Frequent alteration of MDM2 and p53 in the molecular progression of recurring non-Hodgkin's lymphoma
Aims: Recurrence of non‐Hodgkin's lymphoma with or without transformation is often associated with increased clinical drug resistance and poor prognosis indicating molecular progression. The study addresses the currently poorly understood molecular mechanisms underlying relapsing non‐Hodgkin�...
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| Veröffentlicht in: | Histopathology 2002-10, Vol.41 (4), p.322-330 |
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| creator | Møller, M B Nielsen, O Pedersen, N T |
| description | Aims: Recurrence of non‐Hodgkin's lymphoma with or without transformation is often associated with increased clinical drug resistance and poor prognosis indicating molecular progression. The study addresses the currently poorly understood molecular mechanisms underlying relapsing non‐Hodgkin's lymphoma.
Methods and results: We have analysed sequential biopsies from 42 non‐Hodgkin's lymphoma patients immunohistochemically for p53 alterations (based on p53 and p21Waf1 expression), as well as for expression of MDM2, p27Kip1 and cyclin D3. Relapse of follicle centre lymphoma was associated with p53 alterations as 5/6 (83%) follicle centre lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. Of these cases, three showed transformation to diffuse large B‐cell lymphoma. p53 alteration was also associated with relapse of de novo diffuse large B‐cell lymphoma and T‐cell non‐Hodgkin's lymphoma, as 2/5 (40%) diffuse large B‐cell lymphomas and 3/9 (33%) T‐cell non‐Hodgkin's lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. No indolent non‐Hodgkin's lymphoma case showed MDM2 over‐expression at diagnosis, whereas 4/5 (80%) transformed diffuse large B‐cell lymphomas developed MDM2 over‐expression.
Conclusion: Our data are consistent with the notion that p53 alterations are important for the histological transformation of follicle centre lymphoma. However, the data also suggest that relapsing follicle centre lymphomas without overt transformation often have p53 alterations and increased risk of transformation, and that relapse of de novo diffuse large B‐cell lymphomas and T‐cell non‐Hodgkin's lymphomas is associated with p53 alterations. Furthermore, our results are consistent with an association of MDM2 over‐expression with histological transformation of both follicle centre lymphoma and marginal zone B‐cell lymphoma. |
| doi_str_mv | 10.1046/j.1365-2559.2002.01506.x |
| format | Article |
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Methods and results: We have analysed sequential biopsies from 42 non‐Hodgkin's lymphoma patients immunohistochemically for p53 alterations (based on p53 and p21Waf1 expression), as well as for expression of MDM2, p27Kip1 and cyclin D3. Relapse of follicle centre lymphoma was associated with p53 alterations as 5/6 (83%) follicle centre lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. Of these cases, three showed transformation to diffuse large B‐cell lymphoma. p53 alteration was also associated with relapse of de novo diffuse large B‐cell lymphoma and T‐cell non‐Hodgkin's lymphoma, as 2/5 (40%) diffuse large B‐cell lymphomas and 3/9 (33%) T‐cell non‐Hodgkin's lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. No indolent non‐Hodgkin's lymphoma case showed MDM2 over‐expression at diagnosis, whereas 4/5 (80%) transformed diffuse large B‐cell lymphomas developed MDM2 over‐expression.
