Analysis of p53 and Bak gene mutations in lymphoproliferative disorders developing in rheumatoid arthritis
Individuals affected by rheumatoid arthritis (RA) occasionally develop lymphoproliferative disorders (RA-LPD). To study the molecular changes underscoring the RA-LPD, mutations of p53 and Bak gene were analyzed in RA-LPD with (MTX-LPD) or without methotrexate treatment for RA (non-MTX-LPD). Histolog...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2007-02, Vol.133 (2), p.125-133 |
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| container_title | Journal of cancer research and clinical oncology |
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| creator | XU, Jing-Xian HOSHIDA, Yoshihiko HONGYO, Tadashi SASAKI, Toru MIYAZATO, Hajime TOMITA, Yasuhiko AOZASA, Katsuyuki |
| description | Individuals affected by rheumatoid arthritis (RA) occasionally develop lymphoproliferative disorders (RA-LPD). To study the molecular changes underscoring the RA-LPD, mutations of p53 and Bak gene were analyzed in RA-LPD with (MTX-LPD) or without methotrexate treatment for RA (non-MTX-LPD).
Histology and immunophenotype were immunohistochemically examined in 32 cases of MTX-LPD and 21 of non-MTX-LPD. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by direct sequencing was employed to detect the mutations of p53 and Bak gene.
Frequency of p53 mutations in non-MTX-LPD (47.6%) was significantly higher than that in MTX-LPD (15.6%) (P < 0.05). Among the cases with non-Hodgkin's lymphoma (NHL), the largest category of RA-LPD, the frequency of p53 mutations in the non-MTX-NHL (47.6%) was significantly higher than that in the MTX-NHL (14.8%) (P < 0.05). Interval between the onset of RA and LPD development was significantly longer in LPD with p53 gene mutations (median 228 months) than that without mutations (133 months). LPD with p53 gene mutations had more advanced diseases and an unfavorable prognosis than those without mutations.
MTX-LPD and non-MTX-LPD show similar findings in clinical characteristics, histology, EBV positive rate, and frequency of Bak gene mutations. Whereas the non-MTX-LPD is distinct from the MTX-LPD in its significantly higher p53 mutation frequency. |
| doi_str_mv | 10.1007/s00432-006-0152-2 |
| format | Article |
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Histology and immunophenotype were immunohistochemically examined in 32 cases of MTX-LPD and 21 of non-MTX-LPD. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by direct sequencing was employed to detect the mutations of p53 and Bak gene.
Frequency of p53 mutations in non-MTX-LPD (47.6%) was significantly higher than that in MTX-LPD (15.6%) (P < 0.05). Among the cases with non-Hodgkin's lymphoma (NHL), the largest category of RA-LPD, the frequency of p53 mutations in the non-MTX-NHL (47.6%) was significantly higher than that in the MTX-NHL (14.8%) (P < 0.05). Interval between the onset of RA and LPD development was significantly longer in LPD with p53 gene mutations (median 228 months) than that without mutations (133 months). LPD with p53 gene mutations had more advanced diseases and an unfavorable prognosis than those without mutations.
MTX-LPD and non-MTX-LPD show similar findings in clinical characteristics, histology, EBV positive rate, and frequency of Bak gene mutations. Whereas the non-MTX-LPD is distinct from the MTX-LPD in its significantly higher p53 mutation frequency.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-006-0152-2</identifier><identifier>PMID: 16988840</identifier><identifier>CODEN: JCROD7</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Aged ; Aged, 80 and over ; Antineoplastic agents ; Arthritis, Rheumatoid - complications ; Arthritis, Rheumatoid - drug therapy ; Arthritis, Rheumatoid - genetics ; bcl-2 Homologous Antagonist-Killer Protein - genetics ; Biological and medical sciences ; Diseases of the osteoarticular system ; Epstein-Barr virus ; Female ; Genes ; Hematologic and hematopoietic diseases ; Humans ; Immunohistochemistry ; Inflammatory joint diseases ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphoma ; Lymphoproliferative Disorders - etiology ; Lymphoproliferative Disorders - genetics ; Male ; Medical sciences ; Methotrexate - pharmacology ; Middle Aged ; Mutation ; Pharmacology. Drug treatments ; Phenotype ; Prognosis ; Rheumatoid arthritis ; Tumor Suppressor Protein p53 - genetics</subject><ispartof>Journal of cancer research and clinical oncology, 2007-02, Vol.133 (2), p.125-133</ispartof><rights>2007 INIST-CNRS</rights><rights>Springer-Verlag 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-e0dfc04c392a775d1409f7dc4ae0baced934e45996c6c4b1b8e3620923bb86ef3</citedby><cites>FETCH-LOGICAL-c387t-e0dfc04c392a775d1409f7dc4ae0baced934e45996c6c4b1b8e3620923bb86ef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18440416$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16988840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>XU, Jing-Xian</creatorcontrib><creatorcontrib>HOSHIDA, Yoshihiko</creatorcontrib><creatorcontrib>HONGYO, Tadashi</creatorcontrib><creatorcontrib>SASAKI, Toru</creatorcontrib><creatorcontrib>MIYAZATO, Hajime</creatorcontrib><creatorcontrib>TOMITA, Yasuhiko</creatorcontrib><creatorcontrib>AOZASA, Katsuyuki</creatorcontrib><title>Analysis of p53 and Bak gene mutations in lymphoproliferative disorders developing in rheumatoid arthritis</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><description>Individuals affected by rheumatoid arthritis (RA) occasionally develop lymphoproliferative disorders (RA-LPD). To study the molecular changes underscoring the RA-LPD, mutations of p53 and Bak gene were analyzed in RA-LPD with (MTX-LPD) or without methotrexate treatment for RA (non-MTX-LPD).
