250 08 p (DE-627)1544976704 Hochhaus, Andreas 2013 01 DE-16-250 08 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_18 |
| allfields_unstemmed |
10.1111/j.1749-6632.2003.tb03229.x doi (DE-627)1801719640 (DE-599)KXP1801719640 (OCoLC)1341459895 DE-627 ger DE-627 rda eng Brümmendorf, Tim Henrik 1966- verfasserin (DE-588)115060219 (DE-627)47758148X (DE-576)289817625 aut Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus 2003 13 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. chronic myeloid leukemia hematopoietic stem cells imatinib mesylate (Gleevec) prognosis reponse telomeres Ersöz, Inci verfasserin aut Hartmann, Ulrike verfasserin aut Balabanov, Stefan verfasserin aut Wolke, Holger verfasserin aut Paschka, Peter 1970- verfasserin (DE-588)123089840 (DE-627)706156870 (DE-576)293550832 aut Lahaye, Tanja verfasserin aut Berner, Birgit verfasserin aut Bartolovic, Kerol verfasserin aut Kreil, Sebastian 1972- verfasserin (DE-588)1072240564 (DE-627)827077742 (DE-576)433714093 aut Berger, Ute verfasserin (DE-588)1255399929 (DE-627)1799635341 aut Gschaidmeier, Harald 1965- verfasserin (DE-588)172811074 (DE-627)697741354 (DE-576)133667324 aut Bokemeyer, Carsten verfasserin aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Dietz, Klaus verfasserin aut Lansdorp, Peter M. verfasserin aut Kanz, Lothar verfasserin aut Hochhaus, Andreas 1959- verfasserin (DE-588)1107039339 (DE-627)863321976 (DE-576)474976130 aut Enthalten in New York Academy of Sciences Annals of the New York Academy of Sciences Oxford [u.a.] : Wiley-Blackwell, 1877 996(2003), 1, Seite 26-38 Online-Ressource (DE-627)342320122 (DE-600)2071584-5 (DE-576)098305034 1749-6632 nnns volume:996 year:2003 number:1 pages:26-38 extent:13 https://doi.org/10.1111/j.1749-6632.2003.tb03229.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.2003.tb03229.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2897 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 996 2003 1 26-38 13 2013 01 DE-16-250 4133911741 00 --%%-- --%%-- --%%-- --%%-- l01 13-05-22 2013 01 DE-16-250 00 s hd2003 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_13 2013 01 DE-16-250 04 p (DE-627)1799509028 Paschka, Peter 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_6 2013 01 DE-16-250 05 p (DE-627)150371442X Kreil, Sebastian 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_10 2013 01 DE-16-250 06 p (DE-627)1799635562 Berger, Ute 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_11 2013 01 DE-16-250 07 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 07 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_14 2013 01 DE-16-250 08 p (DE-627)1544976704 Hochhaus, Andreas 2013 01 DE-16-250 08 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_18 |
| allfieldsGer |
10.1111/j.1749-6632.2003.tb03229.x doi (DE-627)1801719640 (DE-599)KXP1801719640 (OCoLC)1341459895 DE-627 ger DE-627 rda eng Brümmendorf, Tim Henrik 1966- verfasserin (DE-588)115060219 (DE-627)47758148X (DE-576)289817625 aut Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus 2003 13 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. chronic myeloid leukemia hematopoietic stem cells imatinib mesylate (Gleevec) prognosis reponse telomeres Ersöz, Inci verfasserin aut Hartmann, Ulrike verfasserin aut Balabanov, Stefan verfasserin aut Wolke, Holger verfasserin aut Paschka, Peter 1970- verfasserin (DE-588)123089840 (DE-627)706156870 (DE-576)293550832 aut Lahaye, Tanja verfasserin aut Berner, Birgit verfasserin aut Bartolovic, Kerol verfasserin aut Kreil, Sebastian 1972- verfasserin (DE-588)1072240564 (DE-627)827077742 (DE-576)433714093 aut Berger, Ute verfasserin (DE-588)1255399929 (DE-627)1799635341 aut Gschaidmeier, Harald 1965- verfasserin (DE-588)172811074 (DE-627)697741354 (DE-576)133667324 aut Bokemeyer, Carsten verfasserin aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Dietz, Klaus verfasserin aut Lansdorp, Peter M. verfasserin aut Kanz, Lothar verfasserin aut Hochhaus, Andreas 1959- verfasserin (DE-588)1107039339 (DE-627)863321976 (DE-576)474976130 aut Enthalten in New York Academy of Sciences Annals of the New York Academy of Sciences Oxford [u.a.] : Wiley-Blackwell, 1877 996(2003), 1, Seite 26-38 Online-Ressource (DE-627)342320122 (DE-600)2071584-5 (DE-576)098305034 1749-6632 nnns volume:996 year:2003 number:1 pages:26-38 extent:13 https://doi.org/10.1111/j.1749-6632.2003.tb03229.