Engagement of the CD19 Receptor on Human B-Lineage Leukemia Cells Activates LCK Tyrosine Kinase and Facilitates Radiation-Induced Apoptosis
As presently reported, both ionizing radiation and engagement of the CD19 receptor are capable of inducing apoptosis in B-lineage acute lymphoblastic leukemia (ALL) cells. In both instances, activation of tyrosine kinases appears to be a proximal and mandatory step, since it can be prevented by the...
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| Veröffentlicht in: | Radiation research 1993-12, Vol.136 (3), p.313-319 |
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| container_title | Radiation research |
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| creator | Waddick, Kevin G. Chae, HeonJoo Park Tuel-Ahlgren, Lisa Jarvis, Lisa J. Dibirdik, Ilker Myers, Dorothea E. Uckun, Fatih M. |
| description | As presently reported, both ionizing radiation and engagement of the CD19 receptor are capable of inducing apoptosis in B-lineage acute lymphoblastic leukemia (ALL) cells. In both instances, activation of tyrosine kinases appears to be a proximal and mandatory step, since it can be prevented by the tyrosine kinase inhibitor genistein. This common biochemical signaling pathway involves the rapid activation of the Src family tyrosine kinase LCK ( p56 lck), which is physically associated with the CD19 receptor, and enhanced tyrosine phosphorylation of multiple substrates leading to stimulation of phosphoinositide turnover, and activation of protein kinase C. Importantly, engagement of the CD19 receptor promoted radiation-induced apoptosis in radiation-resistant B-lineage ALL cells in a cell type-specific fashion. Our results prompt the hypothesis that clonogenic B-lineage ALL blasts with an inherent or acquired resistance to radiation could be radiosensitized in clinical settings using anti-CD19 MoAb B43 or its homoconjugate as adjuncts. |
| doi_str_mv | 10.2307/3578542 |
| format | Article |
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In both instances, activation of tyrosine kinases appears to be a proximal and mandatory step, since it can be prevented by the tyrosine kinase inhibitor genistein. This common biochemical signaling pathway involves the rapid activation of the Src family tyrosine kinase LCK ( p56 lck), which is physically associated with the CD19 receptor, and enhanced tyrosine phosphorylation of multiple substrates leading to stimulation of phosphoinositide turnover, and activation of protein kinase C. Importantly, engagement of the CD19 receptor promoted radiation-induced apoptosis in radiation-resistant B-lineage ALL cells in a cell type-specific fashion. Our results prompt the hypothesis that clonogenic B-lineage ALL blasts with an inherent or acquired resistance to radiation could be radiosensitized in clinical settings using anti-CD19 MoAb B43 or its homoconjugate as adjuncts.</description><identifier>ISSN: 0033-7587</identifier><identifier>EISSN: 1938-5404</identifier><identifier>DOI: 10.2307/3578542</identifier><identifier>PMID: 7506428</identifier><identifier>CODEN: RAREAE</identifier><language>eng</language><publisher>Oak Brook, Il: Academic Press, Inc</publisher><subject>Antigens, CD - physiology ; Antigens, CD19 ; Antigens, Differentiation, B-Lymphocyte - physiology ; Apoptosis ; Apoptosis - radiation effects ; B lymphocytes ; Biological and medical sciences ; Blasts ; Burkitt Lymphoma - enzymology ; Burkitt Lymphoma - pathology ; Cell lines ; DNA ; Enzyme Activation ; Ionizing radiation ; Leukemia ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Lymphocytic leukemia ; Medical sciences ; Protein-Tyrosine Kinases - metabolism ; Proto-Oncogene Proteins - metabolism ; Radiation therapy and radiosensitizing agent ; Radiation Tolerance ; Receptors ; Space life sciences ; Symposium: Apoptosis/Programmed Cell Death ; Treatment with physical agents ; Treatment. 