Low Expression of p27 Protein Combined with Altered p53 and Rb/p16 Expression Status Is Associated with Increased Expression of Cyclin A and Cyclin B1 in Diffuse Large B-Cell Lymphomas
The expression of the cyclin-dependent kinase inhibitor (CDKI) p27 protein was investigated in relation to (1) the expression of the cell cycle regulators p53, Rb and p16 and (2) the proliferation profile as determined by the expression of Ki67, cyclin A, and cyclin B1 in 80 cases of de novo diffuse...
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| Veröffentlicht in: | Modern pathology 2001-11, Vol.14 (11), p.1105-1113 |
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| creator | Bai, Maria Vlachonikolis, John Agnantis, Niki J Tsanou, Elena Dimou, Sofia Nicolaides, Constatinos Stefanaki, Stella Pavlidis, Nicolaos Kanavarous, Panagiotis |
| description | The expression of the cyclin-dependent kinase inhibitor (CDKI) p27 protein was investigated in relation to (1) the expression of the cell cycle regulators p53, Rb and p16 and (2) the proliferation profile as determined by the expression of Ki67, cyclin A, and cyclin B1 in 80 cases of de novo diffuse large B-cell lymphomas (DLBCL). P27 expression was low/null in large tumor cells in 58/80 cases and intermediate/high in 22/80 cases. Increased expression of p53 protein was observed in 39/80 cases. Decreased expression of Rb and p16 proteins was mutually exclusive and was observed in 5/80 and 14/80 cases, respectively. The analysis of the p27 expression status (low/null versus intermediate/high) with respect to the p53 and/or Rb/p16 expression status showed that low/null p27 expression was significantly correlated with increased p53 expression (P = .018) and showed a strong trend for correlation with concurrent increased p53 expression and decreased Rb or p16 expression (P = .050). These findings suggest a tendency for concurrent alterations of the cell cycle regulators p27, p53, and Rb or p16 in DLBCL, which might result in impaired tumor growth control. Indeed, the analysis of the combined p27/p53/Rb/p16 expression status with respect to the proliferation profile showed that (1) three alterations in the combined p27/p53/Rb/p16 status (i.e., low/null P27 expression, increased expression of p53, and decreased expression of Rb or p16) were significantly correlated with increased expression of cyclin B1 (P = .005) and (2) two or three alterations were significantly correlated with increased expression of cyclin A (P = .014). These findings suggest combined impairment of a complex cell-cycle control network involving the CDK inhibitor p27, the P53 pathway, and the Rb1 pathway, which exerts a cooperative effect resulting in enhanced tumor cell proliferation. |
| doi_str_mv | 10.1038/modpathol.3880444 |
| format | Article |
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P27 expression was low/null in large tumor cells in 58/80 cases and intermediate/high in 22/80 cases. Increased expression of p53 protein was observed in 39/80 cases. Decreased expression of Rb and p16 proteins was mutually exclusive and was observed in 5/80 and 14/80 cases, respectively. The analysis of the p27 expression status (low/null versus intermediate/high) with respect to the p53 and/or Rb/p16 expression status showed that low/null p27 expression was significantly correlated with increased p53 expression (P = .018) and showed a strong trend for correlation with concurrent increased p53 expression and decreased Rb or p16 expression (P = .050). These findings suggest a tendency for concurrent alterations of the cell cycle regulators p27, p53, and Rb or p16 in DLBCL, which might result in impaired tumor growth control. Indeed, the analysis of the combined p27/p53/Rb/p16 expression status with respect to the proliferation profile showed that (1) three alterations in the combined p27/p53/Rb/p16 status (i.e., low/null P27 expression, increased expression of p53, and decreased expression of Rb or p16) were significantly correlated with increased expression of cyclin B1 (P = .005) and (2) two or three alterations were significantly correlated with increased expression of cyclin A (P = .014). These findings suggest combined impairment of a complex cell-cycle control network involving the CDK inhibitor p27, the P53 pathway, and the Rb1 pathway, which exerts a cooperative effect resulting in enhanced tumor cell proliferation.