Overexpression of the p73 gene is a novel finding in high-risk B-cell chronic lymphocytic leukemia
The p73 protein shares structural and functional similarities with the tumour-suppressor p53, but its role in neoplastic transformation is unknown. Alternative splicing leads to the expression of at least nine p73 C-terminal mRNA splice variants (α β γ δ ε ξ η ηl θ). In this survey, we analyse the e...
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| Veröffentlicht in: | Annals of oncology 2001-07, Vol.12 (7), p.981-986 |
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| creator | Novak, U. Grob, T. J. Baskaynak, G. Peters, U. R. Aebi, S. Zwahlen, D. Tschan, M. P. Kreuzer, K.-A. Leibundgut, E. Oppliger Cajot, J.-F. Tobler, A. Fey, M. F. |
| description | The p73 protein shares structural and functional similarities with the tumour-suppressor p53, but its role in neoplastic transformation is unknown. Alternative splicing leads to the expression of at least nine p73 C-terminal mRNA splice variants (α β γ δ ε ξ η ηl θ). In this survey, we analyse the expression of p73 by real-time quantitative RT-PCR, its known C-terminal variants with an RT-PCR-Southern tech nique and by Western blot in samples of 51 patients with B-CLL, normal B lymphocytes from eight individuals, and five haematopoetic cell lines. p73α protein expression positively correlated with higher risk B-CLL stages (P=0.046). Total p73 mRNA expression was higher (P= 0.01) and p73α protein more frequently detected (P=0.008) in B-CLL compared with normal CD19+—B-lymphocytes. p73 C-terminal mRNA variants were expressed both in B-CLL and in normal B-lymphocytes, but their expression was biased since the γ (P=0.041), the θ (P ≪ 0.001), and the η variant (P=0.033) prevailed in normal B-lymphocytes. In summary, we conclude that the accumulation of p73, the expression pattern of particular p73 variants and its link to progression may play a distinct role in the molecular pathology B-CLL. |
| doi_str_mv | 10.1023/A:1011153206003 |
| format | Article |
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J. ; Baskaynak, G. ; Peters, U. R. ; Aebi, S. ; Zwahlen, D. ; Tschan, M. P. ; Kreuzer, K.-A. ; Leibundgut, E. Oppliger ; Cajot, J.-F. ; Tobler, A. ; Fey, M. F.</creator><creatorcontrib>Novak, U. ; Grob, T. J. ; Baskaynak, G. ; Peters, U. R. ; Aebi, S. ; Zwahlen, D. ; Tschan, M. P. ; Kreuzer, K.-A. ; Leibundgut, E. Oppliger ; Cajot, J.-F. ; Tobler, A. ; Fey, M. F.</creatorcontrib><description>The p73 protein shares structural and functional similarities with the tumour-suppressor p53, but its role in neoplastic transformation is unknown. Alternative splicing leads to the expression of at least nine p73 C-terminal mRNA splice variants (α β γ δ ε ξ η ηl θ). In this survey, we analyse the expression of p73 by real-time quantitative RT-PCR, its known C-terminal variants with an RT-PCR-Southern tech nique and by Western blot in samples of 51 patients with B-CLL, normal B lymphocytes from eight individuals, and five haematopoetic cell lines. p73α protein expression positively correlated with higher risk B-CLL stages (P=0.046). Total p73 mRNA expression was higher (P= 0.01) and p73α protein more frequently detected (P=0.008) in B-CLL compared with normal CD19+—B-lymphocytes. p73 C-terminal mRNA variants were expressed both in B-CLL and in normal B-lymphocytes, but their expression was biased since the γ (P=0.041), the θ (P ≪ 0.001), and the η variant (P=0.033) prevailed in normal B-lymphocytes. In summary, we conclude that the accumulation of p73, the expression pattern of particular p73 variants and its link to progression may play a distinct role in the molecular pathology B-CLL.</description><identifier>ISSN: 0923-7534</identifier><identifier>EISSN: 1569-8041</identifier><identifier>DOI: 10.1023/A:1011153206003</identifier><identifier>PMID: 11521806</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Apoptosis ; B-CLL ; Biological and medical sciences ; Biomarkers, Tumor - analysis ; Biomarkers, Tumor - genetics ; Blotting, Western ; DNA-Binding Proteins - analysis ; DNA-Binding Proteins - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Hematologic and hematopoietic diseases ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell - genetics ; Leukemia, Lymphocytic, Chronic, B-Cell - metabolism ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Middle Aged ; Nuclear Proteins - analysis ; Nuclear Proteins - genetics ; overexpression ; p53 ; p73 ; Reverse Transcriptase Polymerase Chain Reaction ; Risk Factors ; Tumor Protein p73 ; Tumor Suppressor Proteins ; Up-Regulation</subject><ispartof>Annals of oncology, 2001-07, Vol.12 (7), p.981-986</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-71650a069ce17c9a312b96a507b44c31a5eb8eabf0d306980feaa7545e59b8813</citedby><cites>FETCH-LOGICAL-c401t-71650a069ce17c9a312b96a507b44c31a5eb8eabf0d306980feaa7545e59b8813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1110477$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11521806$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Novak, U.