MCL1 as putative target in pancreatoblastoma
Pancreatoblastoma (PB) is a rare tumor of the pancreas. In case of metastases, the treatment options are sparse and targeted approaches are not developed. We here evaluate MCL1 amplification as a putative target in PB. Thirteen samples from adult (10/13) and pediatric patients (3/13) were collected....
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| Veröffentlicht in: | Virchows Archiv : an international journal of pathology 2022-08, Vol.481 (2), p.265-272 |
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| creator | Reissig, Timm M. Uhrig, Sebastian Jost, Philipp J. Luchini, Claudio Vicentini, Caterina Liffers, Sven-Thorsten Allgäuer, Michael Adsay, Volkan Scarpa, Aldo Lawlor, Rita Teresa Fröhling, Stefan Stenzinger, Albrecht Klöppel, Günter Schildhaus, Hans-Ulrich Siveke, Jens T. |
| description | Pancreatoblastoma (PB) is a rare tumor of the pancreas. In case of metastases, the treatment options are sparse and targeted approaches are not developed. We here evaluate
MCL1
amplification as a putative target in PB.
Thirteen samples from adult (10/13) and pediatric patients (3/13) were collected. Three of these samples had been previously subjected to whole-exome sequencing (2 cases) or whole-genome sequencing (1 case) within a precision oncology program (NCT/DKTK MASTER), and this analysis had shown copy number gains of
MCL1
gene. We established a fluorescence in situ hybridization (FISH) test to assess the copy number alterations of
MCL1
gene in 13 formalin-fixed paraffin-embedded PBs, including the 3 cases assessed by genome sequencing. FISH analysis showed the amplification of
MCL1
in 2 cases (both were adult PB), one of which was a case with the highest copy number gain at genomic analysis. In both cases, the average gene copy number per cell was ≥ 5.7 and the MCL1/1p12 ratio was ≥ 2.4. Our data support MCL1 as a putative target in PB. Patients with
MCL1
-amplified PB might benefit from MCL1 inhibition. Sequencing data is useful to screen for amplification; however, the established FISH for
MCL1
can help to determine the level and cellular heterogeneity of
MCL1
amplification more accurately. |
| doi_str_mv | 10.1007/s00428-022-03349-w |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9343273</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2696967485</sourcerecordid><originalsourceid>FETCH-LOGICAL-c404t-16510892372b81a35c367141a944265e2f122d8325fd5fcace9fc9c1a8de82803</originalsourceid><addsrcrecordid>eNp9kctOwzAQRS0EgvL4ARYoEhsWBGZsx7E3SKjiJRWxgbXluk4JSpNiOyD-HkNLeSzQLLyYM3fm-hKyj3CCAOVpAOBU5kBpDoxxlb-ukQFyRnPKoFwnA1C8yAXDcotsh_AEQFGi2CRbrBBCIsoBOb4djjAzIZv30cT6xWXR-KmLWd1mc9Na70zsxo0JsZuZXbJRmSa4veW7Qx4uL-6H1_no7upmeD7KLQcecxQFglSUlXQs0bDCMlEiR6M4p6JwtEJKJ5LRopoUlTXWqcoqi0ZOnKQS2A45W-jO-_HMTaxrozeNnvt6Zvyb7kytf3fa-lFPuxetWHJfsiRwtBTw3XPvQtSzOljXNKZ1XR80FSUHQCFUQg__oE9d79tkL1EqVcllkSi6oKzvQvCuWh2DoD_C0IswdApDf4ahX9PQwU8bq5Gv308AWwAhtdqp89-7_5F9B3kXk8g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2696967485</pqid></control><display><type>article</type><title>MCL1 as putative target in pancreatoblastoma</title><source>Springer Journals</source><creator>Reissig, Timm M. ; Uhrig, Sebastian ; Jost, Philipp J. ; Luchini, Claudio ; Vicentini, Caterina ; Liffers, Sven-Thorsten ; Allgäuer, Michael ; Adsay, Volkan ; Scarpa, Aldo ; Lawlor, Rita Teresa ; Fröhling, Stefan ; Stenzinger, Albrecht ; Klöppel, Günter ; Schildhaus, Hans-Ulrich ; Siveke, Jens T.</creator><creatorcontrib>Reissig, Timm M. ; Uhrig, Sebastian ; Jost, Philipp J. ; Luchini, Claudio ; Vicentini, Caterina ; Liffers, Sven-Thorsten ; Allgäuer, Michael ; Adsay, Volkan ; Scarpa, Aldo ; Lawlor, Rita Teresa ; Fröhling, Stefan ; Stenzinger, Albrecht ; Klöppel, Günter ; Schildhaus, Hans-Ulrich ; Siveke, Jens T.</creatorcontrib><description>Pancreatoblastoma (PB) is a rare tumor of the pancreas. In case of metastases, the treatment options are sparse and targeted approaches are not developed. We here evaluate
MCL1
amplification as a putative target in PB.
