Analysis of cell cycle regulator proteins in non-small cell lung cancer
Background/Aims: Abnormalities of the proteins involved in cell cycle checkpoints are extremely common among almost all neoplasms. This study aimed to investigate the expression of four components of the cell cycle machinery—p21, p16, p53, and proliferating cell nuclear antigen (PCNA)—in non-small c...
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| creator | Esposito, V Baldi, A Tonini, G Vincenzi, B Santini, M Ambrogi, V Mineo, T C Persichetti, P Liuzzi, G Montesarchio, V Wolner, E Baldi, F Groeger, A M |
| description | Background/Aims: Abnormalities of the proteins involved in cell cycle checkpoints are extremely common among almost all neoplasms. This study aimed to investigate the expression of four components of the cell cycle machinery—p21, p16, p53, and proliferating cell nuclear antigen (PCNA)—in non-small cell lung cancer (NSCLC). Methods: The expression of p21, p16, p53, and PCNA was examined in 68 well characterised NSCLC specimens using immunohistochemistry. The coregulation of these proteins and their influence on survival were analysed using both univariate and multivariate analyses. Results: By univariate analysis, the expression of all the proteins examined, except for PCNA, was significantly correlated with survival. In multivariate analysis, the only immunohistochemical parameter able to influence overall survival was p16, confirming the hypothesis that the RB–p16 tumour suppressor pathway is inactivated in most lung cancer samples. Finally, the group of patients with NSCLC who were negative for both p21 and p16 had a significantly shorter overall survival. Conclusions: These results suggest that loss of control of cell cycle checkpoints is a common occurrence in lung cancers, and support the idea that functional cooperation between different cell cycle inhibitor proteins constitutes another level of regulation in cell growth control and tumour suppression. |
| doi_str_mv | 10.1136/jcp.57.1.58 |
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This study aimed to investigate the expression of four components of the cell cycle machinery—p21, p16, p53, and proliferating cell nuclear antigen (PCNA)—in non-small cell lung cancer (NSCLC). Methods: The expression of p21, p16, p53, and PCNA was examined in 68 well characterised NSCLC specimens using immunohistochemistry. The coregulation of these proteins and their influence on survival were analysed using both univariate and multivariate analyses. Results: By univariate analysis, the expression of all the proteins examined, except for PCNA, was significantly correlated with survival. In multivariate analysis, the only immunohistochemical parameter able to influence overall survival was p16, confirming the hypothesis that the RB–p16 tumour suppressor pathway is inactivated in most lung cancer samples. Finally, the group of patients with NSCLC who were negative for both p21 and p16 had a significantly shorter overall survival. Conclusions: These results suggest that loss of control of cell cycle checkpoints is a common occurrence in lung cancers, and support the idea that functional cooperation between different cell cycle inhibitor proteins constitutes another level of regulation in cell growth control and tumour suppression.</description><identifier>ISSN: 0021-9746</identifier><identifier>EISSN: 1472-4146</identifier><identifier>DOI: 10.1136/jcp.57.1.58</identifier><identifier>PMID: 14693837</identifier><identifier>CODEN: JCPAAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and Association of Clinical Pathologists</publisher><subject>Adult ; Aged ; Aged, 80 and over ; ALND ; Analysis of Variance ; Antigens ; axillary lymph node dissection ; Biological and medical sciences ; Biomarkers, Tumor - metabolism ; Cancer therapies ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell cycle ; Cell Cycle Proteins - metabolism ; Cell growth ; Cooperation ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins - metabolism ; Deoxyribonucleic acid ; DNA ; Female ; Genes ; H&E ; haematoxylin and eosin ; Humans ; Hypotheses ; Immunoenzyme Techniques ; Immunoglobulins ; Investigative techniques, diagnostic techniques (general aspects) ; Kinases ; Lung cancer ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; LVI ; lymphovascular invasion ; Male ; Medical prognosis ; Medical sciences ; Middle Aged ; Multivariate analysis ; Neoplasm Proteins - metabolism ; Original ; Pathogenesis ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Pneumology ; Prognosis ; Proportional Hazards Models ; Proteins ; Regulation ; Retrospective Studies ; sentinel lymph node ; SLN ; Statistical analysis ; Studies ; Survival Analysis ; Thoracic surgery ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Tumors of the respiratory system and mediastinum</subject><ispartof>Journal of clinical pathology, 2004-01, Vol.57 (1), p.58-63</ispartof><rights>Copyright 2004 Journal of Clinical Pathology</rights><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 BMJ Publishing Group Ltd.</rights><rights>Copyright: 2004 Copyright 2004 Journal of Clinical Pathology</rights><rights>Copyright © Copyright 2004 Journal of Clinical Pathology 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b581t-26c698c055325bc80d96447b70a81fc6e68a96fc05a4f5ef10f1cd3a2add3ac03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770176/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770176/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15437081$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14693837$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Esposito, V</creatorcontrib><creatorcontrib>Baldi, A</creatorcontrib><creatorcontrib>Tonini, G</creatorcontrib><creatorcontrib>Vincenzi, B</creatorcontrib><creatorcontrib>Santini, M</creatorcontrib><creatorcontrib>Ambrogi, V</creatorcontrib><creatorcontrib>Mineo, T C</creatorcontrib><creatorcontrib>Persichetti, P</creatorcontrib><creatorcontrib>Liuzzi, G</creatorcontrib><creatorcontrib>Montesarchio, V</creatorcontrib><creatorcontrib>Wolner, E</creatorcontrib><creatorcontrib>Baldi, F</creatorcontrib><creatorcontrib>Groeger, A M</creatorcontrib><title>Analysis of cell cycle regulator proteins in non-small cell lung cancer</title><title>Journal of clinical pathology</title><addtitle>J Clin Pathol</addtitle><description>Background/Aims: Abnormalities of the proteins involved in cell cycle checkpoints are extremely common among almost all neoplasms. This study aimed to investigate the expression of four components of the cell cycle machinery—p21, p16, p53, and proliferating cell nuclear antigen (PCNA)—in non-small cell lung cancer (NSCLC). Methods: The expression of p21, p16, p53, and PCNA was examined in 68 well characterised NSCLC specimens using immunohistochemistry. The coregulation of these proteins and their influence on survival were analysed using both univariate and multivariate analyses. Results: By univariate analysis, the expression of all the proteins examined, except for PCNA, was significantly correlated with survival. In multivariate analysis, the only immunohistochemical parameter able to influence overall survival was p16, confirming the hypothesis that the RB–p16 tumour suppressor pathway is inactivated in most lung cancer samples. Finally, the group of patients with NSCLC who were negative for both p21 and p16 had a significantly shorter overall survival. Conclusions: These results suggest that loss of control of cell cycle checkpoints is a common occurrence in lung cancers, and support the idea that functional cooperation between different cell cycle inhibitor proteins constitutes another level of regulation in cell growth control and tumour suppression.