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Evidence for ABL Amplification in Multiple Myeloma and Therapeutic Implications
Background. Cytogenetic abnormalities are considered initiating events in the pathogenesis of multiple myeloma (MM) and are assumed to be of clinical significance. Methods. Fluorescence in situ hybridization (FISH) was used to analyze chromosomal architecture in 101 patients with MM. We evaluated ov...
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Published in: | Journal of oncology 2022-03, Vol.2022, p.4112016-9 |
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description | Background. Cytogenetic abnormalities are considered initiating events in the pathogenesis of multiple myeloma (MM) and are assumed to be of clinical significance. Methods. Fluorescence in situ hybridization (FISH) was used to analyze chromosomal architecture in 101 patients with MM. We evaluated overall patient survival and assessed the cytotoxicity of imatinib against MM cells using a CCK8 assay. Results. ABL gene amplification was detected in 67 patients (66.3%). However, ABL gene amplification was not associated with clinical features, cytogenetic abnormalities (c-Myc amplification, IGH rearrangement, RB1 deletion, p53 deletion, or 1q21 amplification), or overall survival. ABL amplification in MM cell lines (LP-1 and U266) was revealed by FISH. Furthermore, the ABL protein was easily detectable in MM cell lines and some tumor cells by western blotting. A CCK8 assay indicated limited cytotoxicity of imatinib against MM cells. Conclusions. Our study firstly discussed ABL gene amplification was prevalent in MM cells, and we believe that the ABL gene would potentially be a useful target in the treatment of combination strategy for MM with ABL amplification in the future. |
doi_str_mv | 10.1155/2022/4112016 |
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Cytogenetic abnormalities are considered initiating events in the pathogenesis of multiple myeloma (MM) and are assumed to be of clinical significance. Methods. Fluorescence in situ hybridization (FISH) was used to analyze chromosomal architecture in 101 patients with MM. We evaluated overall patient survival and assessed the cytotoxicity of imatinib against MM cells using a CCK8 assay. Results. ABL gene amplification was detected in 67 patients (66.3%). However, ABL gene amplification was not associated with clinical features, cytogenetic abnormalities (c-Myc amplification, IGH rearrangement, RB1 deletion, p53 deletion, or 1q21 amplification), or overall survival. ABL amplification in MM cell lines (LP-1 and U266) was revealed by FISH. Furthermore, the ABL protein was easily detectable in MM cell lines and some tumor cells by western blotting. A CCK8 assay indicated limited cytotoxicity of imatinib against MM cells. Conclusions. Our study firstly discussed ABL gene amplification was prevalent in MM cells, and we believe that the ABL gene would potentially be a useful target in the treatment of combination strategy for MM with ABL amplification in the future.</description><identifier>ISSN: 1687-8450</identifier><identifier>EISSN: 1687-8450</identifier><identifier>DOI: 10.1155/2022/4112016</identifier><identifier>PMID: 35342415</identifier><language>eng</language><publisher>Egypt: Hindawi</publisher><subject>Apoptosis ; B cells ; Biotechnology industry ; Bone marrow ; Cell growth ; Chemotherapy ; Creatinine ; DNA damage ; Ethylenediaminetetraacetic acid ; Gene expression ; Genes ; Genetic aspects ; Genomes ; Health aspects ; Hospitals ; Hybridization ; Inhibitor drugs ; Kinases ; Laboratories ; Medical prognosis ; Medical research ; Medicine, Experimental ; Multiple myeloma ; Patients ; Plasma ; Proteins ; Software ; Targeted cancer therapy ; Tumor proteins ; Vincristine</subject><ispartof>Journal of oncology, 2022-03, Vol.2022, p.4112016-9</ispartof><rights>Copyright © 2022 He Huang et al.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>Copyright © 2022 He Huang et al. This work is licensed 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><rights>Copyright © 2022 He Huang et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c433t-6318a4aea234ac6c6233e05d16b5259e4589fa49991877023dbb2f7ecfff21963</cites><orcidid>0000-0003-3614-9002 ; 0000-0003-2195-3700 ; 0000-0002-1211-2830 ; 0000-0002-8144-0782 ; 0000-0001-9946-9869 ; 0000-0002-1607-5619 ; 0000-0001-5359-8534 ; 0000-0003-3593-4535 ; 0000-0002-8873-3326</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2643813009/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2643813009?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768,74869</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35342415$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Raghavamenon, Achuthan Chathrattil</contributor><creatorcontrib>Huang, He</creatorcontrib><creatorcontrib>Zhou, Shuping</creatorcontrib><creatorcontrib>Lin, Hongdou</creatorcontrib><creatorcontrib>Guo, Wenjian</creatorcontrib><creatorcontrib>Lin, Ying</creatorcontrib><creatorcontrib>Yao, Ronxin</creatorcontrib><creatorcontrib>He, Licai</creatorcontrib><creatorcontrib>Yu, Kang</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><title>Evidence for ABL Amplification in Multiple Myeloma and Therapeutic Implications</title><title>Journal of oncology</title><addtitle>J Oncol</addtitle><description>Background. Cytogenetic abnormalities are considered initiating events in the pathogenesis of multiple myeloma (MM) and are assumed to be of clinical significance. Methods. Fluorescence in situ hybridization (FISH) was used to analyze chromosomal