Histology and immunophenotype were immunohistochemically examined in 32 cases of MTX-LPD and 21 of non-MTX-LPD. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by direct sequencing was employed to detect the mutations of p53 and Bak gene.
Frequency of p53 mutations in non-MTX-LPD (47.6%) was significantly higher than that in MTX-LPD (15.6%) (P < 0.05). Among the cases with non-Hodgkin's lymphoma (NHL), the largest category of RA-LPD, the frequency of p53 mutations in the non-MTX-NHL (47.6%) was significantly higher than that in the MTX-NHL (14.8%) (P < 0.05). Interval between the onset of RA and LPD development was significantly longer in LPD with p53 gene mutations (median 228 months) than that without mutations (133 months). LPD with p53 gene mutations had more advanced diseases and an unfavorable prognosis than those without mutations.
MTX-LPD and non-MTX-LPD show similar findings in clinical characteristics, histology, EBV positive rate, and frequency of Bak gene mutations. Whereas the non-MTX-LPD is distinct from the MTX-LPD in its significantly higher p53 mutation frequency.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antineoplastic agents</subject><subject>Arthritis, Rheumatoid - complications</subject><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>bcl-2 Homologous Antagonist-Killer Protein - genetics</subject><subject>Biological and medical sciences</subject><subject>Diseases of the osteoarticular system</subject><subject>Epstein-Barr virus</subject><subject>Female</subject><subject>Genes</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammatory joint diseases</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphoma</subject><subject>Lymphoproliferative Disorders - etiology</subject><subject>Lymphoproliferative Disorders - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methotrexate - pharmacology</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Pharmacology. Drug treatments</subject><subject>Phenotype</subject><subject>Prognosis</subject><subject>Rheumatoid arthritis</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0U1r3DAQBmBRWppt2h_QSxGF9uZk9GHZOqahH4FAL-lZyNI4q61tuZId2H9fmV0I9NKT0PDMMMxLyHsGVwyguc4AUvAKQFXAal7xF2THtgoTon5JdsAaVtWcqQvyJucDlH_d8Nfkgindtq2EHTncTHY45pBp7OlcC2onT7_Y3_QRJ6TjutglxCnTMNHhOM77OKc4hB5TqT8h9SHH5DFl6vEJhziH6XGzaY_raJcYPLVp2aewhPyWvOrtkPHd-b0kv759fbj9Ud3__H53e3NfOdE2S4XgewfSCc1t09SeSdB94520CJ116LWQKGutlVNOdqxrUSgOmouuaxX24pJ8Ps0tq_5ZMS9mDNnhMNgJ45qNaoWqVfH_g0yXK0mhC_z4DzzENZXDZcM51EJygILYCbkUc07YmzmF0aajYWC2uMwpLlPiMltcZtvgw3nw2o3onzvO-RTw6Qxsdnbok51cyM-ulRIkU-IvoFOeCA</recordid><startdate>20070201</startdate><enddate>20070201</enddate><creator>XU, Jing-Xian</creator><creator>HOSHIDA, Yoshihiko</creator><creator>HONGYO, Tadashi</creator><creator>SASAKI, Toru</creator><creator>MIYAZATO, Hajime</creator><creator>TOMITA, Yasuhiko</creator><creator>AOZASA, Katsuyuki</creator><general>Springer</general><general>Springer Nature B.V</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20070201</creationdate><title>Analysis of p53 and Bak gene mutations in lymphoproliferative disorders developing in rheumatoid arthritis</title><author>XU, Jing-Xian ; HOSHIDA, Yoshihiko ; HONGYO, Tadashi ; SASAKI, Toru ; MIYAZATO, Hajime ; TOMITA, Yasuhiko ; AOZASA, Katsuyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-e0dfc04c392a775d1409f7dc4ae0baced934e45996c6c4b1b8e3620923bb86ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antineoplastic agents</topic><topic>Arthritis, Rheumatoid - complications</topic><topic>Arthritis, Rheumatoid - drug therapy</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>bcl-2 Homologous Antagonist-Killer Protein - genetics</topic><topic>Biological and medical sciences</topic><topic>Diseases of the osteoarticular system</topic><topic>Epstein-Barr virus</topic><topic>Female</topic><topic>Genes</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammatory joint