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.2003.tb03229.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2897 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 996 2003 1 26-38 13 2013 01 DE-16-250 4133911741 00 --%%-- --%%-- --%%-- --%%-- l01 13-05-22 2013 01 DE-16-250 00 s hd2003 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_13 2013 01 DE-16-250 04 p (DE-627)1799509028 Paschka, Peter 2013 01 DE-16-250 04 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_6 2013 01 DE-16-250 05 p (DE-627)150371442X Kreil, Sebastian 2013 01 DE-16-250 05 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_10 2013 01 DE-16-250 06 p (DE-627)1799635562 Berger, Ute 2013 01 DE-16-250 06 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_11 2013 01 DE-16-250 07 p (DE-627)1460943260 Hehlmann, Rüdiger 2013 01 DE-16-250 07 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_14 2013 01 DE-16-250 08 p (DE-627)1544976704 Hochhaus, Andreas 2013 01 DE-16-250 08 k (DE-627)1416468528 III. Medizinische Klinik 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_18 |
| allfieldsSound |
10.1111/j.1749-6632.2003.tb03229.x doi (DE-627)1801719640 (DE-599)KXP1801719640 (OCoLC)1341459895 DE-627 ger DE-627 rda eng Brümmendorf, Tim Henrik 1966- verfasserin (DE-588)115060219 (DE-627)47758148X (DE-576)289817625 aut Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus 2003 13 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. chronic myeloid leukemia hematopoietic stem cells imatinib mesylate (Gleevec) prognosis reponse telomeres Ersöz, Inci verfasserin aut Hartmann, Ulrike verfasserin aut Balabanov, Stefan verfasserin aut Wolke, Holger verfasserin aut Paschka, Peter 1970- verfasserin (DE-588)123089840 (DE-627)706156870 (DE-576)293550832 aut Lahaye, Tanja verfasserin aut Berner, Birgit verfasserin aut Bartolovic, Kerol verfasserin aut Kreil, Sebastian 1972- verfasserin (DE-588)1072240564 (DE-627)827077742 (DE-576)433714093 aut Berger, Ute verfasserin (DE-588)1255399929 (DE-627)1799635341 aut Gschaidmeier, Harald 1965- verfasserin (DE-588)172811074 (DE-627)697741354 (DE-576)133667324 aut Bokemeyer, Carsten verfasserin aut Hehlmann, Rüdiger 1941- verfasserin (DE-588)1037003489 (DE-627)751737879 (DE-576)390939463 aut Dietz, Klaus verfasserin aut Lansdorp, Peter M. verfasserin aut Kanz, Lothar verfasserin aut Hochhaus, Andreas 1959- verfasserin (DE-588)1107039339 (DE-627)863321976 (DE-576)474976130 aut Enthalten in New York Academy of Sciences Annals of the New York Academy of Sciences Oxford [u.a.] : Wiley-Blackwell, 1877 996(2003), 1, Seite 26-38 Online-Ressource (DE-627)342320122 (DE-600)2071584-5 (DE-576)098305034 1749-6632 nnns volume:996 year:2003 number:1 pages:26-38 extent:13 https://doi.org/10.1111/j.1749-6632.2003.tb03229.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.2003.tb03229.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2897 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 996 2003 1 26-38 13 2013 01 DE-16-250 4133911741 00 --%%-- --%%-- --%%-- --%%-- l01 13-05-22 2013 01 DE-16-250 00 s hd2003 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_13 2013 01 DE-16-250 04 p (DE-627)1799509028 Paschka, Peter 2013 01 DE-16-250 04 k (DE-627)1416468528 III. 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Enthalten in Annals of the New York Academy of Sciences 996(2003), 1, Seite 26-38 volume:996 year:2003 number:1 pages:26-38 extent:13 |
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Brümmendorf, Tim Henrik @@aut@@ Ersöz, Inci @@aut@@ Hartmann, Ulrike @@aut@@ Balabanov, Stefan @@aut@@ Wolke, Holger @@aut@@ Paschka, Peter @@aut@@ Lahaye, Tanja @@aut@@ Berner, Birgit @@aut@@ Bartolovic, Kerol @@aut@@ Kreil, Sebastian @@aut@@ Berger, Ute @@aut@@ Gschaidmeier, Harald @@aut@@ Bokemeyer, Carsten @@aut@@ Hehlmann, Rüdiger @@aut@@ Dietz, Klaus @@aut@@ Lansdorp, Peter M. @@aut@@ Kanz, Lothar @@aut@@ Hochhaus, Andreas @@aut@@ |