Thirteen samples from adult (10/13) and pediatric patients (3/13) were collected. Three of these samples had been previously subjected to whole-exome sequencing (2 cases) or whole-genome sequencing (1 case) within a precision oncology program (NCT/DKTK MASTER), and this analysis had shown copy number gains of
MCL1
gene. We established a fluorescence in situ hybridization (FISH) test to assess the copy number alterations of
MCL1
gene in 13 formalin-fixed paraffin-embedded PBs, including the 3 cases assessed by genome sequencing. FISH analysis showed the amplification of
MCL1
in 2 cases (both were adult PB), one of which was a case with the highest copy number gain at genomic analysis. In both cases, the average gene copy number per cell was ≥ 5.7 and the MCL1/1p12 ratio was ≥ 2.4. Our data support MCL1 as a putative target in PB. Patients with
MCL1
-amplified PB might benefit from MCL1 inhibition. Sequencing data is useful to screen for amplification; however, the established FISH for
MCL1
can help to determine the level and cellular heterogeneity of
MCL1
amplification more accurately.</description><identifier>ISSN: 0945-6317</identifier><identifier>EISSN: 1432-2307</identifier><identifier>DOI: 10.1007/s00428-022-03349-w</identifier><identifier>PMID: 35668118</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Amplification ; Copy number ; Fluorescence in situ hybridization ; Gene sequencing ; Genomes ; Genomic analysis ; Heterogeneity ; Mcl-1 protein ; MCL1 gene ; Medicine ; Medicine & Public Health ; Metastases ; Original ; Original Article ; Paraffin ; Paraffins ; Pathology ; Patients ; Pediatrics ; Precision medicine ; Tumors ; Whole genome sequencing</subject><ispartof>Virchows Archiv : an international journal of pathology, 2022-08, Vol.481 (2), p.265-272</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-16510892372b81a35c367141a944265e2f122d8325fd5fcace9fc9c1a8de82803</citedby><cites>FETCH-LOGICAL-c404t-16510892372b81a35c367141a944265e2f122d8325fd5fcace9fc9c1a8de82803</cites><orcidid>0000-0002-9856-7050 ; 0000-0002-8772-4778 ; 0000-0002-9955-5991</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00428-022-03349-w$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00428-022-03349-w$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35668118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reissig, Timm M.</creatorcontrib><creatorcontrib>Uhrig, Sebastian</creatorcontrib><creatorcontrib>Jost, Philipp J.</creatorcontrib><creatorcontrib>Luchini, Claudio</creatorcontrib><creatorcontrib>Vicentini, Caterina</creatorcontrib><creatorcontrib>Liffers, Sven-Thorsten</creatorcontrib><creatorcontrib>Allgäuer, Michael</creatorcontrib><creatorcontrib>Adsay, Volkan</creatorcontrib><creatorcontrib>Scarpa, Aldo</creatorcontrib><creatorcontrib>Lawlor, Rita Teresa</creatorcontrib><creatorcontrib>Fröhling, Stefan</creatorcontrib><creatorcontrib>Stenzinger, Albrecht</creatorcontrib><creatorcontrib>Klöppel, Günter</creatorcontrib><creatorcontrib>Schildhaus, Hans-Ulrich</creatorcontrib><creatorcontrib>Siveke, Jens T.</creatorcontrib><title>MCL1 as putative target in pancreatoblastoma</title><title>Virchows Archiv : an international journal of pathology</title><addtitle>Virchows Arch</addtitle><addtitle>Virchows Arch</addtitle><description>Pancreatoblastoma (PB) is a rare tumor of the pancreas. In case of metastases, the treatment options are sparse and targeted approaches are not developed. We here evaluate
MCL1
amplification as a putative target in PB.
