Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia
The most common human leukemia is B cell chronic lymphocytic leukemia (CLL), a malignancy of mature B cells with a characteristic clinical presentation but a variable clinical course. The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequence or somatically mutated. La...
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| Veröffentlicht in: | The Journal of experimental medicine 2001-12, Vol.194 (11), p.1639-1647 |
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| creator | Rosenwald, A Alizadeh, A A Widhopf, G Simon, R Davis, R E Yu, X Yang, L Pickeral, O K Rassenti, L Z Powell, J Botstein, D Byrd, J C Grever, M R Cheson, B D Chiorazzi, N Wilson, W H Kipps, T J Brown, P O Staudt, L M |
| description | The most common human leukemia is B cell chronic lymphocytic leukemia (CLL), a malignancy of mature B cells with a characteristic clinical presentation but a variable clinical course. The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequence or somatically mutated. Lack of Ig mutations defined a distinctly worse prognostic group of CLL patients raising the possibility that CLL comprises two distinct diseases. Using genomic-scale gene expression profiling, we show that CLL is characterized by a common gene expression "signature," irrespective of Ig mutational status, suggesting that CLL cases share a common mechanism of transformation and/or cell of origin. Nonetheless, the expression of hundreds of other genes correlated with the Ig mutational status, including many genes that are modulated in expression during mitogenic B cell receptor signaling. These genes were used to build a CLL subtype predictor that may help in the clinical classification of patients with this disease. |
| doi_str_mv | 10.1084/jem.194.11.1639 |
| format | Article |
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The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequence or somatically mutated. Lack of Ig mutations defined a distinctly worse prognostic group of CLL patients raising the possibility that CLL comprises two distinct diseases. Using genomic-scale gene expression profiling, we show that CLL is characterized by a common gene expression "signature," irrespective of Ig mutational status, suggesting that CLL cases share a common mechanism of transformation and/or cell of origin. Nonetheless, the expression of hundreds of other genes correlated with the Ig mutational status, including many genes that are modulated in expression during mitogenic B cell receptor signaling. These genes were used to build a CLL subtype predictor that may help in the clinical classification of patients with this disease.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.194.11.1639</identifier><identifier>PMID: 11733578</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Gene Expression ; Genotype ; Humans ; Immunoglobulins - genetics ; Immunophenotyping ; Leukemia, Lymphocytic, Chronic, B-Cell - genetics ; Mutation ; Original</subject><ispartof>The Journal of experimental medicine, 2001-12, Vol.194 (11), p.1639-1647</ispartof><rights>Copyright © 2001, The Rockefeller University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-d58132d98bfda00cd98e05019ce8dbe844552d4f83592d9f6341501d8f242ce3</citedby><cites>FETCH-LOGICAL-c486t-d58132d98bfda00cd98e05019ce8dbe844552d4f83592d9f6341501d8f242ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11733578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rosenwald, A</creatorcontrib><creatorcontrib>Alizadeh, A A</creatorcontrib><creatorcontrib>Widhopf, G</creatorcontrib><creatorcontrib>Simon, R</creatorcontrib><creatorcontrib>Davis, R E</creatorcontrib><creatorcontrib>Yu, X</creatorcontrib><creatorcontrib>Yang, L</creatorcontrib><creatorcontrib>Pickeral, O K</creatorcontrib><creatorcontrib>Rassenti, L Z</creatorcontrib><creatorcontrib>Powell, J</creatorcontrib><creatorcontrib>Botstein, D</creatorcontrib><creatorcontrib>Byrd, J C</creatorcontrib><creatorcontrib>Grever, M R</creatorcontrib><creatorcontrib>Cheson, B D</creatorcontrib><creatorcontrib>Chiorazzi, N</creatorcontrib><creatorcontrib>Wilson, W H</creatorcontrib><creatorcontrib>Kipps, T J</creatorcontrib><creatorcontrib>Brown, P O</creatorcontrib><creatorcontrib>Staudt, L M</creatorcontrib><title>Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>The most common human leukemia is B cell chronic lymphocytic leukemia (CLL), a malignancy of mature B cells with a characteristic clinical presentation but a variable clinical course. The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequence or somatically mutated. Lack of Ig mutations defined a distinctly worse prognostic group of CLL patients raising the possibility that CLL comprises two distinct diseases. Using genomic-scale gene expression profiling, we show that CLL is characterized by a common gene expression "signature," irrespective of Ig mutational status, suggesting that CLL cases share a common mechanism of transformation and/or cell of origin. Nonetheless, the expression of hundreds of other genes correlated with the Ig mutational status, including many genes that are modulated in expression during mitogenic B cell receptor signaling. These genes were used to build a CLL subtype predictor that may help in the clinical classification of patients with this disease.