architecture in 101 patients with MM. We evaluated overall patient survival and assessed the cytotoxicity of imatinib against MM cells using a CCK8 assay. Results. ABL gene amplification was detected in 67 patients (66.3%). However, ABL gene amplification was not associated with clinical features, cytogenetic abnormalities (c-Myc amplification, IGH rearrangement, RB1 deletion, p53 deletion, or 1q21 amplification), or overall survival. ABL amplification in MM cell lines (LP-1 and U266) was revealed by FISH. Furthermore, the ABL protein was easily detectable in MM cell lines and some tumor cells by western blotting. A CCK8 assay indicated limited cytotoxicity of imatinib against MM cells. Conclusions. Our study firstly discussed ABL gene amplification was prevalent in MM cells, and we believe that the ABL gene would potentially be a useful target in the treatment of combination strategy for MM with ABL amplification in the future.</description><subject>Apoptosis</subject><subject>B cells</subject><subject>Biotechnology industry</subject><subject>Bone marrow</subject><subject>Cell growth</subject><subject>Chemotherapy</subject><subject>Creatinine</subject><subject>DNA damage</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Hospitals</subject><subject>Hybridization</subject><subject>Inhibitor drugs</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Multiple myeloma</subject><subject>Patients</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Software</subject><subject>Targeted cancer therapy</subject><subject>Tumor proteins</subject><subject>Vincristine</subject><issn>1687-8450</issn><issn>1687-8450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp90c1rFDEYBvBBFFurN88S8CLo2nxPchHWUrWwpZd6DtnMm25KJhmTmUr_e2fYtVYPnhLIL0_y8jTNa4I_EiLEKcWUnnJCKCbySXNMpGpXigv89NH-qHlR6y3GkmMtnzdHTDBOORHHzdX5XeggOUA-F7T-vEHrfojBB2fHkBMKCV1OcQxDBHR5DzH3FtnUoesdFDvANAaHLpYbe19fNs-8jRVeHdaT5vuX8-uzb6vN1deLs_Vm5Thj40oyoiy3YCnj1kknKWOARUfkVlChgQulveVaa6LaFlPWbbfUt-C895RoyU6aT_vcYdr20DlIY7HRDCX0ttybbIP5-ySFnbnJd0bpeW7RzgHvDgEl_5igjqYP1UGMNkGeqqGScyZxy8lM3_5Db_NU0jzeopgiDGP9R93YCCYkn-d33RJq1lIr3jKtFvVhr1zJtRbwD18m2Cx9mqVPc-hz5m8ej_mAfxc4g_d7sAupsz_D_-N-AZsnpb4</recordid><startdate>20220315</startdate><enddate>20220315</enddate><creator>Huang, He</creator><creator>Zhou, Shuping</creator><creator>Lin, Hongdou</creator><creator>Guo, Wenjian</creator><creator>Lin, Ying</creator><creator>Yao, Ronxin</creator><creator>He, Licai</creator><creator>Yu, Kang</creator><creator>Li, Qian</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3614-9002</orcidid><orcidid>https://orcid.org/0000-0003-2195-3700</orcidid><orcidid>https://orcid.org/0000-0002-1211-2830</orcidid><orcidid>https://orcid.org/0000-0002-8144-0782</orcidid><orcidid>https://orcid.org/0000-0001-9946-9869</orcidid><orcidid>https://orcid.org/0000-0002-1607-5619</orcidid><orcidid>https://orcid.org/0000-0001-5359-8534</orcidid><orcidid>https://orcid.org/0000-0003-3593-4535</orcidid><orcidid>https://orcid.org/0000-0002-8873-3326</orcidid></search><sort><creationdate>20220315</creationdate><title>Evidence for ABL Amplification in Multiple Myeloma and Therapeutic Implications</title><author>Huang, He ; 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Cytogenetic abnormalities are considered initiating events in the pathogenesis of multiple myeloma (MM) and are assumed to be of clinical significance. Methods. Fluorescence in situ hybridization (FISH) was used to analyze chromosomal architecture in 101 patients with MM. We evaluated overall patient survival and assessed the cytotoxicity of imatinib against MM cells using a CCK8 assay. Results. ABL gene amplification was detected in 67 patients (66.3%). However, ABL gene amplification was not associated with clinical features, cytogenetic abnormalities (c-Myc amplification, IGH rearrangement, RB1 deletion, p53 deletion, or 1q21 amplification), or overall survival. ABL amplification in MM cell lines (LP-1 and U266) was revealed by FISH. Furthermore, the ABL protein was easily detectable in MM cell lines and some tumor cells by western blotting. A CCK8 assay indicated limited cytotoxicity of imatinib against MM cells. Conclusions. Our study firstly discussed ABL gene amplification was prevalent in MM cells, and we believe that the ABL gene would potentially be a useful target in the treatment of combination strategy for MM with ABL amplification in the future.</abstract><cop>Egypt</cop><pub>Hindawi</pub><pmid>35342415</pmid><doi>10.1155/2022/4112016</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-3614-9002</orcidid><orcidid>https://orcid.org/0000-0003-2195-3700</orcidid><orcidid>https://orcid.org/0000-0002-1211-2830</orcidid><orcidid>https://orcid.org/0000-0002-8144-0782</orcidid><orcidid>https://orcid.org/0000-0001-9946-9869</orcidid><orcidid>https://orcid.org/0000-0002-1607-5619</orcidid><orcidid>https://orcid.org/0000-0001-5359-8534</orcidid><orcidid>https://orcid.org/0000-0003-3593-4535</orcidid><orcidid>https://orcid.org/0000-0002-8873-3326</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis B cells Biotechnology industry Bone marrow Cell growth Chemotherapy Creatinine DNA damage Ethylenediaminetetraacetic acid Gene expression Genes Genetic aspects Genomes Health aspects Hospitals Hybridization Inhibitor drugs Kinases Laboratories Medical prognosis Medical research Medicine, Experimental Multiple myeloma Patients Plasma Proteins Software Targeted cancer therapy Tumor proteins Vincristine |
title | Evidence for ABL Amplification in Multiple Myeloma and Therapeutic Implications |
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