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>ALND</subject><subject>Analysis of Variance</subject><subject>Antigens</subject><subject>axillary lymph node dissection</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cancer therapies</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell growth</subject><subject>Cooperation</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclins - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Female</subject><subject>Genes</subject><subject>H&E</subject><subject>haematoxylin and eosin</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Immunoenzyme Techniques</subject><subject>Immunoglobulins</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>LVI</subject><subject>lymphovascular invasion</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Multivariate analysis</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Original</subject><subject>Pathogenesis</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Pneumology</subject><subject>Prognosis</subject><subject>Proportional Hazards Models</subject><subject>Proteins</subject><subject>Regulation</subject><subject>Retrospective Studies</subject><subject>sentinel lymph node</subject><subject>SLN</subject><subject>Statistical analysis</subject><subject>Studies</subject><subject>Survival Analysis</subject><subject>Thoracic surgery</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>0021-9746</issn><issn>1472-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kd2LEzEUxYMobq0--S4Doi8yNXfy2RehVF2FroKoD76ENE1q6kxSkxmx_70ZWrarLBJIIPeXc3PPQegx4BkA4S93Zj9jYgYzJu-gCVDR1BQov4smGDdQzwXlF-hBzjuMgQgg99FFKc-JJGKCLhdBt4fscxVdZWzbVuZgWlslux1a3cdU7VPsrQ-58qEKMdS50yM1ou0QtpXRwdj0EN1zus320emcoi9v33xevqtXHy_fLxeres0k9HXDDZ9LgxkjDVsbiTdzTqlYC6wlOMMtl3rOXQE0dcw6wA7MhuhGb8puMJmiV0fd_bDu7MbY0Cfdqn3ynU4HFbVXf1eC_6628ZcCITAIXgSenwRS_DnY3KvO53EaHWwcspIYC0ph7PT0H3AXh1TcykVLAm6ILGZOUX2ktrq1ygcXS1eztcGW5jFY58v1ouREoKFNU_jZLXxZG9t5c-uDF8cHJsWck3XXswJWY_6q5K-YUKCYLPSTm_ac2VPgBXh2AnQ2unWppOfzmWOUCCxvzOVzb39f13X6obgggqkPX5fq2-urT7C6Ymp1tnXd7f77wz9QvNNI</recordid><startdate>200401</startdate><enddate>200401</enddate><creator>Esposito, V</creator><creator>Baldi, A</creator><creator>Tonini, G</creator><creator>Vincenzi, B</creator><creator>Santini, M</creator><creator>Ambrogi, V</creator><creator>Mineo, T C</creator><creator>Persichetti, P</creator><creator>Liuzzi, G</creator><creator>Montesarchio, V</creator><creator>Wolner, E</creator><creator>Baldi, F</creator><creator>Groeger, A M</creator><general>BMJ Publishing Group Ltd and Association of Clinical Pathologists</general><general>BMJ</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><general>Copyright 2004 Journal of Clinical Pathology</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200401</creationdate><title>Analysis of cell cycle regulator proteins in non-small cell lung cancer</title><author>Esposito, V ; Baldi, A ; Tonini, G ; Vincenzi, B ; Santini, M ; Ambrogi, V ; Mineo, T C ; Persichetti, P ; Liuzzi, G ; Montesarchio, V ; Wolner, E ; Baldi, F ; Groeger, A M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b581t-26c698c055325bc80d96447b70a81fc6e68a96fc05a4f5ef10f1cd3a2add3ac03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>ALND</topic><topic>Analysis of Variance</topic><topic>Antigens</topic><topic>axillary lymph node dissection</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cancer therapies</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell cycle</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell growth</topic><topic>Cooperation</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclins - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Female</topic><topic>Genes</topic><topic>H&E</topic><topic>haematoxylin and eosin</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Immunoenzyme Techniques</topic><topic>Immunoglobulins</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>LVI</topic><topic>lymphovascular invasion</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Multivariate analysis</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Original</topic><topic>Pathogenesis</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Pneumology</topic><topic>Prognosis</topic><topic>Proportional Hazards Models</topic><topic>Proteins</topic><topic>Regulation</topic><topic>Retrospective Studies</topic><topic>sentinel lymph node</topic><topic>SLN</topic><topic>Statistical analysis</topic><topic>Studies</topic><topic>Survival Analysis</topic><topic>Thoracic surgery</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Tumors of the respiratory system and mediastinum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Esposito, V</creatorcontrib><creatorcontrib>Baldi, A</creatorcontrib><creatorcontrib>Tonini, G</creatorcontrib><creatorcontrib>Vincenzi, B</creatorcontrib><creatorcontrib>Santini, M</creatorcontrib><creatorcontrib>Ambrogi, V</creatorcontrib><creatorcontrib>Mineo, T