</creatorcontrib><creatorcontrib>Grob, T. J.</creatorcontrib><creatorcontrib>Baskaynak, G.</creatorcontrib><creatorcontrib>Peters, U. R.</creatorcontrib><creatorcontrib>Aebi, S.</creatorcontrib><creatorcontrib>Zwahlen, D.</creatorcontrib><creatorcontrib>Tschan, M. P.</creatorcontrib><creatorcontrib>Kreuzer, K.-A.</creatorcontrib><creatorcontrib>Leibundgut, E. Oppliger</creatorcontrib><creatorcontrib>Cajot, J.-F.</creatorcontrib><creatorcontrib>Tobler, A.</creatorcontrib><creatorcontrib>Fey, M. F.</creatorcontrib><title>Overexpression of the p73 gene is a novel finding in high-risk B-cell chronic lymphocytic leukemia</title><title>Annals of oncology</title><addtitle>Ann Oncol</addtitle><description>The p73 protein shares structural and functional similarities with the tumour-suppressor p53, but its role in neoplastic transformation is unknown. Alternative splicing leads to the expression of at least nine p73 C-terminal mRNA splice variants (α β γ δ ε ξ η ηl θ). In this survey, we analyse the expression of p73 by real-time quantitative RT-PCR, its known C-terminal variants with an RT-PCR-Southern tech nique and by Western blot in samples of 51 patients with B-CLL, normal B lymphocytes from eight individuals, and five haematopoetic cell lines. p73α protein expression positively correlated with higher risk B-CLL stages (P=0.046). Total p73 mRNA expression was higher (P= 0.01) and p73α protein more frequently detected (P=0.008) in B-CLL compared with normal CD19+—B-lymphocytes. p73 C-terminal mRNA variants were expressed both in B-CLL and in normal B-lymphocytes, but their expression was biased since the γ (P=0.041), the θ (P ≪ 0.001), and the η variant (P=0.033) prevailed in normal B-lymphocytes. In summary, we conclude that the accumulation of p73, the expression pattern of particular p73 variants and its link to progression may play a distinct role in the molecular pathology B-CLL.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Apoptosis</subject><subject>B-CLL</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Blotting, Western</subject><subject>DNA-Binding Proteins - analysis</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - metabolism</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nuclear Proteins - analysis</subject><subject>Nuclear Proteins - genetics</subject><subject>overexpression</subject><subject>p53</subject><subject>p73</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Risk Factors</subject><subject>Tumor Protein p73</subject><subject>Tumor Suppressor Proteins</subject><subject>Up-Regulation</subject><issn>0923-7534</issn><issn>1569-8041</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkE1v00AQhleIiqaBMze0B8TNdMbr9drcQqCkaqVeiqi4rNabcbzEXru7TtX8exwl4uM0I83zvho9jL1F-IiQisvFJwRElCKFHEC8YDOUeZkUkOFLNoMyFYmSIjtnFzH-AoC8TMtX7HxKpFhAPmPV3RMFeh4Cxeh6z_uajw3xQQm-IU_cRW6475-o5bXza-c33HneuE2TBBe3_HNiqW25bULvneXtvhua3u7Hw067LXXOvGZntWkjvTnNOft-9fV-uUpu775dLxe3ic0Ax0RhLsFMH1pCZUsjMK3K3EhQVZZZgUZSVZCpaliLiSqgJmOUzCTJsioKFHP24dg7hP5xR3HUnYuH74ynfhe1QkxFNrmas8sjaEMfY6BaD8F1Juw1gj5o1Qv9n9Yp8e5Uvas6Wv_lTx4n4P0JMNGatg7GWxf_4RAypSYsOWIujvT852zCVudKKKlXDz_1DwEPX5Y3K52J3xuGjUg</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>Novak, U.</creator><creator>Grob, T. J.</creator><creator>Baskaynak, G.</creator><creator>Peters, U. R.</creator><creator>Aebi, S.</creator><creator>Zwahlen, D.</creator><creator>Tschan, M. P.</creator><creator>Kreuzer, K.-A.</creator><creator>Leibundgut, E. Oppliger</creator><creator>Cajot, J.-F.</creator><creator>Tobler, A.</creator><creator>Fey, M. F.</creator><general>Oxford University Press</general><scope>BSCLL</scope><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>20010701</creationdate><title>Overexpression of the p73 gene is a novel finding in high-risk B-cell chronic lymphocytic leukemia</title><author>Novak, U. ; Grob, T. J. ; Baskaynak, G. ; Peters, U. R. ; Aebi, S. ; Zwahlen, D. ; Tschan, M. P. ; Kreuzer, K.