The repertoire of genetic alterations in salivary duct carcinoma including a novel

Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targetin...
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Autor*in:	Dogan, Snjezana [verfasserIn] Ng, Charlotte K.Y. [verfasserIn] Xu, Bin [verfasserIn] Kumar, Rahul [verfasserIn] Wang, Lu [verfasserIn] Edelweiss, Marcia [verfasserIn] Scott, Sasinya N. [verfasserIn] Zehir, Ahmet [verfasserIn] Drilon, Alexander [verfasserIn] Morris, Luc G.T. [verfasserIn] Lee, Nancy Y. [verfasserIn] Antonescu, Cristina R. [verfasserIn] Ho, Alan L. [verfasserIn] Katabi, Nora [verfasserIn] Berger, Michael F. [verfasserIn] Reis-Filho, Jorge S. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Salivary duct carcinoma

Übergeordnetes Werk:	Enthalten in: Human pathology - New York, NY [u.a.] : Elsevier, 1970, 88, Seite 66-77
Übergeordnetes Werk:	volume:88 ; pages:66-77

DOI / URN:	10.1016/j.humpath.2019.03.004

Katalog-ID:	ELV002422395

Internformat


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245	1	0	\|a The repertoire of genetic alterations in salivary duct carcinoma including a novel
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520			\|a Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC.
650		4	\|a Salivary duct carcinoma
700	1		\|a Ng, Charlotte K.Y. \|e verfasserin \|4 aut
700	1		\|a Xu, Bin \|e verfasserin \|4 aut
700	1		\|a Kumar, Rahul \|e verfasserin \|4 aut
700	1		\|a Wang, Lu \|e verfasserin \|4 aut
700	1		\|a Edelweiss, Marcia \|e verfasserin \|4 aut
700	1		\|a Scott, Sasinya N. \|e verfasserin \|4 aut
700	1		\|a Zehir, Ahmet \|e verfasserin \|4 aut
700	1		\|a Drilon, Alexander \|e verfasserin \|4 aut
700	1		\|a Morris, Luc G.T. \|e verfasserin \|4 aut
700	1		\|a Lee, Nancy Y. \|e verfasserin \|4 aut
700	1		\|a Antonescu, Cristina R. \|e verfasserin \|4 aut
700	1		\|a Ho, Alan L. \|e verfasserin \|4 aut
700	1		\|a Katabi, Nora \|e verfasserin \|4 aut
700	1		\|a Berger, Michael F. \|e verfasserin \|4 aut
700	1		\|a Reis-Filho, Jorge S. \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Human pathology \|d New York, NY [u.a.] : Elsevier, 1970 \|g 88, Seite 66-77 \|h Online-Ressource \|w (DE-627)326644784 \|w (DE-600)2041481-X \|w (DE-576)094477272 \|x 1532-8392 \|7 nnns
773	1	8	\|g volume:88 \|g pages:66-77
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912			\|a GBV_ILN_370
912			\|a GBV_ILN_602
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2004
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2011
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2015
912			\|a GBV_ILN_2020
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2025
912			\|a GBV_ILN_2027
912			\|a GBV_ILN_2034
912			\|a GBV_ILN_2038
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
912			\|a GBV_ILN_2049
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912			\|a GBV_ILN_2059
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912			\|a GBV_ILN_2129
912			\|a GBV_ILN_2143
912			\|a GBV_ILN_2147
912			\|a GBV_ILN_2148
912			\|a GBV_ILN_2152
912			\|a GBV_ILN_2153
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_2336
912			\|a GBV_ILN_2507
912			\|a GBV_ILN_2522
912			\|a GBV_ILN_4035
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4242
912			\|a GBV_ILN_4251
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4326
912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4393
936	b	k	\|a 44.46 \|j Klinische Pathologie
936	b	k	\|a 44.47 \|j Pathologie \|x Medizin
951			\|a AR
952			\|d 88 \|h 66-77