Conclusion: Our data are consistent with the notion that p53 alterations are important for the histological transformation of follicle centre lymphoma. However, the data also suggest that relapsing follicle centre lymphomas without overt transformation often have p53 alterations and increased risk of transformation, and that relapse of de novo diffuse large B‐cell lymphomas and T‐cell non‐Hodgkin's lymphomas is associated with p53 alterations. Furthermore, our results are consistent with an association of MDM2 over‐expression with histological transformation of both follicle centre lymphoma and marginal zone B‐cell lymphoma.</description><identifier>ISSN: 0309-0167</identifier><identifier>EISSN: 1365-2559</identifier><identifier>DOI: 10.1046/j.1365-2559.2002.01506.x</identifier><identifier>PMID: 12383214</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Aged ; Aged, 80 and over ; Biological and medical sciences ; Biomarkers, Tumor ; Cell Cycle Proteins - biosynthesis ; Cell Transformation, Neoplastic - genetics ; Cyclin D3 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclins - biosynthesis ; Disease Progression ; Female ; Genes, p53 - genetics ; Hematologic and hematopoietic diseases ; Humans ; Immunohistochemistry ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphoma, B-Cell - genetics ; Lymphoma, B-Cell - metabolism ; Lymphoma, B-Cell - pathology ; Lymphoma, Follicular - genetics ; Lymphoma, Follicular - metabolism ; Lymphoma, Follicular - pathology ; Lymphoma, Large B-Cell, Diffuse - genetics ; Lymphoma, Large B-Cell, Diffuse - metabolism ; Lymphoma, Large B-Cell, Diffuse - pathology ; Lymphoma, Non-Hodgkin - genetics ; Lymphoma, Non-Hodgkin - metabolism ; Lymphoma, Non-Hodgkin - pathology ; Lymphoma, T-Cell - genetics ; Lymphoma, T-Cell - metabolism ; Lymphoma, T-Cell - pathology ; Male ; MDM2 ; Medical sciences ; Mutation ; non-Hodgkin's lymphoma ; Nuclear Proteins ; p27Kip1 ; p53 ; progression ; Proto-Oncogene Proteins - biosynthesis ; Proto-Oncogene Proteins c-mdm2 ; Recurrence ; relapse ; transformation ; Tumor Suppressor Proteins - biosynthesis</subject><ispartof>Histopathology, 2002-10, Vol.41 (4), p.322-330</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5016-b745f216ea8588bfb89a1c8249883c727d1a7fafa6b389a0e49668b046e6fe663</citedby><cites>FETCH-LOGICAL-c5016-b745f216ea8588bfb89a1c8249883c727d1a7fafa6b389a0e49668b046e6fe663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2559.2002.01506.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2559.2002.01506.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13946716$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12383214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Møller, M B</creatorcontrib><creatorcontrib>Nielsen, O</creatorcontrib><creatorcontrib>Pedersen, N T</creatorcontrib><title>Frequent alteration of MDM2 and p53 in the molecular progression of recurring non-Hodgkin's lymphoma</title><title>Histopathology</title><addtitle>Histopathology</addtitle><description>Aims: Recurrence of non‐Hodgkin's lymphoma with or without transformation is often associated with increased clinical drug resistance and poor prognosis indicating molecular progression. The study addresses the currently poorly understood molecular mechanisms underlying relapsing non‐Hodgkin's lymphoma.
Methods and results: We have analysed sequential biopsies from 42 non‐Hodgkin's lymphoma patients immunohistochemically for p53 alterations (based on p53 and p21Waf1 expression), as well as for expression of MDM2, p27Kip1 and cyclin D3. Relapse of follicle centre lymphoma was associated with p53 alterations as 5/6 (83%) follicle centre lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. Of these cases, three showed transformation to diffuse large B‐cell lymphoma. p53 alteration was also associated with relapse of de novo diffuse large B‐cell lymphoma and T‐cell non‐Hodgkin's lymphoma, as 2/5 (40%) diffuse large B‐cell lymphomas and 3/9 (33%) T‐cell non‐Hodgkin's lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. No indolent non‐Hodgkin's lymphoma case showed MDM2 over‐expression at diagnosis, whereas 4/5 (80%) transformed diffuse large B‐cell lymphomas developed MDM2 over‐expression.
