Protein expression analysis of chromosome 12 candidate genes in chronic lymphocytic leukemia (CLL)
The pathogenic role of trisomy 12 in chronic lymphocytic leukemia (CLL) remains unresolved, but recently an upregulated RNA expression level has been observed for chromosome 12 candidate genes. In the current study, the protein expression of chromosome 12 candidate genes was characterized by compari...
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| Veröffentlicht in: | Leukemia 2005-07, Vol.19 (7), p.1211-1215 |
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| creator | WINKLER, D SCHNEIDER, C KRÖBER, A PASQUALUCCI, L LICHTER, P DÖHNER, H STILGENBAUER, S |
| description | The pathogenic role of trisomy 12 in chronic lymphocytic leukemia (CLL) remains unresolved, but recently an upregulated RNA expression level has been observed for chromosome 12 candidate genes. In the current study, the protein expression of chromosome 12 candidate genes was characterized by comparing CLL cases with (n=58) or without (n=16) trisomy 12, CD19+-B-cells and cell lines (JVM-2, EHEB, JURKAT). Immunoblotting was performed to quantify the levels of AID, APAF-1, ARF3, CCND2, CDK2, CKD4, GLI, MDM-2, p27, Smac/DIABLO and STAT6 (signal transducer and activator of transcription 6). The cell lines showed distinct expression patterns for CCND2, MDM-2, p27, Smac/DIABLO and STAT6, and displayed higher levels of CDK2 and CDK4 than the CLL cases. JURKAT and the CLL cases expressed uniformly high levels of p27, but low levels of CCND2. AID expression in the CLL cases was weak with slight variations regardless of the subgroup affiliation. The expression of the investigated proteins was independent of the trisomy 12 status as well as of the VH mutation status. The comparison of CD19+-B-cells with CLL revealed higher protein levels in CLL for CDK4, p27, Smac/DIABLO and STAT6. Further studies including protein expression experiments in genetic high-risk subgroups of CLL have to elucidate whether these proteins qualify as candidates for targeted CLL therapies. |
| doi_str_mv | 10.1038/sj.leu.2403778 |
| format | Article |
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In the current study, the protein expression of chromosome 12 candidate genes was characterized by comparing CLL cases with (n=58) or without (n=16) trisomy 12, CD19+-B-cells and cell lines (JVM-2, EHEB, JURKAT). Immunoblotting was performed to quantify the levels of AID, APAF-1, ARF3, CCND2, CDK2, CKD4, GLI, MDM-2, p27, Smac/DIABLO and STAT6 (signal transducer and activator of transcription 6). The cell lines showed distinct expression patterns for CCND2, MDM-2, p27, Smac/DIABLO and STAT6, and displayed higher levels of CDK2 and CDK4 than the CLL cases. JURKAT and the CLL cases expressed uniformly high levels of p27, but low levels of CCND2. AID expression in the CLL cases was weak with slight variations regardless of the subgroup affiliation. The expression of the investigated proteins was independent of the trisomy 12 status as well as of the VH mutation status. The comparison of CD19+-B-cells with CLL revealed higher protein levels in CLL for CDK4, p27, Smac/DIABLO and STAT6. Further studies including protein expression experiments in genetic high-risk subgroups of CLL have to elucidate whether these proteins qualify as candidates for targeted CLL therapies.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/sj.leu.2403778</identifier><identifier>PMID: 15902296</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing</publisher><subject>Antigens, CD19 - biosynthesis ; Apaf-1 protein ; Biological and medical sciences ; CD19 antigen ; Cell Line, Tumor ; Chromosome 12 ; Chromosomes ; Chromosomes, Human, Pair 12 - genetics ; Chronic lymphocytic leukemia ; Compilers ; Cyclin-dependent kinase 2 ; Cyclin-dependent kinase 4 ; DIABLO protein ; Gene expression ; Genes ; Hematologic and hematopoietic diseases ; Humans ; Immunoblotting ; Leukemia ; Leukemia, Lymphocytic, Chronic, B-Cell - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphatic leukemia ; Lymphocytes B ; Medical sciences ; Molecular Weight ; Mutation ; Protein expression ; Proteins ; Proto-Oncogene Proteins - analysis ; Proto-Oncogene Proteins - biosynthesis ; Proto-Oncogene Proteins - genetics ; Risk groups ; Stat6 protein ; Subgroups ; Transcription ; Trisomy</subject><ispartof>Leukemia, 2005-07, Vol.19 (7), p.1211-1215</ispartof><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2005</rights><rights>Nature Publishing Group 2005.