Indexfelder

author_variant	s d sd c k n ck ckn b x bx r k rk l w lw m e me s n s sn sns a z az a d ad l g m lg lgm n y l ny nyl c r a cr cra a l h al alh n k nk m f b mf mfb j s r f jsr jsrf
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bklnumber	44.46 44.47
publishDate	2019
allfields	10.1016/j.humpath.2019.03.004 doi (DE-627)ELV002422395 (ELSEVIER)S0046-8177(19)30049-8 DE-627 ger DE-627 rda eng 610 DE-600 44.46 bkl 44.47 bkl Dogan, Snjezana verfasserin aut The repertoire of genetic alterations in salivary duct carcinoma including a novel 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC. Salivary duct carcinoma Ng, Charlotte K.Y. verfasserin aut Xu, Bin verfasserin aut Kumar, Rahul verfasserin aut Wang, Lu verfasserin aut Edelweiss, Marcia verfasserin aut Scott, Sasinya N. verfasserin aut Zehir, Ahmet verfasserin aut Drilon, Alexander verfasserin aut Morris, Luc G.T. verfasserin aut Lee, Nancy Y. verfasserin aut Antonescu, Cristina R. verfasserin aut Ho, Alan L. verfasserin aut Katabi, Nora verfasserin aut Berger, Michael F. verfasserin aut Reis-Filho, Jorge S. verfasserin aut Enthalten in Human pathology New York, NY [u.a.] : Elsevier, 1970 88, Seite 66-77 Online-Ressource (DE-627)326644784 (DE-600)2041481-X (DE-576)094477272 1532-8392 nnns volume:88 pages:66-77 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.46 Klinische Pathologie 44.47 Pathologie Medizin AR 88 66-77
spelling	10.1016/j.humpath.2019.03.004 doi (DE-627)ELV002422395 (ELSEVIER)S0046-8177(19)30049-8 DE-627 ger DE-627 rda eng 610 DE-600 44.46 bkl 44.47 bkl Dogan, Snjezana verfasserin aut The repertoire of genetic alterations in salivary duct carcinoma including a novel 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC. Salivary duct carcinoma Ng, Charlotte K.Y. verfasserin aut Xu, Bin verfasserin aut Kumar, Rahul verfasserin aut Wang, Lu verfasserin aut Edelweiss, Marcia verfasserin aut Scott, Sasinya N. verfasserin aut Zehir, Ahmet verfasserin aut Drilon, Alexander verfasserin aut Morris, Luc G.T. verfasserin aut Lee, Nancy Y. verfasserin aut Antonescu, Cristina R. verfasserin aut Ho, Alan L. verfasserin aut Katabi, Nora verfasserin aut Berger, Michael F. verfasserin aut Reis-Filho, Jorge S. verfasserin aut Enthalten in Human pathology New York, NY [u.a.] : Elsevier, 1970 88, Seite 66-77 Online-Ressource (DE-627)326644784 (DE-600)2041481-X (DE-576)094477272 1532-8392 nnns volume:88 pages:66-77 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.46 Klinische Pathologie 44.47 Pathologie Medizin AR 88 66-77
allfields_unstemmed	10.1016/j.humpath.2019.03.004 doi (DE-627)ELV002422395 (ELSEVIER)S0046-8177(19)30049-8 DE-627 ger DE-627 rda eng 610 DE-600 44.46 bkl 44.47 bkl Dogan, Snjezana verfasserin aut The repertoire of genetic alterations in salivary duct carcinoma including a novel 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC. Salivary duct carcinoma Ng, Charlotte K.Y. verfasserin aut Xu, Bin verfasserin aut Kumar, Rahul verfasserin aut Wang, Lu verfasserin aut Edelweiss, Marcia verfasserin aut Scott, Sasinya N. verfasserin aut Zehir, Ahmet verfasserin aut Drilon, Alexander verfasserin aut Morris, Luc G.T. verfasserin aut Lee, Nancy Y. verfasserin aut Antonescu, Cristina R. verfasserin aut Ho, Alan L. verfasserin aut Katabi, Nora verfasserin aut Berger, Michael F. verfasserin aut Reis-Filho, Jorge S. verfasserin aut Enthalten in Human pathology New York, NY [u.a.] : Elsevier, 1970 88, Seite 66-77 Online-Ressource (DE-627)326644784 (DE-600)2041481-X (DE-576)094477272 1532-8392 nnns volume:88 pages:66-77 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.46 Klinische Pathologie 44.47 Pathologie Medizin AR 88 66-77
