Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient
Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has bee...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kawashima-Goto, Sachiko [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014 |
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| Schlagwörter: |
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| Anmerkung: |
© The Japanese Society of Hematology 2014 |
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| Übergeordnetes Werk: |
Enthalten in: International journal of hematology - Tokyo [u.a.] : Springer, 1995, 101(2014), 4 vom: 28. Nov., Seite 411-416 |
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| Übergeordnetes Werk: |
volume:101 ; year:2014 ; number:4 ; day:28 ; month:11 ; pages:411-416 |
| Links: |
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| DOI / URN: |
10.1007/s12185-014-1711-y |
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| Katalog-ID: |
SPR025117866 |
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| 100 | 1 | |a Kawashima-Goto, Sachiko |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient |
| 264 | 1 | |c 2014 | |
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| 520 | |a Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. | ||
| 650 | 4 | |a ETP-ALL |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a JAK3 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Acquired UPD |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a SNP array |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Whole-exome sequencing |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Imamura, Toshihiko |4 aut | |
| 700 | 1 | |a Seki, Masafumi |4 aut | |
| 700 | 1 | |a Kato, Motohiro |4 aut | |
| 700 | 1 | |a Yoshida, Kenichi |4 aut | |
| 700 | 1 | |a Sugimoto, Atsuya |4 aut | |
| 700 | 1 | |a Kaneda, Daisuke |4 aut | |
| 700 | 1 | |a Fujiki, Atsushi |4 aut | |
| 700 | 1 | |a Miyachi, Mitsuru |4 aut | |
| 700 | 1 | |a Nakatani, Takuya |4 aut | |
| 700 | 1 | |a Osone, Shinya |4 aut | |
| 700 | 1 | |a Ishida, Hiroyuki |4 aut | |
| 700 | 1 | |a Taki, Tomohiko |4 aut | |
| 700 | 1 | |a Takita, Junko |4 aut | |
| 700 | 1 | |a Shiraishi, Yuichi |4 aut | |
| 700 | 1 | |a Chiba, Kenichi |4 aut | |
| 700 | 1 | |a Tanaka, Hiroko |4 aut | |
| 700 | 1 | |a Miyano, Satoru |4 aut | |
| 700 | 1 | |a Ogawa, Seishi |4 aut | |
| 700 | 1 | |a Hosoi, Hajime |4 aut | |
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10.1007/s12185-014-1711-y doi (DE-627)SPR025117866 (SPR)s12185-014-1711-y-e DE-627 ger DE-627 rakwb eng Kawashima-Goto, Sachiko verfasserin aut Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. ETP-ALL (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Acquired UPD (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Whole-exome sequencing (dpeaa)DE-He213 Imamura, Toshihiko aut Seki, Masafumi aut Kato, Motohiro aut Yoshida, Kenichi aut Sugimoto, Atsuya aut Kaneda, Daisuke aut Fujiki, Atsushi aut Miyachi, Mitsuru aut Nakatani, Takuya aut Osone, Shinya aut Ishida, Hiroyuki aut Taki, Tomohiko aut Takita, Junko aut Shiraishi, Yuichi aut Chiba, Kenichi aut Tanaka, Hiroko aut Miyano, Satoru aut Ogawa, Seishi aut Hosoi, Hajime aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 101(2014), 4 vom: 28. Nov., Seite 411-416 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:101 year:2014 number:4 day:28 month:11 pages:411-416 https://dx.doi.org/10.1007/s12185-014-1711-y 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 101 2014 4 28 11 411-416 |
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10.1007/s12185-014-1711-y doi (DE-627)SPR025117866 (SPR)s12185-014-1711-y-e DE-627 ger DE-627 rakwb eng Kawashima-Goto, Sachiko verfasserin aut Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. ETP-ALL (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Acquired UPD (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Whole-exome sequencing (dpeaa)DE-He213 Imamura, Toshihiko aut Seki, Masafumi aut Kato, Motohiro aut Yoshida, Kenichi aut Sugimoto, Atsuya aut Kaneda, Daisuke aut Fujiki, Atsushi aut Miyachi, Mitsuru aut Nakatani, Takuya aut Osone, Shinya aut Ishida, Hiroyuki aut Taki, Tomohiko aut Takita, Junko aut Shiraishi, Yuichi aut Chiba, Kenichi aut Tanaka, Hiroko aut Miyano, Satoru aut Ogawa, Seishi aut Hosoi, Hajime aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 101(2014), 4 vom: 28. Nov., Seite 411-416 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:101 year:2014 number:4 day:28 month:11 pages:411-416 https://dx.doi.org/10.1007/s12185-014-1711-y 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 101 2014 4 28 11 411-416 |