Conclusion: Our data are consistent with the notion that p53 alterations are important for the histological transformation of follicle centre lymphoma. However, the data also suggest that relapsing follicle centre lymphomas without overt transformation often have p53 alterations and increased risk of transformation, and that relapse of de novo diffuse large B‐cell lymphomas and T‐cell non‐Hodgkin's lymphomas is associated with p53 alterations. Furthermore, our results are consistent with an association of MDM2 over‐expression with histological transformation of both follicle centre lymphoma and marginal zone B‐cell lymphoma.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor</subject><subject>Cell Cycle Proteins - biosynthesis</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cyclin D3</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclin-Dependent Kinase Inhibitor p27</subject><subject>Cyclins - biosynthesis</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Genes, p53 - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphoma, B-Cell - genetics</subject><subject>Lymphoma, B-Cell - metabolism</subject><subject>Lymphoma, B-Cell - pathology</subject><subject>Lymphoma, Follicular - genetics</subject><subject>Lymphoma, Follicular - metabolism</subject><subject>Lymphoma, Follicular - pathology</subject><subject>Lymphoma, Large B-Cell, Diffuse - genetics</subject><subject>Lymphoma, Large B-Cell, Diffuse - metabolism</subject><subject>Lymphoma, Large B-Cell, Diffuse - pathology</subject><subject>Lymphoma, Non-Hodgkin - genetics</subject><subject>Lymphoma, Non-Hodgkin - metabolism</subject><subject>Lymphoma, Non-Hodgkin - pathology</subject><subject>Lymphoma, T-Cell - genetics</subject><subject>Lymphoma, T-Cell - metabolism</subject><subject>Lymphoma, T-Cell - pathology</subject><subject>Male</subject><subject>MDM2</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>non-Hodgkin's lymphoma</subject><subject>Nuclear Proteins</subject><subject>p27Kip1</subject><subject>p53</subject><subject>progression</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>Proto-Oncogene Proteins c-mdm2</subject><subject>Recurrence</subject><subject>relapse</subject><subject>transformation</subject><subject>Tumor Suppressor Proteins - biosynthesis</subject><issn>0309-0167</issn><issn>1365-2559</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1v0zAchy0EYt3gKyBfgFOCX-KXHDig7qWTusE00CQulpPYXTrHKXaqtd9-zhptV062_H9-9s8PABCjHKOCf1vnmHKWEcbKnCBEcoQZ4vnuDZi9DN6CGaKozBDm4ggcx7hGCAtKyHtwhAmVlOBiBprzYP5tjR-gdoMJemh7D3sLr06vCNS-gRtGYevhcG9g1ztTb50OcBP6VTAxTnBIxyG0fgV977NF36weWv81QrfvNvd9pz-Ad1a7aD5O6wn4c372e77Ilj8vLuc_llnNUsusEgWzBHOjJZOyspUsNa4lKUopaS2IaLAWVlvNK5pGyBQl57JKQgy3hnN6Ar4c7k390qfioLo21sY57U2_jUoQLLnEIygPYB36GIOxahPaToe9wkiNhtVajSLVKFKNhtWzYbVL0U_TG9uqM81rcFKagM8ToGOtnQ3a12185WhZcPHc4fuBe2yd2f93AbW4vB13KZ8d8m0czO4lr8OD4oIKpu6uL9T1zd_53a8lUqf0CTpmpcA</recordid><startdate>200210</startdate><enddate>200210</enddate><creator>Møller, M B</creator><creator>Nielsen, O</creator><creator>Pedersen, N T</creator><general>Blackwell Science Ltd</general><general>Blackwell</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>200210</creationdate><title>Frequent alteration of MDM2 and p53 in the molecular progression of recurring non-Hodgkin's lymphoma</title><author>Møller, M B ; Nielsen, O ; Pedersen, N T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5016-b745f216ea8588bfb89a1c8249883c727d1a7fafa6b389a0e49668b046e6fe663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor</topic><topic>Cell Cycle Proteins - biosynthesis</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cyclin D3</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclin-Dependent Kinase Inhibitor p27</topic><topic>Cyclins - biosynthesis</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Genes, p53 - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphoma, B-Cell - genetics</topic><topic>Lymphoma, B-Cell - metabolism</topic><topic>Lymphoma, B-Cell - pathology</topic><topic>Lymphoma, Follicular - genetics</topic><topic>Lymphoma, Follicular - metabolism</topic><topic>Lymphoma, Follicular - pathology</topic><topic>Lymphoma, Large B-Cell, Diffuse - genetics</topic><topic>Lymphoma, Large B-Cell, Diffuse - metabolism</topic><topic>Lymphoma, Large B-Cell, Diffuse - pathology</topic><topic>Lymphoma, Non-Hodgkin - genetics</topic><topic>Lymphoma, Non-Hodgkin - metabolism</topic><topic>Lymphoma, Non-Hodgkin - pathology</topic><topic>Lymphoma, T-Cell - genetics</topic><topic>Lymphoma, T-Cell - metabolism</topic><topic>Lymphoma, T-Cell - pathology</topic><topic>Male</topic><topic>MDM2</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>non-Hodgkin's lymphoma</topic><topic>Nuclear Proteins</topic><topic>p27Kip1</topic><topic>p53</topic><topic>progression</topic><topic>Proto-Oncogene Proteins - biosynthesis</topic><topic>Proto-Oncogene Proteins c-mdm2</topic><topic>Recurrence</topic><topic>relapse</topic><topic>transformation</topic><topic>Tumor Suppressor Proteins - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Møller, M B</creatorcontrib><creatorcontrib>Nielsen, O</creatorcontrib><creatorcontrib>Pedersen, N T</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>Histopathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Møller, M B</au><au>Nielsen, O</au><au>Pedersen, N T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Frequent alteration of MDM2 and p53 in the molecular progression of recurring non-Hodgkin's lymphoma</atitle><jtitle>Histopathology</jtitle><addtitle>Histopathology</addtitle><date>2002-10</date><risdate>2002</risdate><volume>41</volume><issue>4</issue><spage>322</spage><epage>330</epage><pages>322-330</pages><issn>0309-0167</issn><eissn>1365-2559</eissn><abstract>Aims: Recurrence of non‐Hodgkin's lymphoma with or without transformation is often associated with increased clinical drug resistance and poor prognosis indicating molecular progression. The study addresses the currently poorly understood molecular mechanisms underlying relapsing non‐Hodgkin's lymphoma.