allfieldsGer	10.1016/j.humpath.2019.03.004 doi (DE-627)ELV002422395 (ELSEVIER)S0046-8177(19)30049-8 DE-627 ger DE-627 rda eng 610 DE-600 44.46 bkl 44.47 bkl Dogan, Snjezana verfasserin aut The repertoire of genetic alterations in salivary duct carcinoma including a novel 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC. Salivary duct carcinoma Ng, Charlotte K.Y. verfasserin aut Xu, Bin verfasserin aut Kumar, Rahul verfasserin aut Wang, Lu verfasserin aut Edelweiss, Marcia verfasserin aut Scott, Sasinya N. verfasserin aut Zehir, Ahmet verfasserin aut Drilon, Alexander verfasserin aut Morris, Luc G.T. verfasserin aut Lee, Nancy Y. verfasserin aut Antonescu, Cristina R. verfasserin aut Ho, Alan L. verfasserin aut Katabi, Nora verfasserin aut Berger, Michael F. verfasserin aut Reis-Filho, Jorge S. verfasserin aut Enthalten in Human pathology New York, NY [u.a.] : Elsevier, 1970 88, Seite 66-77 Online-Ressource (DE-627)326644784 (DE-600)2041481-X (DE-576)094477272 1532-8392 nnns volume:88 pages:66-77 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.46 Klinische Pathologie 44.47 Pathologie Medizin AR 88 66-77
allfieldsSound	10.1016/j.humpath.2019.03.004 doi (DE-627)ELV002422395 (ELSEVIER)S0046-8177(19)30049-8 DE-627 ger DE-627 rda eng 610 DE-600 44.46 bkl 44.47 bkl Dogan, Snjezana verfasserin aut The repertoire of genetic alterations in salivary duct carcinoma including a novel 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC. Salivary duct carcinoma Ng, Charlotte K.Y. verfasserin aut Xu, Bin verfasserin aut Kumar, Rahul verfasserin aut Wang, Lu verfasserin aut Edelweiss, Marcia verfasserin aut Scott, Sasinya N. verfasserin aut Zehir, Ahmet verfasserin aut Drilon, Alexander verfasserin aut Morris, Luc G.T. verfasserin aut Lee, Nancy Y. verfasserin aut Antonescu, Cristina R. verfasserin aut Ho, Alan L. verfasserin aut Katabi, Nora verfasserin aut Berger, Michael F. verfasserin aut Reis-Filho, Jorge S. verfasserin aut Enthalten in Human pathology New York, NY [u.a.] : Elsevier, 1970 88, Seite 66-77 Online-Ressource (DE-627)326644784 (DE-600)2041481-X (DE-576)094477272 1532-8392 nnns volume:88 pages:66-77 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.46 Klinische Pathologie 44.47 Pathologie Medizin AR 88 66-77
language	English
source	Enthalten in Human pathology 88, Seite 66-77 volume:88 pages:66-77
sourceStr	Enthalten in Human pathology 88, Seite 66-77 volume:88 pages:66-77
format_phy_str_mv	Article
bklname	Klinische Pathologie Pathologie
institution	findex.gbv.de
topic_facet	Salivary duct carcinoma
dewey-raw	610
isfreeaccess_bool	false
container_title	Human pathology
authorswithroles_txt_mv	Dogan, Snjezana @@aut@@ Ng, Charlotte K.Y. @@aut@@ Xu, Bin @@aut@@ Kumar, Rahul @@aut@@ Wang, Lu @@aut@@ Edelweiss, Marcia @@aut@@ Scott, Sasinya N. @@aut@@ Zehir, Ahmet @@aut@@ Drilon, Alexander @@aut@@ Morris, Luc G.T. @@aut@@ Lee, Nancy Y. @@aut@@ Antonescu, Cristina R. @@aut@@ Ho, Alan L. @@aut@@ Katabi, Nora @@aut@@ Berger, Michael F. @@aut@@ Reis-Filho, Jorge S. @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	326644784
dewey-sort	3610
id	ELV002422395
language_de	englisch
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author	Dogan, Snjezana
