Functional consequence and therapeutic targeting of cryptic ALK fusions in monosomy 7 acute myeloid leukemia
Acute myeloid leukemia (AML) patients have a wide array of cytogenetic and molecular aberrations, which can influence response to therapy. Monosomy 7 is a rare subset within pediatric AML (prevalence of
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| Veröffentlicht in: | Pediatric blood & cancer 2023-04, Vol.70 (4), p.e30180-n/a |
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| container_issue | 4 |
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| container_title | Pediatric blood & cancer |
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| creator | Manselle, Makia K. Ries, Rhonda E. Hylkema, Tiffany Leonti, Amanda Kirkey, Danielle C. Furlan, Scott N. Meshinchi, Soheil |
| description | Acute myeloid leukemia (AML) patients have a wide array of cytogenetic and molecular aberrations, which can influence response to therapy. Monosomy 7 is a rare subset within pediatric AML (prevalence of |
| doi_str_mv | 10.1002/pbc.30180 |
| format | Article |
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Monosomy 7 is a rare subset within pediatric AML (prevalence of <2%) that is highly associated with poor outcomes. Fusions involving the anaplastic tyrosine kinase (ALK) gene were exclusively identified in 14.3% of this high‐risk cohort, while absent across all other AML. Given the dismal outcomes of monosomy 7, we evaluated the use of crizotinib, an FDA‐approved tyrosine kinase inhibitor, used to treat patients with ALK fusions. Our findings suggest that crizotinib may serve as a novel therapy for these patients.</description><identifier>ISSN: 1545-5009</identifier><identifier>EISSN: 1545-5017</identifier><identifier>DOI: 10.1002/pbc.30180</identifier><identifier>PMID: 36720638</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acute myeloid leukemia ; AML ; cancer genetics ; chemotherapy ; Child ; Chromosome Deletion ; Crizotinib - therapeutic use ; Cytogenetics ; Hematology ; hematology/oncology ; Humans ; Leukemia, Myeloid, Acute - drug therapy ; Monosomy ; Oncology ; Pediatrics ; Protein Kinase Inhibitors - therapeutic use ; Protein-tyrosine kinase ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor Protein-Tyrosine Kinases - therapeutic use ; Therapeutic targets</subject><ispartof>Pediatric blood & cancer, 2023-04, Vol.70 (4), p.e30180-n/a</ispartof><rights>2023 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-d17bd771abce459bf246ccfbed48a534501684314730fb8a064fdd9da171d9723</citedby><cites>FETCH-LOGICAL-c3530-d17bd771abce459bf246ccfbed48a534501684314730fb8a064fdd9da171d9723</cites><orcidid>0000-0002-1639-8311</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpbc.30180$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpbc.30180$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36720638$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Manselle, Makia K.</creatorcontrib><creatorcontrib>Ries, Rhonda E.</creatorcontrib><creatorcontrib>Hylkema, Tiffany</creatorcontrib><creatorcontrib>Leonti, Amanda</creatorcontrib><creatorcontrib>Kirkey, Danielle C.</creatorcontrib><creatorcontrib>Furlan, Scott N.</creatorcontrib><creatorcontrib>Meshinchi, Soheil</creatorcontrib><title>Functional consequence and therapeutic targeting of cryptic ALK fusions in monosomy 7 acute myeloid leukemia</title><title>Pediatric blood & cancer</title><addtitle>Pediatr Blood Cancer</addtitle><description>Acute myeloid leukemia (AML) patients have a wide array of cytogenetic and molecular aberrations, which can influence response to therapy. Monosomy 7 is a rare subset within pediatric AML (prevalence of <2%) that is highly associated with poor outcomes. Fusions involving the anaplastic tyrosine kinase (ALK) gene were exclusively identified in 14.3% of this high‐risk cohort, while absent across all other AML. Given the dismal outcomes of monosomy 7, we evaluated the use of crizotinib, an FDA‐approved tyrosine kinase inhibitor, used to treat patients with ALK fusions. Our findings suggest that crizotinib may serve as a novel therapy for these patients.</description><subject>Acute myeloid leukemia</subject><subject>AML</subject><subject>cancer genetics</subject><subject>chemotherapy</subject><subject>Child</subject><subject>Chromosome Deletion</subject><subject>Crizotinib - therapeutic use</subject><subject>Cytogenetics</subject><subject>Hematology</subject><subject>hematology/oncology</subject><subject>Humans</subject><subject>Leukemia, Myeloid, Acute - drug therapy</subject><subject>Monosomy</subject><subject>Oncology</subject><subject>Pediatrics</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Protein-tyrosine kinase</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - therapeutic use</subject><subject>Therapeutic targets</subject><issn>1545-5009</issn><issn>1545-5017</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10c1OxCAUBWBiNP4vfAFD4kYXo1DaQpc6cdQ4iS503VC4VbSFCiWmby866sLEFYR8nOTeg9ABJaeUkOxsaNQpI1SQNbRNi7yYFYTy9d87qbbQTggviZakEJtoi5U8IyUT26hbRKtG46zssHI2wFsEqwBLq_H4DF4OEEej8Cj9E4zGPmHXYuWn4fPxfHmL2xjS74CNxb2zLrh-whxLFUfA_QSdMxp3EF-hN3IPbbSyC7D_fe6ix8Xlw_x6try7upmfL2eKFYzMNOWN5pzKRkFeVE2b5aVSbQM6F7JgeZquFDmjOWekbYQkZd5qXWlJOdUVz9guOl7lDt6lecJY9yYo6DppwcVQZym8ZCWtWKJHf-iLiz5t40sJIWjGi6ROVkp5F4KHth686aWfakrqzwrqVEH9VUGyh9-JselB_8qfnSdwtgLvpoPp_6T6_mK-ivwAAOOQNQ</recordid><startdate>202304</startdate><enddate>202304</enddate><creator>Manselle, Makia K.</creator><creator>Ries, Rhonda E.</creator><creator>Hylkema, Tiffany</creator><creator>Leonti, Amanda</creator><creator>Kirkey, Danielle C.</creator><creator>Furlan, Scott N.</creator><creator>Meshinchi, Soheil</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1639-8311</orcidid></search><sort><creationdate>202304</creationdate><title>Functional consequence and therapeutic targeting of cryptic ALK fusions in monosomy 7 acute myeloid leukemia</title><author>Manselle, Makia K. ; 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| subjects | Acute myeloid leukemia AML cancer genetics chemotherapy Child Chromosome Deletion Crizotinib - therapeutic use Cytogenetics Hematology hematology/oncology Humans Leukemia, Myeloid, Acute - drug therapy Monosomy Oncology Pediatrics Protein Kinase Inhibitors - therapeutic use Protein-tyrosine kinase Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - therapeutic use Therapeutic targets |
| title | Functional consequence and therapeutic targeting of cryptic ALK fusions in monosomy 7 acute myeloid leukemia |
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