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10.1007/s12185-014-1711-y doi (DE-627)SPR025117866 (SPR)s12185-014-1711-y-e DE-627 ger DE-627 rakwb eng Kawashima-Goto, Sachiko verfasserin aut Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. ETP-ALL (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Acquired UPD (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Whole-exome sequencing (dpeaa)DE-He213 Imamura, Toshihiko aut Seki, Masafumi aut Kato, Motohiro aut Yoshida, Kenichi aut Sugimoto, Atsuya aut Kaneda, Daisuke aut Fujiki, Atsushi aut Miyachi, Mitsuru aut Nakatani, Takuya aut Osone, Shinya aut Ishida, Hiroyuki aut Taki, Tomohiko aut Takita, Junko aut Shiraishi, Yuichi aut Chiba, Kenichi aut Tanaka, Hiroko aut Miyano, Satoru aut Ogawa, Seishi aut Hosoi, Hajime aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 101(2014), 4 vom: 28. Nov., Seite 411-416 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:101 year:2014 number:4 day:28 month:11 pages:411-416 https://dx.doi.org/10.1007/s12185-014-1711-y 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 101 2014 4 28 11 411-416 |
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10.1007/s12185-014-1711-y doi (DE-627)SPR025117866 (SPR)s12185-014-1711-y-e DE-627 ger DE-627 rakwb eng Kawashima-Goto, Sachiko verfasserin aut Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. ETP-ALL (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Acquired UPD (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Whole-exome sequencing (dpeaa)DE-He213 Imamura, Toshihiko aut Seki, Masafumi aut Kato, Motohiro aut Yoshida, Kenichi aut Sugimoto, Atsuya aut Kaneda, Daisuke aut Fujiki, Atsushi aut Miyachi, Mitsuru aut Nakatani, Takuya aut Osone, Shinya aut Ishida, Hiroyuki aut Taki, Tomohiko aut Takita, Junko aut Shiraishi, Yuichi aut Chiba, Kenichi aut Tanaka, Hiroko aut Miyano, Satoru aut Ogawa, Seishi aut Hosoi, Hajime aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 101(2014), 4 vom: 28. Nov., Seite 411-416 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:101 year:2014 number:4 day:28 month:11 pages:411-416 https://dx.doi.org/10.1007/s12185-014-1711-y 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 101 2014 4 28 11 411-416 |
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10.1007/s12185-014-1711-y doi (DE-627)SPR025117866 (SPR)s12185-014-1711-y-e DE-627 ger DE-627 rakwb eng Kawashima-Goto, Sachiko verfasserin aut Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. ETP-ALL (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Acquired UPD (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Whole-exome sequencing (dpeaa)DE-He213 Imamura, Toshihiko aut Seki, Masafumi aut Kato, Motohiro aut Yoshida, Kenichi aut Sugimoto, Atsuya aut Kaneda, Daisuke aut Fujiki, Atsushi aut Miyachi, Mitsuru aut Nakatani, Takuya aut Osone, Shinya aut Ishida, Hiroyuki aut Taki, Tomohiko aut Takita, Junko aut Shiraishi, Yuichi aut Chiba, Kenichi aut Tanaka, Hiroko aut Miyano, Satoru aut Ogawa, Seishi aut Hosoi, Hajime aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 101(2014), 4 vom: 28. Nov., Seite 411-416 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:101 year:2014 number:4 day:28 month:11 pages:411-416 https://dx.doi.org/10.1007/s12185-014-1711-y 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 101 2014 4 28 11 411-416 |
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Enthalten in International journal of hematology 101(2014), 4 vom: 28. Nov., Seite 411-416 volume:101 year:2014 number:4 day:28 month:11 pages:411-416 |
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Enthalten in International journal of hematology 101(2014), 4 vom: 28. Nov., Seite 411-416 volume:101 year:2014 number:4 day:28 month:11 pages:411-416 |
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ETP-ALL JAK3 Acquired UPD SNP array Whole-exome sequencing |
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Kawashima-Goto, Sachiko @@aut@@ Imamura, Toshihiko @@aut@@ Seki, Masafumi @@aut@@ Kato, Motohiro @@aut@@ Yoshida, Kenichi @@aut@@ Sugimoto, Atsuya @@aut@@ Kaneda, Daisuke @@aut@@ Fujiki, Atsushi @@aut@@ Miyachi, Mitsuru @@aut@@ Nakatani, Takuya @@aut@@ Osone, Shinya @@aut@@ Ishida, Hiroyuki @@aut@@ Taki, Tomohiko @@aut@@ Takita, Junko @@aut@@ Shiraishi, Yuichi @@aut@@ Chiba, Kenichi @@aut@@ Tanaka, Hiroko @@aut@@ Miyano, Satoru @@aut@@ Ogawa, Seishi @@aut@@ Hosoi, Hajime @@aut@@ |
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Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. 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|
