Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma
Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging fr...
Ausführliche Beschreibung
Autor*in: |
Micale, Mark A. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2017 |
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Schlagwörter: |
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Anmerkung: |
© Springer-Verlag GmbH Germany, part of Springer Nature 2017 |
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Übergeordnetes Werk: |
Enthalten in: Journal of hematopathology - Berlin : Springer, 2008, 10(2017), 3-4 vom: 21. Nov., Seite 133-140 |
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Übergeordnetes Werk: |
volume:10 ; year:2017 ; number:3-4 ; day:21 ; month:11 ; pages:133-140 |
Links: |
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DOI / URN: |
10.1007/s12308-017-0309-8 |
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Katalog-ID: |
SPR024893056 |
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520 | |a Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. | ||
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650 | 4 | |a Plasmablastic myeloma |7 (dpeaa)DE-He213 | |
650 | 4 | |a Clonal evolution |7 (dpeaa)DE-He213 | |
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700 | 1 | |a Williams, Jacqueline |4 aut | |
700 | 1 | |a Burroughs, Michael |4 aut | |
700 | 1 | |a Huang, James Z. |4 aut | |
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10.1007/s12308-017-0309-8 doi (DE-627)SPR024893056 (SPR)s12308-017-0309-8-e DE-627 ger DE-627 rakwb eng Micale, Mark A. verfasserin (orcid)0000-0001-5143-4712 aut Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2017 Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. Plasma cell myeloma (dpeaa)DE-He213 Plasmablastic myeloma (dpeaa)DE-He213 Clonal evolution (dpeaa)DE-He213 Clonal heterogeneity (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Powers, Stephanie aut Embrey, Bedford aut Williams, Jacqueline aut Burroughs, Michael aut Huang, James Z. aut Enthalten in Journal of hematopathology Berlin : Springer, 2008 10(2017), 3-4 vom: 21. Nov., Seite 133-140 (DE-627)572421230 (DE-600)2438687-X 1865-5785 nnns volume:10 year:2017 number:3-4 day:21 month:11 pages:133-140 https://dx.doi.org/10.1007/s12308-017-0309-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2017 3-4 21 11 133-140 |
spelling |
10.1007/s12308-017-0309-8 doi (DE-627)SPR024893056 (SPR)s12308-017-0309-8-e DE-627 ger DE-627 rakwb eng Micale, Mark A. verfasserin (orcid)0000-0001-5143-4712 aut Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2017 Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. Plasma cell myeloma (dpeaa)DE-He213 Plasmablastic myeloma (dpeaa)DE-He213 Clonal evolution (dpeaa)DE-He213 Clonal heterogeneity (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Powers, Stephanie aut Embrey, Bedford aut Williams, Jacqueline aut Burroughs, Michael aut Huang, James Z. aut Enthalten in Journal of hematopathology Berlin : Springer, 2008 10(2017), 3-4 vom: 21. Nov., Seite 133-140 (DE-627)572421230 (DE-600)2438687-X 1865-5785 nnns volume:10 year:2017 number:3-4 day:21 month:11 pages:133-140 https://dx.doi.org/10.1007/s12308-017-0309-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2017 3-4 21 11 133-140 |
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10.1007/s12308-017-0309-8 doi (DE-627)SPR024893056 (SPR)s12308-017-0309-8-e DE-627 ger DE-627 rakwb eng Micale, Mark A. verfasserin (orcid)0000-0001-5143-4712 aut Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2017 Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. Plasma cell myeloma (dpeaa)DE-He213 Plasmablastic myeloma (dpeaa)DE-He213 Clonal evolution (dpeaa)DE-He213 Clonal heterogeneity (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Powers, Stephanie aut Embrey, Bedford aut Williams, Jacqueline aut Burroughs, Michael aut Huang, James Z. aut Enthalten in Journal of hematopathology Berlin : Springer, 2008 10(2017), 3-4 vom: 21. Nov., Seite 133-140 (DE-627)572421230 (DE-600)2438687-X 1865-5785 nnns volume:10 year:2017 number:3-4 day:21 month:11 pages:133-140 https://dx.doi.org/10.1007/s12308-017-0309-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2017 3-4 21 11 133-140 |
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10.1007/s12308-017-0309-8 doi (DE-627)SPR024893056 (SPR)s12308-017-0309-8-e DE-627 ger DE-627 rakwb eng Micale, Mark A. verfasserin (orcid)0000-0001-5143-4712 aut Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2017 Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. Plasma cell myeloma (dpeaa)DE-He213 Plasmablastic myeloma (dpeaa)DE-He213 Clonal evolution (dpeaa)DE-He213 Clonal heterogeneity (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Powers, Stephanie aut Embrey, Bedford aut Williams, Jacqueline aut Burroughs, Michael aut Huang, James Z. aut Enthalten in Journal of hematopathology Berlin : Springer, 2008 10(2017), 3-4 vom: 21. Nov., Seite 133-140 (DE-627)572421230 (DE-600)2438687-X 1865-5785 nnns volume:10 year:2017 number:3-4 day:21 month:11 pages:133-140 https://dx.doi.org/10.1007/s12308-017-0309-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2017 3-4 21 11 133-140 |