</description><subject>Gene Expression</subject><subject>Genotype</subject><subject>Humans</subject><subject>Immunoglobulins - genetics</subject><subject>Immunophenotyping</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</subject><subject>Mutation</subject><subject>Original</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctr3DAQxkVpaTaPc29Fp9680eixli-BNuRRCARK7sIrj3eVWpJj2SH730dmt216yknDzG8-5tNHyBdgS2Banj-iX0IllwBLWInqA1mAkqyolNAfyYIxzgtgrDwixyk9MgZSqtVncgRQCqFKvSD9L-zq0cVAY0s3GJDiSz9gSnOr32KI465HOkbqvJ9C3HRxPXUuUD-N-73NHyY3f1CLXUftdojBWdrtfL-NdjfONU6_0bv6lHxq6y7h2eE9IQ_XVw-Xt8Xd_c3Py-93hZV6NRaN0iB4U-l129SM2VwhUwwqi7pZo85GFG9kq4WqMtauhIQ8bnTLJbcoTsjFXraf1h4bi2Ec6s70g_P1sDOxdub_SXBbs4nPhkMlFBdZ4NtBYIhPE6bReJdmd3XAOCVTcsHL-R_fA0HzUrKyyuD5HrRDTGnA9u81wMycpslpmpymATBzmnnj61sT__hDfOIVdmae8w</recordid><startdate>20011203</startdate><enddate>20011203</enddate><creator>Rosenwald, A</creator><creator>Alizadeh, A A</creator><creator>Widhopf, G</creator><creator>Simon, R</creator><creator>Davis, R E</creator><creator>Yu, X</creator><creator>Yang, L</creator><creator>Pickeral, O K</creator><creator>Rassenti, L Z</creator><creator>Powell, J</creator><creator>Botstein, D</creator><creator>Byrd, J C</creator><creator>Grever, M R</creator><creator>Cheson, B D</creator><creator>Chiorazzi, N</creator><creator>Wilson, W H</creator><creator>Kipps, T J</creator><creator>Brown, P O</creator><creator>Staudt, L M</creator><general>The Rockefeller University Press</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>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20011203</creationdate><title>Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia</title><author>Rosenwald, A ; Alizadeh, A A ; Widhopf, G ; Simon, R ; Davis, R E ; Yu, X ; Yang, L ; Pickeral, O K ; Rassenti, L Z ; Powell, J ; Botstein, D ; Byrd, J C ; Grever, M R ; Cheson, B D ; Chiorazzi, N ; Wilson, W H ; Kipps, T J ; Brown, P O ; Staudt, L M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-d58132d98bfda00cd98e05019ce8dbe844552d4f83592d9f6341501d8f242ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Gene Expression</topic><topic>Genotype</topic><topic>Humans</topic><topic>Immunoglobulins - genetics</topic><topic>Immunophenotyping</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</topic><topic>Mutation</topic><topic>Original</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rosenwald, A</creatorcontrib><creatorcontrib>Alizadeh, A A</creatorcontrib><creatorcontrib>Widhopf, G</creatorcontrib><creatorcontrib>Simon, R</creatorcontrib><creatorcontrib>Davis, R E</creatorcontrib><creatorcontrib>Yu, X</creatorcontrib><creatorcontrib>Yang, L</creatorcontrib><creatorcontrib>Pickeral, O K</creatorcontrib><creatorcontrib>Rassenti, L Z</creatorcontrib><creatorcontrib>Powell, J</creatorcontrib><creatorcontrib>Botstein, D</creatorcontrib><creatorcontrib>Byrd, J C</creatorcontrib><creatorcontrib>Grever, M R</creatorcontrib><creatorcontrib>Cheson, B D</creatorcontrib><creatorcontrib>Chiorazzi, N</creatorcontrib><creatorcontrib>Wilson, W H</creatorcontrib><creatorcontrib>Kipps, T J</creatorcontrib><creatorcontrib>Brown, P O</creatorcontrib><creatorcontrib>Staudt, L M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rosenwald, A</au><au>Alizadeh, A A</au><au>Widhopf, G</au><au>Simon, R</au><au>Davis, R E</au><au>Yu, X</au><au>Yang, L</au><au>Pickeral, O K</au><au>Rassenti, L Z</au><au>Powell, J</au><au>Botstein, D</au><au>Byrd, J C</au><au>Grever, M R</au><au>Cheson, B D</au><au>Chiorazzi, N</au><au>Wilson, W H</au><au>Kipps, T J</au><au>Brown, P O</au><au>Staudt, L M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2001-12-03</date><risdate>2001</risdate><volume>194</volume><issue>11</issue><spage>1639</spage><epage>1647</epage><pages>1639-1647</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>The most common human leukemia is B cell chronic lymphocytic leukemia (CLL), a malignancy of mature B cells with a characteristic clinical presentation but a variable clinical course. The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequence or somatically mutated. Lack of Ig mutations defined a distinctly worse prognostic group of CLL patients raising the possibility that CLL comprises two distinct diseases. Using genomic-scale gene expression profiling, we show that CLL is characterized by a common gene expression "signature," irrespective of Ig mutational status, suggesting that CLL cases share a common mechanism of transformation and/or cell of origin. Nonetheless, the expression of hundreds of other genes correlated with the Ig mutational status, including many genes that are modulated in expression during mitogenic B cell receptor signaling. 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| subjects | Gene Expression Genotype Humans Immunoglobulins - genetics Immunophenotyping Leukemia, Lymphocytic, Chronic, B-Cell - genetics Mutation Original |
| title | Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia |
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