C</creatorcontrib><creatorcontrib>Persichetti, P</creatorcontrib><creatorcontrib>Liuzzi, G</creatorcontrib><creatorcontrib>Montesarchio, V</creatorcontrib><creatorcontrib>Wolner, E</creatorcontrib><creatorcontrib>Baldi, F</creatorcontrib><creatorcontrib>Groeger, A M</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</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>ProQuest Central</collection><collection>BMJ Journals</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>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Esposito, V</au><au>Baldi, A</au><au>Tonini, G</au><au>Vincenzi, B</au><au>Santini, M</au><au>Ambrogi, V</au><au>Mineo, T C</au><au>Persichetti, P</au><au>Liuzzi, G</au><au>Montesarchio, V</au><au>Wolner, E</au><au>Baldi, F</au><au>Groeger, A M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of cell cycle regulator proteins in non-small cell lung cancer</atitle><jtitle>Journal of clinical pathology</jtitle><addtitle>J Clin Pathol</addtitle><date>2004-01</date><risdate>2004</risdate><volume>57</volume><issue>1</issue><spage>58</spage><epage>63</epage><pages>58-63</pages><issn>0021-9746</issn><eissn>1472-4146</eissn><coden>JCPAAK</coden><abstract>Background/Aims: Abnormalities of the proteins involved in cell cycle checkpoints are extremely common among almost all neoplasms. This study aimed to investigate the expression of four components of the cell cycle machinery—p21, p16, p53, and proliferating cell nuclear antigen (PCNA)—in non-small cell lung cancer (NSCLC). Methods: The expression of p21, p16, p53, and PCNA was examined in 68 well characterised NSCLC specimens using immunohistochemistry. The coregulation of these proteins and their influence on survival were analysed using both univariate and multivariate analyses. Results: By univariate analysis, the expression of all the proteins examined, except for PCNA, was significantly correlated with survival. In multivariate analysis, the only immunohistochemical parameter able to influence overall survival was p16, confirming the hypothesis that the RB–p16 tumour suppressor pathway is inactivated in most lung cancer samples. Finally, the group of patients with NSCLC who were negative for both p21 and p16 had a significantly shorter overall survival. Conclusions: These results suggest that loss of control of cell cycle checkpoints is a common occurrence in lung cancers, and support the idea that functional cooperation between different cell cycle inhibitor proteins constitutes another level of regulation in cell growth control and tumour suppression.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and Association of Clinical Pathologists</pub><pmid>14693837</pmid><doi>10.1136/jcp.57.1.58</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over ALND Analysis of Variance Antigens axillary lymph node dissection Biological and medical sciences Biomarkers, Tumor - metabolism Cancer therapies Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell cycle Cell Cycle Proteins - metabolism Cell growth Cooperation Cyclin-Dependent Kinase Inhibitor p16 - metabolism Cyclin-Dependent Kinase Inhibitor p21 Cyclins - metabolism Deoxyribonucleic acid DNA Female Genes H&E haematoxylin and eosin Humans Hypotheses Immunoenzyme Techniques Immunoglobulins Investigative techniques, diagnostic techniques (general aspects) Kinases Lung cancer Lung Neoplasms - metabolism Lung Neoplasms - pathology LVI lymphovascular invasion Male Medical prognosis Medical sciences Middle Aged Multivariate analysis Neoplasm Proteins - metabolism Original Pathogenesis Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Pneumology Prognosis Proportional Hazards Models Proteins Regulation Retrospective Studies sentinel lymph node SLN Statistical analysis Studies Survival Analysis Thoracic surgery Tumor Suppressor Protein p53 - metabolism Tumors Tumors of the respiratory system and mediastinum |
| title | Analysis of cell cycle regulator proteins in non-small cell lung cancer |
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