| author |
Kawashima-Goto, Sachiko |
| spellingShingle |
Kawashima-Goto, Sachiko misc ETP-ALL misc JAK3 misc Acquired UPD misc SNP array misc Whole-exome sequencing Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient |
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Kawashima-Goto, Sachiko |
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1865-3774 |
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Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient ETP-ALL (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Acquired UPD (dpeaa)DE-He213 SNP array (dpeaa)DE-He213 Whole-exome sequencing (dpeaa)DE-He213 |
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misc ETP-ALL misc JAK3 misc Acquired UPD misc SNP array misc Whole-exome sequencing |
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misc ETP-ALL misc JAK3 misc Acquired UPD misc SNP array misc Whole-exome sequencing |
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misc ETP-ALL misc JAK3 misc Acquired UPD misc SNP array misc Whole-exome sequencing |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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International journal of hematology |
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Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient |
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Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient |
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Kawashima-Goto, Sachiko |
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International journal of hematology |
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Kawashima-Goto, Sachiko Imamura, Toshihiko Seki, Masafumi Kato, Motohiro Yoshida, Kenichi Sugimoto, Atsuya Kaneda, Daisuke Fujiki, Atsushi Miyachi, Mitsuru Nakatani, Takuya Osone, Shinya Ishida, Hiroyuki Taki, Tomohiko Takita, Junko Shiraishi, Yuichi Chiba, Kenichi Tanaka, Hiroko Miyano, Satoru Ogawa, Seishi Hosoi, Hajime |
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Elektronische Aufsätze |
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Kawashima-Goto, Sachiko |
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10.1007/s12185-014-1711-y |
| title_sort |
identification of a homozygous jak3 v674a mutation caused by acquired uniparental disomy in a relapsed early t-cell precursor all patient |
| title_auth |
Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient |
| abstract |
Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. © The Japanese Society of Hematology 2014 |
| abstractGer |
Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. © The Japanese Society of Hematology 2014 |
| abstract_unstemmed |
Abstract Investigation of genetic alterations associated with relapse in acute lymphoblastic leukemia (ALL) may help to identify druggable targets for specific therapies. Early T-cell precursor ALL (ETP-ALL) is a subtype of T-ALL with poor prognosis. Although the genetic landscape of ETP-ALL has been determined, genetic alterations related to the relapse of ETP-ALL have not been fully investigated. Here, we report the first patient with relapsed pediatric ETP-ALL to exhibit a homozygous JAK3 activating mutation, V674A, caused by acquired uniparental disomy (UPD). Single nucleotide polymorphism array analysis revealed acquired UPD (aUPD) at the 19p13.3-p12 locus only in leukemic cells at relapse. Sanger sequence of the JAK3 gene, which was located at 19p13.1 and frequently mutated in ETP-ALL, was performed in paired leukemic samples to determine homozygous JAK3 V674A mutation only in relapsed leukemic cells. In contrast, leukemic cells at initial diagnosis harbored hemizygous JAK3 V674A mutation. Further, whole-exome sequencing revealed mutations in 18 genes only in relapsed samples, although none of these was recurrent in T-ALL. These findings suggest that aUPD at 19p13.1 is partly associated with relapse in this patient. Pharmacological inhibition of JAK3 may be therapeutic in such cases. © The Japanese Society of Hematology 2014 |
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Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient |
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Imamura, Toshihiko Seki, Masafumi Kato, Motohiro Yoshida, Kenichi Sugimoto, Atsuya Kaneda, Daisuke Fujiki, Atsushi Miyachi, Mitsuru Nakatani, Takuya Osone, Shinya Ishida, Hiroyuki Taki, Tomohiko Takita, Junko Shiraishi, Yuichi Chiba, Kenichi Tanaka, Hiroko Miyano, Satoru Ogawa, Seishi Hosoi, Hajime |
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| score |
7.3994675 |