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c604t-ff943f0f1f06eb041fe11b72cb5e3bbaae71b8f0186daeb97e2b211c1415d1453</citedby><cites>FETCH-LOGICAL-c604t-ff943f0f1f06eb041fe11b72cb5e3bbaae71b8f0186daeb97e2b211c1415d1453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,2728,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16897211$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15902296$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WINKLER, D</creatorcontrib><creatorcontrib>SCHNEIDER, C</creatorcontrib><creatorcontrib>KRÖBER, A</creatorcontrib><creatorcontrib>PASQUALUCCI, L</creatorcontrib><creatorcontrib>LICHTER, P</creatorcontrib><creatorcontrib>DÖHNER, H</creatorcontrib><creatorcontrib>STILGENBAUER, S</creatorcontrib><title>Protein expression analysis of chromosome 12 candidate genes in chronic lymphocytic leukemia (CLL)</title><title>Leukemia</title><addtitle>Leukemia</addtitle><description>The pathogenic role of trisomy 12 in chronic lymphocytic leukemia (CLL) remains unresolved, but recently an upregulated RNA expression level has been observed for chromosome 12 candidate genes. In the current study, the protein expression of chromosome 12 candidate genes was characterized by comparing CLL cases with (n=58) or without (n=16) trisomy 12, CD19+-B-cells and cell lines (JVM-2, EHEB, JURKAT). Immunoblotting was performed to quantify the levels of AID, APAF-1, ARF3, CCND2, CDK2, CKD4, GLI, MDM-2, p27, Smac/DIABLO and STAT6 (signal transducer and activator of transcription 6). The cell lines showed distinct expression patterns for CCND2, MDM-2, p27, Smac/DIABLO and STAT6, and displayed higher levels of CDK2 and CDK4 than the CLL cases. JURKAT and the CLL cases expressed uniformly high levels of p27, but low levels of CCND2. AID expression in the CLL cases was weak with slight variations regardless of the subgroup affiliation. The expression of the investigated proteins was independent of the trisomy 12 status as well as of the VH mutation status. The comparison of CD19+-B-cells with CLL revealed higher protein levels in CLL for CDK4, p27, Smac/DIABLO and STAT6. Further studies including protein expression experiments in genetic high-risk subgroups of CLL have to elucidate whether these proteins qualify as candidates for targeted CLL therapies.</description><subject>Antigens, CD19 - biosynthesis</subject><subject>Apaf-1 protein</subject><subject>Biological and medical sciences</subject><subject>CD19 antigen</subject><subject>Cell Line, Tumor</subject><subject>Chromosome 12</subject><subject>Chromosomes</subject><subject>Chromosomes, Human, Pair 12 - genetics</subject><subject>Chronic lymphocytic leukemia</subject><subject>Compilers</subject><subject>Cyclin-dependent kinase 2</subject><subject>Cyclin-dependent kinase 4</subject><subject>DIABLO protein</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Leukemia</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphatic leukemia</subject><subject>Lymphocytes B</subject><subject>Medical sciences</subject><subject>Molecular Weight</subject><subject>Mutation</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - analysis</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Risk groups</subject><subject>Stat6 protein</subject><subject>Subgroups</subject><subject>Transcription</subject><subject>Trisomy</subject><issn>0887-6924</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1ksuP0zAQxiMEYsvClRsoArGCQ4vt-JXjquIlVYIDnC3HGW9dErt4Eon-97jawi5okQ-2xr_vG82jqp5SsqKk0W9xtxpgXjFOGqX0vWpBuZJLIQS9Xy2I1mopW8bPqkeIO0KOn_JhdUZFSxhr5aLqvuQ0QYg1_NxnQAwp1jba4YAB6-Rrt81pTJhGqCmrnY196O0E9RVEwLrojkAMrh4O436b3GE6vmH-DmOw9ev1ZvPmcfXA2wHhyek-r769f_d1_XG5-fzh0_pys3SS8GnpfcsbTzz1REJHOPVAaaeY6wQ0XWctKNppT6iWvYWuVcA6RqmjnIqectGcVxfXvvucfsyAkxkDOhgGGyHNaKTmjdKqLeDLf8BdmnMpGg2TXCgqBFOFevFfihHRUE1uWV3ZAUyIPk3ZumNec0m1Foy3sinU6g6qnL50yaUIPpT4X4KLW4It2GHaYhrmqYwH73R2OSFm8Gafw2jzwVBijgticGfKOMxpQYrg-amquRuhv8FPG1GAVyfAorODzza6gDec1K0qbS_cs2su2mnO8Af4negXnAXK8w</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>WINKLER, D</creator><creator>SCHNEIDER, C</creator><creator>KRÖBER, A</creator><creator>PASQUALUCCI, L</creator><creator>LICHTER, P</creator><creator>DÖHNER, H</creator><creator>STILGENBAUER, S</creator><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7QL</scope><scope>7RV</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20050701</creationdate><title>Protein expression analysis of chromosome 12 candidate genes in chronic lymphocytic leukemia (CLL)</title><author>WINKLER, D ; SCHNEIDER, C ; KRÖBER, A ; PASQUALUCCI, L ; LICHTER, P ; DÖHNER, H ; STILGENBAUER, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c604t-ff943f0f1f06eb041fe11b72cb5e3bbaae71b8f0186daeb97e2b211c1415d1453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Antigens, CD19 - biosynthesis</topic><topic>Apaf-1 protein</topic><topic>Biological and medical sciences</topic><topic>CD19 antigen</topic><topic>Cell Line, Tumor</topic><topic>Chromosome 12</topic><topic>Chromosomes</topic><topic>Chromosomes, Human, Pair 12 - genetics</topic><topic>Chronic lymphocytic leukemia</topic><topic>Compilers</topic><topic>Cyclin-dependent kinase 2</topic><topic>Cyclin-dependent kinase 4</topic><topic>DIABLO protein</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Leukemia</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphatic leukemia</topic><topic>Lymphocytes B</topic><topic>Medical sciences</topic><topic>Molecular Weight</topic><topic>Mutation</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - analysis</topic><topic>Proto-Oncogene Proteins - biosynthesis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Risk groups</topic><topic>Stat6 protein</topic><topic>Subgroups</topic><topic>Transcription</topic><topic>Trisomy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WINKLER, D</creatorcontrib><creatorcontrib>SCHNEIDER, C</creatorcontrib><creatorcontrib>KRÖBER, A</creatorcontrib><creatorcontrib>PASQUALUCCI, L</creatorcontrib><creatorcontrib>LICHTER, P</creatorcontrib><creatorcontrib>DÖHNER, H</creatorcontrib><creatorcontrib>STILGENBAUER, S</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>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Leukemia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WINKLER, D</au><au>SCHNEIDER, C</au><au>KRÖBER, A</au><au>PASQUALUCCI, L</au><au>LICHTER, P</au><au>DÖHNER, H</au><au>STILGENBAUER, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protein expression analysis of chromosome 12 candidate genes in chronic lymphocytic leukemia (CLL)</atitle><jtitle>Leukemia</jtitle><addtitle>Leukemia</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>19</volume><issue>7</issue><spage>1211</spage><epage>1215</epage><pages>1211-1215</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><coden>LEUKED</coden><abstract>The pathogenic role of trisomy 12 in chronic lymphocytic leukemia (CLL) remains unresolved, but recently an upregulated RNA expression level has been observed for chromosome 12 candidate genes. In the current study, the protein expression of chromosome 12 candidate genes was characterized by comparing CLL cases with (n=58) or without (n=16) trisomy 12, CD19+-B-cells and cell lines (JVM-2, EHEB, JURKAT). Immunoblotting was performed to quantify the levels of AID, APAF-1, ARF3, CCND2, CDK2, CKD4, GLI, MDM-2, p27, Smac/DIABLO and STAT6 (signal transducer and activator of transcription 6). The cell lines showed distinct expression patterns for CCND2, MDM-2, p27, Smac/DIABLO and STAT6, and displayed higher levels of CDK2 and CDK4 than the CLL cases. JURKAT and the CLL cases expressed uniformly high levels of p27, but low levels of CCND2. AID expression in the CLL cases was weak with slight variations regardless of the subgroup affiliation. The expression of the investigated proteins was independent of the trisomy 12 status as well as of the VH mutation status. The comparison of CD19+-B-cells with CLL revealed higher protein levels in CLL for CDK4, p27, Smac/DIABLO and STAT6. Further studies including protein expression experiments in genetic high-risk subgroups of CLL have to elucidate whether these proteins qualify as candidates for targeted CLL therapies.</abstract><cop>London</cop><pub>Nature Publishing</pub><pmid>15902296</pmid><doi>10.1038/sj.leu.2403778</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antigens, CD19 - biosynthesis Apaf-1 protein Biological and medical sciences CD19 antigen Cell Line, Tumor Chromosome 12 Chromosomes Chromosomes, Human, Pair 12 - genetics Chronic lymphocytic leukemia Compilers Cyclin-dependent kinase 2 Cyclin-dependent kinase 4 DIABLO protein Gene expression Genes Hematologic and hematopoietic diseases Humans Immunoblotting Leukemia Leukemia, Lymphocytic, Chronic, B-Cell - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphatic leukemia Lymphocytes B Medical sciences Molecular Weight Mutation Protein expression Proteins Proto-Oncogene Proteins - analysis Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins - genetics Risk groups Stat6 protein Subgroups Transcription Trisomy |
| title | Protein expression analysis of chromosome 12 candidate genes in chronic lymphocytic leukemia (CLL) |
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