Thirteen samples from adult (10/13) and pediatric patients (3/13) were collected. Three of these samples had been previously subjected to whole-exome sequencing (2 cases) or whole-genome sequencing (1 case) within a precision oncology program (NCT/DKTK MASTER), and this analysis had shown copy number gains of
MCL1
gene. We established a fluorescence in situ hybridization (FISH) test to assess the copy number alterations of
MCL1
gene in 13 formalin-fixed paraffin-embedded PBs, including the 3 cases assessed by genome sequencing. FISH analysis showed the amplification of
MCL1
in 2 cases (both were adult PB), one of which was a case with the highest copy number gain at genomic analysis. In both cases, the average gene copy number per cell was ≥ 5.7 and the MCL1/1p12 ratio was ≥ 2.4. Our data support MCL1 as a putative target in PB. Patients with
MCL1
-amplified PB might benefit from MCL1 inhibition. Sequencing data is useful to screen for amplification; however, the established FISH for
MCL1
can help to determine the level and cellular heterogeneity of
MCL1
amplification more accurately.</description><subject>Amplification</subject><subject>Copy number</subject><subject>Fluorescence in situ hybridization</subject><subject>Gene sequencing</subject><subject>Genomes</subject><subject>Genomic analysis</subject><subject>Heterogeneity</subject><subject>Mcl-1 protein</subject><subject>MCL1 gene</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Original</subject><subject>Original Article</subject><subject>Paraffin</subject><subject>Paraffins</subject><subject>Pathology</subject><subject>Patients</subject><subject>Pediatrics</subject><subject>Precision medicine</subject><subject>Tumors</subject><subject>Whole genome 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Participant titles)</collection><jtitle>Virchows Archiv : an international journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reissig, Timm M.</au><au>Uhrig, Sebastian</au><au>Jost, Philipp J.</au><au>Luchini, Claudio</au><au>Vicentini, Caterina</au><au>Liffers, Sven-Thorsten</au><au>Allgäuer, Michael</au><au>Adsay, Volkan</au><au>Scarpa, Aldo</au><au>Lawlor, Rita Teresa</au><au>Fröhling, Stefan</au><au>Stenzinger, Albrecht</au><au>Klöppel, Günter</au><au>Schildhaus, Hans-Ulrich</au><au>Siveke, Jens T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MCL1 as putative target in pancreatoblastoma</atitle><jtitle>Virchows Archiv : an international journal of pathology</jtitle><stitle>Virchows Arch</stitle><addtitle>Virchows Arch</addtitle><date>2022-08-01</date><risdate>2022</risdate><volume>481</volume><issue>2</issue><spage>265</spage><epage>272</epage><pages>265-272</pages><issn>0945-6317</issn><eissn>1432-2307</eissn><abstract>Pancreatoblastoma (PB) is a rare tumor of the pancreas. In case of metastases, the treatment options are sparse and targeted approaches are not developed. We here evaluate
MCL1
amplification as a putative target in PB.
Thirteen samples from adult (10/13) and pediatric patients (3/13) were collected. Three of these samples had been previously subjected to whole-exome sequencing (2 cases) or whole-genome sequencing (1 case) within a precision oncology program (NCT/DKTK MASTER), and this analysis had shown copy number gains of
MCL1
gene. We established a fluorescence in situ hybridization (FISH) test to assess the copy number alterations of
MCL1
gene in 13 formalin-fixed paraffin-embedded PBs, including the 3 cases assessed by genome sequencing. FISH analysis showed the amplification of
MCL1
in 2 cases (both were adult PB), one of which was a case with the highest copy number gain at genomic analysis. In both cases, the average gene copy number per cell was ≥ 5.7 and the MCL1/1p12 ratio was ≥ 2.4. Our data support MCL1 as a putative target in PB. Patients with
MCL1
-amplified PB might benefit from MCL1 inhibition. Sequencing data is useful to screen for amplification; however, the established FISH for
MCL1
can help to determine the level and cellular heterogeneity of
MCL1
amplification more accurately.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>35668118</pmid><doi>10.1007/s00428-022-03349-w</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-9856-7050</orcidid><orcidid>https://orcid.org/0000-0002-8772-4778</orcidid><orcidid>https://orcid.org/0000-0002-9955-5991</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Virchows Archiv : an international journal of pathology, 2022-08, Vol.481 (2), p.265-272 |
| issn | 0945-6317 1432-2307 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9343273 |
| source | Springer Journals |
| subjects | Amplification Copy number Fluorescence in situ hybridization Gene sequencing Genomes Genomic analysis Heterogeneity Mcl-1 protein MCL1 gene Medicine Medicine & Public Health Metastases Original Original Article Paraffin Paraffins Pathology Patients Pediatrics Precision medicine Tumors Whole genome sequencing |
| title | MCL1 as putative target in pancreatoblastoma |
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