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In both instances, activation of tyrosine kinases appears to be a proximal and mandatory step, since it can be prevented by the tyrosine kinase inhibitor genistein. This common biochemical signaling pathway involves the rapid activation of the Src family tyrosine kinase LCK ( p56 lck), which is physically associated with the CD19 receptor, and enhanced tyrosine phosphorylation of multiple substrates leading to stimulation of phosphoinositide turnover, and activation of protein kinase C. Importantly, engagement of the CD19 receptor promoted radiation-induced apoptosis in radiation-resistant B-lineage ALL cells in a cell type-specific fashion. Our results prompt the hypothesis that clonogenic B-lineage ALL blasts with an inherent or acquired resistance to radiation could be radiosensitized in clinical settings using anti-CD19 MoAb B43 or its homoconjugate as adjuncts.</description><subject>Antigens, CD - physiology</subject><subject>Antigens, CD19</subject><subject>Antigens, Differentiation, B-Lymphocyte - physiology</subject><subject>Apoptosis</subject><subject>Apoptosis - radiation effects</subject><subject>B lymphocytes</subject><subject>Biological and medical sciences</subject><subject>Blasts</subject><subject>Burkitt Lymphoma - enzymology</subject><subject>Burkitt Lymphoma - pathology</subject><subject>Cell lines</subject><subject>DNA</subject><subject>Enzyme Activation</subject><subject>Ionizing radiation</subject><subject>Leukemia</subject><subject>Lymphocyte Specific Protein Tyrosine Kinase p56(lck)</subject><subject>Lymphocytic leukemia</subject><subject>Medical sciences</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Radiation therapy and radiosensitizing agent</subject><subject>Radiation Tolerance</subject><subject>Receptors</subject><subject>Space life sciences</subject><subject>Symposium: Apoptosis/Programmed Cell Death</subject><subject>Treatment with physical agents</subject><subject>Treatment. General aspects</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0033-7587</issn><issn>1938-5404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MtO3TAQBmALtaIHiniCSl5UZZXWjmM7WR5SbiJSJUTX0cQZg2ninMZOJZ6Bl66BiK668ljzaUbzE3LM2ddcMP1NSF3KIt8jG16JMpMFK96RDWNCZFqW-gM5COGBpT9X1T7Z15KpIi835OnM38EdjugjnSyN90jr77yiN2hwF6eZTp5eLiN4epo1zmOytMHlF44OaI3DEOjWRPcHIgba1Nf09nGeQoL02nkISMH39ByMG1x8MTfQO4hu8tmV7xeDPd3uprQpuPCRvLcwBDxa30Py8_zstr7Mmh8XV_W2yUyRVzHTFkVnDetUp1SfKs6NtJ00VY-yZMZwrSCXwigrFRYcGEDeKW25RqYlikPy5XXubp5-LxhiO7pg0i3gcVpCqxWXQsgywZNXaNJNYUbb7mY3wvzYctY-x96usSf5aR25dCP2b27NOfU_r30IBgY7gzcuvLGCK8Vk8Y89hJT9f7f9BUxAlTk</recordid><startdate>19931201</startdate><enddate>19931201</enddate><creator>Waddick, Kevin G.</creator><creator>Chae, HeonJoo Park</creator><creator>Tuel-Ahlgren, Lisa</creator><creator>Jarvis, Lisa J.</creator><creator>Dibirdik, Ilker</creator><creator>Myers, Dorothea E.</creator><creator>Uckun, Fatih M.</creator><general>Academic Press, Inc</general><general>Radiation Research Society</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>19931201</creationdate><title>Engagement of the CD19 Receptor on Human B-Lineage Leukemia Cells Activates LCK Tyrosine Kinase and Facilitates Radiation-Induced Apoptosis</title><author>Waddick, Kevin G. ; Chae, HeonJoo Park ; Tuel-Ahlgren, Lisa ; Jarvis, Lisa J. ; Dibirdik, Ilker ; Myers, Dorothea E. ; Uckun, Fatih M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c429t-7fe3bfc0b6b66dbfc11c5fb5c9de580cc176a253c6f56e41a0aa2b67f17e075e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Antigens, CD - physiology</topic><topic>Antigens, CD19</topic><topic>Antigens, Differentiation, B-Lymphocyte - physiology</topic><topic>Apoptosis</topic><topic>Apoptosis - radiation effects</topic><topic>B lymphocytes</topic><topic>Biological and medical sciences</topic><topic>Blasts</topic><topic>Burkitt Lymphoma - enzymology</topic><topic>Burkitt Lymphoma - pathology</topic><topic>Cell lines</topic><topic>DNA</topic><topic>Enzyme Activation</topic><topic>Ionizing radiation</topic><topic>Leukemia</topic><topic>Lymphocyte Specific Protein Tyrosine Kinase p56(lck)</topic><topic>Lymphocytic leukemia</topic><topic>Medical sciences</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Radiation therapy and radiosensitizing agent</topic><topic>Radiation Tolerance</topic><topic>Receptors</topic><topic>Space life sciences</topic><topic>Symposium: Apoptosis/Programmed Cell Death</topic><topic>Treatment with physical agents</topic><topic>Treatment. General aspects</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Waddick, Kevin G.