-A. ; Leibundgut, E. Oppliger ; Cajot, J.-F. ; Tobler, A. ; Fey, M. F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-71650a069ce17c9a312b96a507b44c31a5eb8eabf0d306980feaa7545e59b8813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Apoptosis</topic><topic>B-CLL</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Blotting, Western</topic><topic>DNA-Binding Proteins - analysis</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Tumor Suppressor</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - metabolism</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nuclear Proteins - analysis</topic><topic>Nuclear Proteins - genetics</topic><topic>overexpression</topic><topic>p53</topic><topic>p73</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Risk Factors</topic><topic>Tumor Protein p73</topic><topic>Tumor Suppressor Proteins</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Novak, U.</creatorcontrib><creatorcontrib>Grob, T. J.</creatorcontrib><creatorcontrib>Baskaynak, G.</creatorcontrib><creatorcontrib>Peters, U. R.</creatorcontrib><creatorcontrib>Aebi, S.</creatorcontrib><creatorcontrib>Zwahlen, D.</creatorcontrib><creatorcontrib>Tschan, M. P.</creatorcontrib><creatorcontrib>Kreuzer, K.-A.</creatorcontrib><creatorcontrib>Leibundgut, E. Oppliger</creatorcontrib><creatorcontrib>Cajot, J.-F.</creatorcontrib><creatorcontrib>Tobler, A.</creatorcontrib><creatorcontrib>Fey, M. F.</creatorcontrib><collection>Istex</collection><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>Annals of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Novak, U.</au><au>Grob, T. J.</au><au>Baskaynak, G.</au><au>Peters, U. R.</au><au>Aebi, S.</au><au>Zwahlen, D.</au><au>Tschan, M. P.</au><au>Kreuzer, K.-A.</au><au>Leibundgut, E. Oppliger</au><au>Cajot, J.-F.</au><au>Tobler, A.</au><au>Fey, M. F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of the p73 gene is a novel finding in high-risk B-cell chronic lymphocytic leukemia</atitle><jtitle>Annals of oncology</jtitle><addtitle>Ann Oncol</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>12</volume><issue>7</issue><spage>981</spage><epage>986</epage><pages>981-986</pages><issn>0923-7534</issn><eissn>1569-8041</eissn><abstract>The p73 protein shares structural and functional similarities with the tumour-suppressor p53, but its role in neoplastic transformation is unknown. Alternative splicing leads to the expression of at least nine p73 C-terminal mRNA splice variants (α β γ δ ε ξ η ηl θ). In this survey, we analyse the expression of p73 by real-time quantitative RT-PCR, its known C-terminal variants with an RT-PCR-Southern tech nique and by Western blot in samples of 51 patients with B-CLL, normal B lymphocytes from eight individuals, and five haematopoetic cell lines. p73α protein expression positively correlated with higher risk B-CLL stages (P=0.046). Total p73 mRNA expression was higher (P= 0.01) and p73α protein more frequently detected (P=0.008) in B-CLL compared with normal CD19+—B-lymphocytes. p73 C-terminal mRNA variants were expressed both in B-CLL and in normal B-lymphocytes, but their expression was biased since the γ (P=0.041), the θ (P ≪ 0.001), and the η variant (P=0.033) prevailed in normal B-lymphocytes. In summary, we conclude that the accumulation of p73, the expression pattern of particular p73 variants and its link to progression may play a distinct role in the molecular pathology B-CLL.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>11521806</pmid><doi>10.1023/A:1011153206003</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Apoptosis B-CLL Biological and medical sciences Biomarkers, Tumor - analysis Biomarkers, Tumor - genetics Blotting, Western DNA-Binding Proteins - analysis DNA-Binding Proteins - genetics Female Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Hematologic and hematopoietic diseases Humans Leukemia, Lymphocytic, Chronic, B-Cell - genetics Leukemia, Lymphocytic, Chronic, B-Cell - metabolism Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Middle Aged Nuclear Proteins - analysis Nuclear Proteins - genetics overexpression p53 p73 Reverse Transcriptase Polymerase Chain Reaction Risk Factors Tumor Protein p73 Tumor Suppressor Proteins Up-Regulation |
| title | Overexpression of the p73 gene is a novel finding in high-risk B-cell chronic lymphocytic leukemia |
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