</description><identifier>ISSN: 0893-3952</identifier><identifier>EISSN: 1530-0285</identifier><identifier>DOI: 10.1038/modpathol.3880444</identifier><identifier>PMID: 11706071</identifier><identifier>CODEN: MODPEO</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>Analysis of Variance ; B-cell lymphoma ; Biomarkers - analysis ; Cell cycle ; Cell Cycle Proteins - biosynthesis ; Cell Division ; Cell growth ; Cyclin A - biosynthesis ; Cyclin B - biosynthesis ; Cyclin B1 ; Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-dependent kinases ; Genes ; Humans ; Immuno-histochemistry ; Immunohistochemistry ; Kinases ; Laboratory Medicine ; Lymphoma ; Lymphoma, B-Cell - metabolism ; Lymphoma, B-Cell - pathology ; Lymphoma, Large B-Cell, Diffuse - metabolism ; Lymphoma, Large B-Cell, Diffuse - pathology ; Medicine ; Medicine & Public Health ; original-article ; Pathology ; Phosphorylation ; Proteins ; Retinoblastoma Protein - biosynthesis ; Tumor Suppressor Protein p53 - biosynthesis ; Tumor Suppressor Proteins - biosynthesis</subject><ispartof>Modern pathology, 2001-11, Vol.14 (11), p.1105-1113</ispartof><rights>2001 United States & Canadian Academy of Pathology</rights><rights>The United States and Canadian Academy of Pathology, Inc. 2001</rights><rights>Copyright Nature Publishing Group Nov 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-9b44cfffea021f9a466cddd6df96ccea30f3ed2dbdf35c1e8196f8d057a363153</citedby><cites>FETCH-LOGICAL-c516t-9b44cfffea021f9a466cddd6df96ccea30f3ed2dbdf35c1e8196f8d057a363153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/221208468?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11706071$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, Maria</creatorcontrib><creatorcontrib>Vlachonikolis, John</creatorcontrib><creatorcontrib>Agnantis, Niki J</creatorcontrib><creatorcontrib>Tsanou, Elena</creatorcontrib><creatorcontrib>Dimou, Sofia</creatorcontrib><creatorcontrib>Nicolaides, Constatinos</creatorcontrib><creatorcontrib>Stefanaki, Stella</creatorcontrib><creatorcontrib>Pavlidis, Nicolaos</creatorcontrib><creatorcontrib>Kanavarous, Panagiotis</creatorcontrib><title>Low Expression of p27 Protein Combined with Altered p53 and Rb/p16 Expression Status Is Associated with Increased Expression of Cyclin A and Cyclin B1 in Diffuse Large B-Cell Lymphomas</title><title>Modern pathology</title><addtitle>Mod Pathol</addtitle><addtitle>Mod Pathol</addtitle><description>The expression of the cyclin-dependent kinase inhibitor (CDKI) p27 protein was investigated in relation to (1) the expression of the cell cycle regulators p53, Rb and p16 and (2) the proliferation profile as determined by the expression of Ki67, cyclin A, and cyclin B1 in 80 cases of de novo diffuse large B-cell lymphomas (DLBCL). P27 expression was low/null in large tumor cells in 58/80 cases and intermediate/high in 22/80 cases. Increased expression of p53 protein was observed in 39/80 cases. Decreased expression of Rb and p16 proteins was mutually exclusive and was observed in 5/80 and 14/80 cases, respectively. The analysis of the p27 expression status (low/null versus intermediate/high) with respect to the p53 and/or Rb/p16 expression status showed that low/null p27 expression was significantly correlated with increased p53 expression (P = .018) and showed a strong trend for correlation with concurrent increased p53 expression and decreased Rb or p16 expression (P = .050). These findings suggest a tendency for concurrent alterations of the cell cycle regulators p27, p53, and Rb or p16 in DLBCL, which might result in impaired tumor growth control. 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These findings suggest combined impairment of a complex cell-cycle control network involving the CDK inhibitor p27, the P53 pathway, and the Rb1 pathway, which exerts a cooperative effect resulting in enhanced tumor cell proliferation.</description><subject>Analysis of Variance</subject><subject>B-cell lymphoma</subject><subject>Biomarkers - analysis</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - biosynthesis</subject><subject>Cell Division</subject><subject>Cell growth</subject><subject>Cyclin A - biosynthesis</subject><subject>Cyclin B - biosynthesis</subject><subject>Cyclin B1</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis</subject><subject>Cyclin-Dependent Kinase Inhibitor p27</subject><subject>Cyclin-dependent kinases</subject><subject>Genes</subject><subject>Humans</subject><subject>Immuno-histochemistry</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Laboratory Medicine</subject><subject>Lymphoma</subject><subject>Lymphoma, B-Cell - 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biosynthesis</topic><topic>Tumor Suppressor