A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia
Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 d...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Dutcher, Janice P. [verfasserIn] Morris, Evelyn L. [verfasserIn] Gaynor, Bruce [verfasserIn] Paietta, Elisabeth [verfasserIn] Wiernik, Peter H. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Medical oncology - New York, NY : Springer, 1984, 27(2009), 3 vom: 21. Aug., Seite 728-735 |
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| Übergeordnetes Werk: |
volume:27 ; year:2009 ; number:3 ; day:21 ; month:08 ; pages:728-735 |
| Links: |
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| DOI / URN: |
10.1007/s12032-009-9276-y |
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| Katalog-ID: |
SPR023868635 |
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| 100 | 1 | |a Dutcher, Janice P. |e verfasserin |4 aut | |
| 245 | 1 | 2 | |a A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia |
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| 520 | |a Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. | ||
| 650 | 4 | |a Carboplatin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mitoxantrone |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a CML |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Blast crisis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Chronic myeloid leukemia-blast crisis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Morris, Evelyn L. |e verfasserin |4 aut | |
| 700 | 1 | |a Gaynor, Bruce |e verfasserin |4 aut | |
| 700 | 1 | |a Paietta, Elisabeth |e verfasserin |4 aut | |
| 700 | 1 | |a Wiernik, Peter H. |e verfasserin |4 aut | |
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| 773 | 1 | 8 | |g volume:27 |g year:2009 |g number:3 |g day:21 |g month:08 |g pages:728-735 |
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10.1007/s12032-009-9276-y doi (DE-627)SPR023868635 (SPR)s12032-009-9276-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Dutcher, Janice P. verfasserin aut A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. Carboplatin (dpeaa)DE-He213 Mitoxantrone (dpeaa)DE-He213 CML (dpeaa)DE-He213 Blast crisis (dpeaa)DE-He213 Chronic myeloid leukemia-blast crisis (dpeaa)DE-He213 Morris, Evelyn L. verfasserin aut Gaynor, Bruce verfasserin aut Paietta, Elisabeth verfasserin aut Wiernik, Peter H. verfasserin aut Enthalten in Medical oncology New York, NY : Springer, 1984 27(2009), 3 vom: 21. Aug., Seite 728-735 (DE-627)320468240 (DE-600)2008172-8 1559-131X nnns volume:27 year:2009 number:3 day:21 month:08 pages:728-735 https://dx.doi.org/10.1007/s12032-009-9276-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4393 GBV_ILN_4700 44.81 ASE AR 27 2009 3 21 08 728-735 |
| spelling |
10.1007/s12032-009-9276-y doi (DE-627)SPR023868635 (SPR)s12032-009-9276-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Dutcher, Janice P. verfasserin aut A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. Carboplatin (dpeaa)DE-He213 Mitoxantrone (dpeaa)DE-He213 CML (dpeaa)DE-He213 Blast crisis (dpeaa)DE-He213 Chronic myeloid leukemia-blast crisis (dpeaa)DE-He213 Morris, Evelyn L. verfasserin aut Gaynor, Bruce verfasserin aut Paietta, Elisabeth verfasserin aut Wiernik, Peter H. verfasserin aut Enthalten in Medical oncology New York, NY : Springer, 1984 27(2009), 3 vom: 21. Aug., Seite 728-735 (DE-627)320468240 (DE-600)2008172-8 1559-131X nnns volume:27 year:2009 number:3 day:21 month:08 pages:728-735 https://dx.doi.org/10.1007/s12032-009-9276-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4393 GBV_ILN_4700 44.81 ASE AR 27 2009 3 21 08 728-735 |
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10.1007/s12032-009-9276-y doi (DE-627)SPR023868635 (SPR)s12032-009-9276-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Dutcher, Janice P. verfasserin aut A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. Carboplatin (dpeaa)DE-He213 Mitoxantrone (dpeaa)DE-He213 CML (dpeaa)DE-He213 Blast crisis (dpeaa)DE-He213 Chronic myeloid leukemia-blast crisis (dpeaa)DE-He213 Morris, Evelyn L. verfasserin aut Gaynor, Bruce verfasserin aut Paietta, Elisabeth verfasserin aut Wiernik, Peter H. verfasserin aut Enthalten in Medical oncology New York, NY : Springer, 1984 27(2009), 3 vom: 21. Aug., Seite 728-735 (DE-627)320468240 (DE-600)2008172-8 1559-131X nnns volume:27 year:2009 number:3 day:21 month:08 pages:728-735 https://dx.doi.org/10.1007/s12032-009-9276-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4393 GBV_ILN_4700 44.81 ASE AR 27 2009 3 21 08 728-735 |
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10.1007/s12032-009-9276-y doi (DE-627)SPR023868635 (SPR)s12032-009-9276-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Dutcher, Janice P. verfasserin aut A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. Carboplatin (dpeaa)DE-He213 Mitoxantrone (dpeaa)DE-He213 CML (dpeaa)DE-He213 Blast crisis (dpeaa)DE-He213 Chronic myeloid leukemia-blast crisis (dpeaa)DE-He213 Morris, Evelyn L. verfasserin aut Gaynor, Bruce verfasserin aut Paietta, Elisabeth verfasserin aut Wiernik, Peter H. verfasserin aut Enthalten in Medical oncology New York, NY : Springer, 1984 27(2009), 3 vom: 21. Aug., Seite 728-735 (DE-627)320468240 (DE-600)2008172-8 1559-131X nnns volume:27 year:2009 number:3 day:21 month:08 pages:728-735 https://dx.doi.org/10.1007/s12032-009-9276-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4393 GBV_ILN_4700 44.81 ASE AR 27 2009 3 21 08 728-735 |