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Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. 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In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). 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|
| standort_str_mv |
--%%-- |
| standort_iln_str_mv |
2013:--%%-- DE-16-250:--%%-- |
| author |
Brümmendorf, Tim Henrik 1966- |
| spellingShingle |
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Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia |
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Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia Tim H. Brümmendorf, Inci Ersöz, Ulrike Hartmann, Stefan Balabanov, Holger Wolke, Peter Paschka, Tanja Lahaye, Birgit Berner, Kerol Bartolovic, Sebastian Kreil, Ute Berger, Harald Gschaidmeier, Carsten Bokemeyer, Rüdiger Hehlmann, Klaus Dietz, Peter M. Lansdorp, Lothar Kanz, and Andreas Hochhaus |
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normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia |
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Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia |
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Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 |
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Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 |
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Abstract: Telomeres are composed of TTAGGG repeats and associated proteins. In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML. Elektronische Reproduktion der Druckausgabe Gesehen am 13.05.2022 |
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Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia |
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In somatic cells, telomere repeats are lost with each cell division, eventually leading to genetic instability and cellular senescence. In previous studies, we described substantial and disease stage-specific telomere shortening in peripheral blood (PB) leukocytes from patients with chronic myeloid leukemia (CML). Here, we sought to determine whether age-adjusted telomere length in PB granulocytes (delta℡gran) is associated with response to treatment with the selective tyrosine kinase inhibitor imatinib. A total of 517 samples from 206 patients in chronic phase (CP), accelerated phase (AP), and blast crisis (BC) before and up to 706 days after initiation of imatinib therapy (median: 144 days) were analyzed by quantitative fluorescence in situ hybridization of interphase cells in suspension (Flow-FISH); telomere fluorescence was expressed in molecular equivalents of soluble fluorochrome units (MESF). Telomere length in samples from start of treatment up to day 144 was significantly shorter (mean ± SE; −1.5 ± 0.3 kMESF) compared to samples from patients treated for more than 144 days (−0.8 ± 0.3 kMESF, p= 0.035). In patients with repeated measurements, a significant increase in telomere length under treatment was observed. Median telomere length in major remission was found to be significantly longer compared to patients without response to treatment measured either by cytogenetics (n= 246, p < 0.05), interphase FISH (n= 204, p= 0.002), or quantitative RT-PCR (n= 371, p < 0.05). In conclusion, the increase in telomere length under treatment with imatinib reflects a shift from Ph+ to Ph− cells in the PB of patients with CML.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">chronic myeloid leukemia</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hematopoietic stem cells</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">imatinib mesylate (Gleevec)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">prognosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">reponse</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">telomeres</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ersöz, Inci</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hartmann, 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code="b">4133911741</subfield><subfield code="c">00</subfield><subfield code="f">--%%--</subfield><subfield code="d">--%%--</subfield><subfield code="e">--%%--</subfield><subfield code="j">--%%--</subfield><subfield code="y">l01</subfield><subfield