Methods and results: We have analysed sequential biopsies from 42 non‐Hodgkin's lymphoma patients immunohistochemically for p53 alterations (based on p53 and p21Waf1 expression), as well as for expression of MDM2, p27Kip1 and cyclin D3. Relapse of follicle centre lymphoma was associated with p53 alterations as 5/6 (83%) follicle centre lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. Of these cases, three showed transformation to diffuse large B‐cell lymphoma. p53 alteration was also associated with relapse of de novo diffuse large B‐cell lymphoma and T‐cell non‐Hodgkin's lymphoma, as 2/5 (40%) diffuse large B‐cell lymphomas and 3/9 (33%) T‐cell non‐Hodgkin's lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. No indolent non‐Hodgkin's lymphoma case showed MDM2 over‐expression at diagnosis, whereas 4/5 (80%) transformed diffuse large B‐cell lymphomas developed MDM2 over‐expression.
Conclusion: Our data are consistent with the notion that p53 alterations are important for the histological transformation of follicle centre lymphoma. However, the data also suggest that relapsing follicle centre lymphomas without overt transformation often have p53 alterations and increased risk of transformation, and that relapse of de novo diffuse large B‐cell lymphomas and T‐cell non‐Hodgkin's lymphomas is associated with p53 alterations. Furthermore, our results are consistent with an association of MDM2 over‐expression with histological transformation of both follicle centre lymphoma and marginal zone B‐cell lymphoma.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12383214</pmid><doi>10.1046/j.1365-2559.2002.01506.x</doi><tpages>9</tpages></addata></record> |
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| subjects | Aged Aged, 80 and over Biological and medical sciences Biomarkers, Tumor Cell Cycle Proteins - biosynthesis Cell Transformation, Neoplastic - genetics Cyclin D3 Cyclin-Dependent Kinase Inhibitor p21 Cyclin-Dependent Kinase Inhibitor p27 Cyclins - biosynthesis Disease Progression Female Genes, p53 - genetics Hematologic and hematopoietic diseases Humans Immunohistochemistry Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphoma, B-Cell - genetics Lymphoma, B-Cell - metabolism Lymphoma, B-Cell - pathology Lymphoma, Follicular - genetics Lymphoma, Follicular - metabolism Lymphoma, Follicular - pathology Lymphoma, Large B-Cell, Diffuse - genetics Lymphoma, Large B-Cell, Diffuse - metabolism Lymphoma, Large B-Cell, Diffuse - pathology Lymphoma, Non-Hodgkin - genetics Lymphoma, Non-Hodgkin - metabolism Lymphoma, Non-Hodgkin - pathology Lymphoma, T-Cell - genetics Lymphoma, T-Cell - metabolism Lymphoma, T-Cell - pathology Male MDM2 Medical sciences Mutation non-Hodgkin's lymphoma Nuclear Proteins p27Kip1 p53 progression Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins c-mdm2 Recurrence relapse transformation Tumor Suppressor Proteins - biosynthesis |
| title | Frequent alteration of MDM2 and p53 in the molecular progression of recurring non-Hodgkin's lymphoma |
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