diseases</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphoma</topic><topic>Lymphoproliferative Disorders - etiology</topic><topic>Lymphoproliferative Disorders - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methotrexate - pharmacology</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Pharmacology. Drug treatments</topic><topic>Phenotype</topic><topic>Prognosis</topic><topic>Rheumatoid arthritis</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>XU, Jing-Xian</creatorcontrib><creatorcontrib>HOSHIDA, Yoshihiko</creatorcontrib><creatorcontrib>HONGYO, Tadashi</creatorcontrib><creatorcontrib>SASAKI, Toru</creatorcontrib><creatorcontrib>MIYAZATO, Hajime</creatorcontrib><creatorcontrib>TOMITA, Yasuhiko</creatorcontrib><creatorcontrib>AOZASA, Katsuyuki</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>Oncogenes and Growth Factors 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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>XU, Jing-Xian</au><au>HOSHIDA, Yoshihiko</au><au>HONGYO, Tadashi</au><au>SASAKI, Toru</au><au>MIYAZATO, Hajime</au><au>TOMITA, Yasuhiko</au><au>AOZASA, Katsuyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of p53 and Bak gene mutations in lymphoproliferative disorders developing in rheumatoid arthritis</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>133</volume><issue>2</issue><spage>125</spage><epage>133</epage><pages>125-133</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><coden>JCROD7</coden><abstract>Individuals affected by rheumatoid arthritis (RA) occasionally develop lymphoproliferative disorders (RA-LPD). To study the molecular changes underscoring the RA-LPD, mutations of p53 and Bak gene were analyzed in RA-LPD with (MTX-LPD) or without methotrexate treatment for RA (non-MTX-LPD).
Histology and immunophenotype were immunohistochemically examined in 32 cases of MTX-LPD and 21 of non-MTX-LPD. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by direct sequencing was employed to detect the mutations of p53 and Bak gene.
Frequency of p53 mutations in non-MTX-LPD (47.6%) was significantly higher than that in MTX-LPD (15.6%) (P < 0.05). Among the cases with non-Hodgkin's lymphoma (NHL), the largest category of RA-LPD, the frequency of p53 mutations in the non-MTX-NHL (47.6%) was significantly higher than that in the MTX-NHL (14.8%) (P < 0.05). Interval between the onset of RA and LPD development was significantly longer in LPD with p53 gene mutations (median 228 months) than that without mutations (133 months). LPD with p53 gene mutations had more advanced diseases and an unfavorable prognosis than those without mutations.
MTX-LPD and non-MTX-LPD show similar findings in clinical characteristics, histology, EBV positive rate, and frequency of Bak gene mutations. Whereas the non-MTX-LPD is distinct from the MTX-LPD in its significantly higher p53 mutation frequency.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>16988840</pmid><doi>10.1007/s00432-006-0152-2</doi><tpages>9</tpages></addata></record> |
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| subjects | Aged Aged, 80 and over Antineoplastic agents Arthritis, Rheumatoid - complications Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - genetics bcl-2 Homologous Antagonist-Killer Protein - genetics Biological and medical sciences Diseases of the osteoarticular system Epstein-Barr virus Female Genes Hematologic and hematopoietic diseases Humans Immunohistochemistry Inflammatory joint diseases Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphoma Lymphoproliferative Disorders - etiology Lymphoproliferative Disorders - genetics Male Medical sciences Methotrexate - pharmacology Middle Aged Mutation Pharmacology. Drug treatments Phenotype Prognosis Rheumatoid arthritis Tumor Suppressor Protein p53 - genetics |
| title | Analysis of p53 and Bak gene mutations in lymphoproliferative disorders developing in rheumatoid arthritis |
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