Proteins - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bai, Maria</creatorcontrib><creatorcontrib>Vlachonikolis, John</creatorcontrib><creatorcontrib>Agnantis, Niki J</creatorcontrib><creatorcontrib>Tsanou, Elena</creatorcontrib><creatorcontrib>Dimou, Sofia</creatorcontrib><creatorcontrib>Nicolaides, Constatinos</creatorcontrib><creatorcontrib>Stefanaki, Stella</creatorcontrib><creatorcontrib>Pavlidis, Nicolaos</creatorcontrib><creatorcontrib>Kanavarous, Panagiotis</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>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>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>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Modern pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bai, Maria</au><au>Vlachonikolis, John</au><au>Agnantis, Niki J</au><au>Tsanou, Elena</au><au>Dimou, Sofia</au><au>Nicolaides, Constatinos</au><au>Stefanaki, Stella</au><au>Pavlidis, Nicolaos</au><au>Kanavarous, Panagiotis</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low Expression of p27 Protein Combined with Altered p53 and Rb/p16 Expression Status Is Associated with Increased Expression of Cyclin A and Cyclin B1 in Diffuse Large B-Cell Lymphomas</atitle><jtitle>Modern pathology</jtitle><stitle>Mod Pathol</stitle><addtitle>Mod Pathol</addtitle><date>2001-11-01</date><risdate>2001</risdate><volume>14</volume><issue>11</issue><spage>1105</spage><epage>1113</epage><pages>1105-1113</pages><issn>0893-3952</issn><eissn>1530-0285</eissn><coden>MODPEO</coden><abstract>The expression of the cyclin-dependent kinase inhibitor (CDKI) p27 protein was investigated in relation to (1) the expression of the cell cycle regulators p53, Rb and p16 and (2) the proliferation profile as determined by the expression of Ki67, cyclin A, and cyclin B1 in 80 cases of de novo diffuse large B-cell lymphomas (DLBCL). P27 expression was low/null in large tumor cells in 58/80 cases and intermediate/high in 22/80 cases. Increased expression of p53 protein was observed in 39/80 cases. Decreased expression of Rb and p16 proteins was mutually exclusive and was observed in 5/80 and 14/80 cases, respectively. The analysis of the p27 expression status (low/null versus intermediate/high) with respect to the p53 and/or Rb/p16 expression status showed that low/null p27 expression was significantly correlated with increased p53 expression (P = .018) and showed a strong trend for correlation with concurrent increased p53 expression and decreased Rb or p16 expression (P = .050). These findings suggest a tendency for concurrent alterations of the cell cycle regulators p27, p53, and Rb or p16 in DLBCL, which might result in impaired tumor growth control. Indeed, the analysis of the combined p27/p53/Rb/p16 expression status with respect to the proliferation profile showed that (1) three alterations in the combined p27/p53/Rb/p16 status (i.e., low/null P27 expression, increased expression of p53, and decreased expression of Rb or p16) were significantly correlated with increased expression of cyclin B1 (P = .005) and (2) two or three alterations were significantly correlated with increased expression of cyclin A (P = .014). These findings suggest combined impairment of a complex cell-cycle control network involving the CDK inhibitor p27, the P53 pathway, and the Rb1 pathway, which exerts a cooperative effect resulting in enhanced tumor cell proliferation.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>11706071</pmid><doi>10.1038/modpathol.3880444</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis of Variance B-cell lymphoma Biomarkers - analysis Cell cycle Cell Cycle Proteins - biosynthesis Cell Division Cell growth Cyclin A - biosynthesis Cyclin B - biosynthesis Cyclin B1 Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis Cyclin-Dependent Kinase Inhibitor p27 Cyclin-dependent kinases Genes Humans Immuno-histochemistry Immunohistochemistry Kinases Laboratory Medicine Lymphoma Lymphoma, B-Cell - metabolism Lymphoma, B-Cell - pathology Lymphoma, Large B-Cell, Diffuse - metabolism Lymphoma, Large B-Cell, Diffuse - pathology Medicine Medicine & Public Health original-article Pathology Phosphorylation Proteins Retinoblastoma Protein - biosynthesis Tumor Suppressor Protein p53 - biosynthesis Tumor Suppressor Proteins - biosynthesis |
| title | Low Expression of p27 Protein Combined with Altered p53 and Rb/p16 Expression Status Is Associated with Increased Expression of Cyclin A and Cyclin B1 in Diffuse Large B-Cell Lymphomas |
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