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10.1007/s12032-009-9276-y doi (DE-627)SPR023868635 (SPR)s12032-009-9276-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Dutcher, Janice P. verfasserin aut A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. Carboplatin (dpeaa)DE-He213 Mitoxantrone (dpeaa)DE-He213 CML (dpeaa)DE-He213 Blast crisis (dpeaa)DE-He213 Chronic myeloid leukemia-blast crisis (dpeaa)DE-He213 Morris, Evelyn L. verfasserin aut Gaynor, Bruce verfasserin aut Paietta, Elisabeth verfasserin aut Wiernik, Peter H. verfasserin aut Enthalten in Medical oncology New York, NY : Springer, 1984 27(2009), 3 vom: 21. Aug., Seite 728-735 (DE-627)320468240 (DE-600)2008172-8 1559-131X nnns volume:27 year:2009 number:3 day:21 month:08 pages:728-735 https://dx.doi.org/10.1007/s12032-009-9276-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4393 GBV_ILN_4700 44.81 ASE AR 27 2009 3 21 08 728-735 |
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Enthalten in Medical oncology 27(2009), 3 vom: 21. Aug., Seite 728-735 volume:27 year:2009 number:3 day:21 month:08 pages:728-735 |
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Enthalten in Medical oncology 27(2009), 3 vom: 21. Aug., Seite 728-735 volume:27 year:2009 number:3 day:21 month:08 pages:728-735 |
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Carboplatin Mitoxantrone CML Blast crisis Chronic myeloid leukemia-blast crisis |
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Dutcher, Janice P. @@aut@@ Morris, Evelyn L. @@aut@@ Gaynor, Bruce @@aut@@ Paietta, Elisabeth @@aut@@ Wiernik, Peter H. @@aut@@ |
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2009-08-21T00:00:00Z |
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Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Carboplatin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mitoxantrone</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CML</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Blast crisis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chronic myeloid leukemia-blast crisis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Morris, Evelyn L.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gaynor, Bruce</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Paietta, Elisabeth</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wiernik, Peter H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Medical oncology</subfield><subfield code="d">New York, NY : Springer, 1984</subfield><subfield code="g">27(2009), 3 vom: 21. 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Dutcher, Janice P. |
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Dutcher, Janice P. ddc 610 bkl 44.81 misc Carboplatin misc Mitoxantrone misc CML misc Blast crisis misc Chronic myeloid leukemia-blast crisis A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia |
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610 ASE 44.81 bkl A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia Carboplatin (dpeaa)DE-He213 Mitoxantrone (dpeaa)DE-He213 CML (dpeaa)DE-He213 Blast crisis (dpeaa)DE-He213 Chronic myeloid leukemia-blast crisis (dpeaa)DE-He213 |
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ddc 610 bkl 44.81 misc Carboplatin misc Mitoxantrone misc CML misc Blast crisis misc Chronic myeloid leukemia-blast crisis |
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pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia |
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A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia |
| abstract |
Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. |
| abstractGer |
Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. |
| abstract_unstemmed |
Abstract The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated. Between 1990 and 1996, 20 patients (11 males and nine females, median age of 49 years [range 30–75 years]) were treated with carboplatin, 250 mg/$ m^{2} $/day × 5 days as an infusion and mitoxantrone, 10 mg/$ m^{2} $/day × 3 days, IV bolus. Median time from diagnosis of CML to BC was 4.25 years (range 0–11 years). CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one. All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities. Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-α (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients). Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months). Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months. Seven patients died too early to evaluate (TETE): three died pancytopenic in <30 days from initiation of chemotherapy, two patients had pancytopenia for >30 days but had only blasts in their day 30 bone marrow, and two patients were pancytopenic >30 days but demonstrated trilineage marrow regeneration. Three of eight responders survived ≥1 year. Toxicity was primarily hematologic. The objective response rate was 61% (8/13) among those who did not die TETE and 40% among all treated patients. Carboplatin plus mitoxantrone are highly active in CMLBC, with marrow aplasia as the dose-limiting toxicity, and these agents deserve further study in CMLBC, perhaps in combination with tyrosine kinase inhibitors. |
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| score |
7.3994074 |