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10.1007/s12308-017-0309-8 doi (DE-627)SPR024893056 (SPR)s12308-017-0309-8-e DE-627 ger DE-627 rakwb eng Micale, Mark A. verfasserin (orcid)0000-0001-5143-4712 aut Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2017 Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. Plasma cell myeloma (dpeaa)DE-He213 Plasmablastic myeloma (dpeaa)DE-He213 Clonal evolution (dpeaa)DE-He213 Clonal heterogeneity (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Powers, Stephanie aut Embrey, Bedford aut Williams, Jacqueline aut Burroughs, Michael aut Huang, James Z. aut Enthalten in Journal of hematopathology Berlin : Springer, 2008 10(2017), 3-4 vom: 21. Nov., Seite 133-140 (DE-627)572421230 (DE-600)2438687-X 1865-5785 nnns volume:10 year:2017 number:3-4 day:21 month:11 pages:133-140 https://dx.doi.org/10.1007/s12308-017-0309-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2017 3-4 21 11 133-140 |
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Micale, Mark A. @@aut@@ Powers, Stephanie @@aut@@ Embrey, Bedford @@aut@@ Williams, Jacqueline @@aut@@ Burroughs, Michael @@aut@@ Huang, James Z. @@aut@@ |
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Micale, Mark A. |
spellingShingle |
Micale, Mark A. misc Plasma cell myeloma misc Plasmablastic myeloma misc Clonal evolution misc Clonal heterogeneity misc SNP array Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma |
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Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma Plasma cell myeloma (dpeaa)DE-He213 Plasmablastic myeloma (dpeaa)DE-He213 Clonal evolution (dpeaa)DE-He213 Clonal heterogeneity (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 |
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Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma |
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significant cytogenomic evolution identified by snp chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma |
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Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma |
abstract |
Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. © Springer-Verlag GmbH Germany, part of Springer Nature 2017 |
abstractGer |
Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. © Springer-Verlag GmbH Germany, part of Springer Nature 2017 |
abstract_unstemmed |
Abstract Plasma cell myeloma (PCM) is a hematological malignancy involving clonal proliferation of plasma cells in bone marrow. It is the third most common hematolymphoid malignancy in the USA and primarily affects elderly people with a median onset age of 69 years and a survival duration ranging from a few months to more than 10 years. This variation is due largely to the fact that PCM is a genetically complex and heterogeneous disease. The tumor cells demonstrate a wide range of morphological features, from mature and recognizable plasma cells to pleomorphic forms. In a subset of cases, however, the tumor cells demonstrate plasmablastic morphology which predicts a poor prognosis. We present a patient with an initial diagnosis of plasma cell myeloma with typical morphology and a hyperdiploid karyotype predictive of a favorable outcome. The patient’s disease was unresponsive to chemotherapy and evolved over the course of 43 months into a myeloma with plasmablastic features characterized by a highly complex abnormal karyotype demonstrating previously unidentified poor cytogenetic markers including CKS1B gene duplication and p53 gene deletion by fluorescence in situ hybridization (FISH). Post-mortem evaluation by single nucleotide polymorphism (SNP array) chromosome microarray analysis revealed additional structural abnormalities in the diagnostic specimen as well as significant genomic evolution in the plasmablastic myeloma. © Springer-Verlag GmbH Germany, part of Springer Nature 2017 |
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Significant cytogenomic evolution identified by SNP chromosome microarray analysis accompanies plasmablastic transformation of a hyperdiploid plasma cell myeloma |
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https://dx.doi.org/10.1007/s12308-017-0309-8 |
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Powers, Stephanie Embrey, Bedford Williams, Jacqueline Burroughs, Michael Huang, James Z. |
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|
score |
7.401017 |