spellingShingle	Dogan, Snjezana ddc 610 bkl 44.46 bkl 44.47 misc Salivary duct carcinoma The repertoire of genetic alterations in salivary duct carcinoma including a novel
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topic_title	610 DE-600 44.46 bkl 44.47 bkl The repertoire of genetic alterations in salivary duct carcinoma including a novel Salivary duct carcinoma
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title	The repertoire of genetic alterations in salivary duct carcinoma including a novel
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title_full	The repertoire of genetic alterations in salivary duct carcinoma including a novel
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author_browse	Dogan, Snjezana Ng, Charlotte K.Y. Xu, Bin Kumar, Rahul Wang, Lu Edelweiss, Marcia Scott, Sasinya N. Zehir, Ahmet Drilon, Alexander Morris, Luc G.T. Lee, Nancy Y. Antonescu, Cristina R. Ho, Alan L. Katabi, Nora Berger, Michael F. Reis-Filho, Jorge S.
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title_sort	the repertoire of genetic alterations in salivary duct carcinoma including a novel
title_auth	The repertoire of genetic alterations in salivary duct carcinoma including a novel
abstract	Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC.
abstractGer	Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC.
abstract_unstemmed	Salivary duct carcinoma (SDC) is a rare, aggressive malignancy with limited treatment options and poor outcome. Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. A broad genomic profiling is necessary to ensure detection of rare but clinically actionable somatic alterations in SDC.
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title_short	The repertoire of genetic alterations in salivary duct carcinoma including a novel
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author2	Ng, Charlotte K.Y. Xu, Bin Kumar, Rahul Wang, Lu Edelweiss, Marcia Scott, Sasinya N. Zehir, Ahmet Drilon, Alexander Morris, Luc G.T. Lee, Nancy Y. Antonescu, Cristina R. Ho, Alan L. Katabi, Nora Berger, Michael F. Reis-Filho, Jorge S.
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up_date	2024-07-07T00:40:31.876Z
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Twenty-nine primary resected SDC, including 15 SDC de novo (SDCDN), and 14 SDC ex pleomorphic adenoma (SDCXPA) were subjected to the massive parallel sequencing assay (MSK-IMPACT) targeting 287 to 468 cancer-related genes. TP53 was the most frequently altered gene (69%). TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively). Potentially targetable mutations were detected in 79% (23/29) of SDC involving ERBB2 (31%), PIK3CA (28%), HRAS (21%), ALK (7%) and BRAF (3%), and 22% (5/23) of those cases harbored possible primary resistance mutations involving CCNE1, NF1 and PTEN. A novel HNRNPH3-ALK rearrangement was found in one SDCDN. In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis. A germline analysis of the DNA repair genes revealed a case with a pathogenic BRCA1 E23fs germline variant. SDCDN and SDCXPA are genetically distinct. Although the majority of SDC may be amenable to molecular targeted therapy, concurrent possible resistance mutations may be found in a significant minority of cases. 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The repertoire of genetic alterations in salivary duct carcinoma including a novel

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