</creatorcontrib><creatorcontrib>Chae, HeonJoo Park</creatorcontrib><creatorcontrib>Tuel-Ahlgren, Lisa</creatorcontrib><creatorcontrib>Jarvis, Lisa J.</creatorcontrib><creatorcontrib>Dibirdik, Ilker</creatorcontrib><creatorcontrib>Myers, Dorothea E.</creatorcontrib><creatorcontrib>Uckun, Fatih M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Radiation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Waddick, Kevin G.</au><au>Chae, HeonJoo Park</au><au>Tuel-Ahlgren, Lisa</au><au>Jarvis, Lisa J.</au><au>Dibirdik, Ilker</au><au>Myers, Dorothea E.</au><au>Uckun, Fatih M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Engagement of the CD19 Receptor on Human B-Lineage Leukemia Cells Activates LCK Tyrosine Kinase and Facilitates Radiation-Induced Apoptosis</atitle><jtitle>Radiation research</jtitle><addtitle>Radiat Res</addtitle><date>1993-12-01</date><risdate>1993</risdate><volume>136</volume><issue>3</issue><spage>313</spage><epage>319</epage><pages>313-319</pages><issn>0033-7587</issn><eissn>1938-5404</eissn><coden>RAREAE</coden><abstract>As presently reported, both ionizing radiation and engagement of the CD19 receptor are capable of inducing apoptosis in B-lineage acute lymphoblastic leukemia (ALL) cells. In both instances, activation of tyrosine kinases appears to be a proximal and mandatory step, since it can be prevented by the tyrosine kinase inhibitor genistein. This common biochemical signaling pathway involves the rapid activation of the Src family tyrosine kinase LCK ( p56 lck), which is physically associated with the CD19 receptor, and enhanced tyrosine phosphorylation of multiple substrates leading to stimulation of phosphoinositide turnover, and activation of protein kinase C. Importantly, engagement of the CD19 receptor promoted radiation-induced apoptosis in radiation-resistant B-lineage ALL cells in a cell type-specific fashion. Our results prompt the hypothesis that clonogenic B-lineage ALL blasts with an inherent or acquired resistance to radiation could be radiosensitized in clinical settings using anti-CD19 MoAb B43 or its homoconjugate as adjuncts.</abstract><cop>Oak Brook, Il</cop><pub>Academic Press, Inc</pub><pmid>7506428</pmid><doi>10.2307/3578542</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0033-7587 |
| ispartof | Radiation research, 1993-12, Vol.136 (3), p.313-319 |
| issn | 0033-7587 1938-5404 |
| language | eng |
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| source | Jstor Complete Legacy; MEDLINE |
| subjects | Antigens, CD - physiology Antigens, CD19 Antigens, Differentiation, B-Lymphocyte - physiology Apoptosis Apoptosis - radiation effects B lymphocytes Biological and medical sciences Blasts Burkitt Lymphoma - enzymology Burkitt Lymphoma - pathology Cell lines DNA Enzyme Activation Ionizing radiation Leukemia Lymphocyte Specific Protein Tyrosine Kinase p56(lck) Lymphocytic leukemia Medical sciences Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins - metabolism Radiation therapy and radiosensitizing agent Radiation Tolerance Receptors Space life sciences Symposium: Apoptosis/Programmed Cell Death Treatment with physical agents Treatment. General aspects Tumor Cells, Cultured Tumors |
| title | Engagement of the CD19 Receptor on Human B-Lineage Leukemia Cells Activates LCK Tyrosine Kinase and Facilitates Radiation-Induced Apoptosis |
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