code="z">13-05-22</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">00</subfield><subfield code="s">s</subfield><subfield code="a">hd2003</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">01</subfield><subfield code="s">s</subfield><subfield code="0">(DE-627)1410508463</subfield><subfield code="a">wissenschaftlicher Artikel (Zeitschrift)</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">02</subfield><subfield code="s">s</subfield><subfield code="a">per_18</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">03</subfield><subfield code="s">s</subfield><subfield code="a">s_13</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">04</subfield><subfield code="s">p</subfield><subfield code="0">(DE-627)1799509028</subfield><subfield code="a">Paschka, Peter</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">04</subfield><subfield code="s">k</subfield><subfield code="0">(DE-627)1416468528</subfield><subfield code="a">III. Medizinische Klinik</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">04</subfield><subfield code="s">s</subfield><subfield code="0">(DE-627)1410501914</subfield><subfield code="a">Verfasser</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">04</subfield><subfield code="s">s</subfield><subfield code="a">pos_6</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">05</subfield><subfield code="s">p</subfield><subfield code="0">(DE-627)150371442X</subfield><subfield code="a">Kreil, Sebastian</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">05</subfield><subfield code="s">k</subfield><subfield code="0">(DE-627)1416468528</subfield><subfield code="a">III. Medizinische Klinik</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">05</subfield><subfield code="s">s</subfield><subfield code="0">(DE-627)1410501914</subfield><subfield code="a">Verfasser</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">05</subfield><subfield code="s">s</subfield><subfield code="a">pos_10</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">06</subfield><subfield code="s">p</subfield><subfield code="0">(DE-627)1799635562</subfield><subfield code="a">Berger, Ute</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">06</subfield><subfield code="s">k</subfield><subfield code="0">(DE-627)1416468528</subfield><subfield code="a">III. Medizinische Klinik</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">06</subfield><subfield code="s">s</subfield><subfield code="0">(DE-627)1410501914</subfield><subfield code="a">Verfasser</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">06</subfield><subfield code="s">s</subfield><subfield code="a">pos_11</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">07</subfield><subfield code="s">p</subfield><subfield code="0">(DE-627)1460943260</subfield><subfield code="a">Hehlmann, Rüdiger</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">07</subfield><subfield code="s">k</subfield><subfield code="0">(DE-627)1416468528</subfield><subfield code="a">III. Medizinische Klinik</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">07</subfield><subfield code="s">s</subfield><subfield code="0">(DE-627)1410501914</subfield><subfield code="a">Verfasser</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">07</subfield><subfield code="s">s</subfield><subfield code="a">pos_14</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">08</subfield><subfield code="s">p</subfield><subfield code="0">(DE-627)1544976704</subfield><subfield code="a">Hochhaus, Andreas</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">08</subfield><subfield code="s">k</subfield><subfield code="0">(DE-627)1416468528</subfield><subfield code="a">III. Medizinische Klinik</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">08</subfield><subfield code="s">s</subfield><subfield code="0">(DE-627)1410501914</subfield><subfield code="a">Verfasser</subfield></datafield><datafield tag="982" ind1=" " ind2=" "><subfield code="2">2013</subfield><subfield code="1">01</subfield><subfield code="x">DE-16-250</subfield><subfield code="8">08</subfield><subfield code="s">s</subfield><subfield code="a">pos_18</subfield></datafield></record></collection>
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