Long-Term Impact of Smoking on Lung Epithelial Proliferation in Current and Former Smokers
Background: Lung cancer risk remains elevated for many years after quitting smoking. To assess using proliferation indices in bronchial tissues as an intermediate endpoint biomarker in lung cancer chemoprevention trials, we determined the relationship between the extent, intensity, and cessation of...
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| Veröffentlicht in: | JNCI : Journal of the National Cancer Institute 2001-07, Vol.93 (14), p.1081-1088 |
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| creator | Lee, J. Jack Liu, Diane Lee, Jin Soo Kurie, Jonathan M. Khuri, Fadlo R. Ibarguen, Heladio Morice, Rodolfo C. Walsh, Garrett Ro, Jae Y. Broxson, Anita Hong, Waun Ki Hittelman, Walter N. |
| description | Background: Lung cancer risk remains elevated for many years after quitting smoking. To assess using proliferation indices in bronchial tissues as an intermediate endpoint biomarker in lung cancer chemoprevention trials, we determined the relationship between the extent, intensity, and cessation of tobacco smoking and proliferative changes in bronchial epithelial biopsy specimens. Methods: Bronchial biopsy specimens were obtained from up to six epithelial sites in 120 current smokers (median pack-years, 42) and 207 former smokers (median pack-years, 40; median quit-years, 8.1). Sections from the paraffin-embedded specimens were stained with hematoxylin–eosin to determine the metaplasia index and with an antibody to Ki-67 to determine the proliferative (labeling) index for the basal and parabasal (Ki-67 PLI) layers. All statistical tests were two-sided. Results: Biopsy sites with metaplasia had statistically significantly higher Ki-67-labeling indices than those without metaplasia (P |
| doi_str_mv | 10.1093/jnci/93.14.1081 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71019271</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>544772111</sourcerecordid><originalsourceid>FETCH-LOGICAL-c495t-5f5265f4ff7ad495d8a2ab8754db1425c6fb4ecf2880e9eb42688fd45f64a38a3</originalsourceid><addsrcrecordid>eNpdkFtrFDEYhoModq1eeydB0Lvp5ny41KW1hUEL1gO9CZmZpGY7k6zJDOi_N-suFszNS_I930t4AHiJ0RlGmq63sQ9rTc8wq3eFH4EVZgI1BCP-GKwQIrJRSrIT8KyULapHE_YUnGDMuFZCr8Btm-Jdc-PyBK-mne1nmDz8PKX7EO9girBdap7vwvzDjcGO8DqnMXiX7RzqNES4WXJ2cYY2DvAi5cnlv-sul-fgibdjcS-OeQq-XJzfbC6b9tOHq827tumZ5nPDPSeCe-a9tEN9GZQltlOSs6HDjPBe-I653hOlkNOuY0Qo5QfGvWCWKktPwdtD7y6nn4srs5lC6d042ujSUozECGsicQVf_wdu05Jj_Zsh1RgliqMKrQ9Qn1Mp2Xmzy2Gy-bfByOydm71zUxMzs3deN14da5ducsMDf5RcgTdHwJbejj7b2lAeOEqlkHrPNQculNn9-je3-d4ISSU3l99vjWi_tu-_kWvzkf4Bu5KZIg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>221032850</pqid></control><display><type>article</type><title>Long-Term Impact of Smoking on Lung Epithelial Proliferation in Current and Former Smokers</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Lee, J. Jack ; Liu, Diane ; Lee, Jin Soo ; Kurie, Jonathan M. ; Khuri, Fadlo R. ; Ibarguen, Heladio ; Morice, Rodolfo C. ; Walsh, Garrett ; Ro, Jae Y. ; Broxson, Anita ; Hong, Waun Ki ; Hittelman, Walter N.</creator><creatorcontrib>Lee, J. Jack ; Liu, Diane ; Lee, Jin Soo ; Kurie, Jonathan M. ; Khuri, Fadlo R. ; Ibarguen, Heladio ; Morice, Rodolfo C. ; Walsh, Garrett ; Ro, Jae Y. ; Broxson, Anita ; Hong, Waun Ki ; Hittelman, Walter N.</creatorcontrib><description>Background: Lung cancer risk remains elevated for many years after quitting smoking. To assess using proliferation indices in bronchial tissues as an intermediate endpoint biomarker in lung cancer chemoprevention trials, we determined the relationship between the extent, intensity, and cessation of tobacco smoking and proliferative changes in bronchial epithelial biopsy specimens. Methods: Bronchial biopsy specimens were obtained from up to six epithelial sites in 120 current smokers (median pack-years, 42) and 207 former smokers (median pack-years, 40; median quit-years, 8.1). Sections from the paraffin-embedded specimens were stained with hematoxylin–eosin to determine the metaplasia index and with an antibody to Ki-67 to determine the proliferative (labeling) index for the basal and parabasal (Ki-67 PLI) layers. All statistical tests were two-sided. Results: Biopsy sites with metaplasia had statistically significantly higher Ki-67-labeling indices than those without metaplasia (P<.001) in both current and former smokers. Increased proliferation was observed in multiple biopsy sites, with the average Ki-67 PLI of the subject strongly correlating with the metaplasia index (r = .72 for current smokers; P<.001), even in sites without metaplasia (r = .23 for current smokers; P<.001). In current smokers, the Ki-67 PLI was associated with the number of packs smoked/day (P = .02) but not with smoking years or pack-years. In subjects who had quit smoking, the Ki-67 PLI dropped statistically significantly within 1 year (P = .008) but remained detectable for more than 20 years, even in the absence of squamous metaplasia. Conclusion: Smoking appears to elicit a dose-related proliferative response in the bronchial epithelia of active smokers. Although the proliferative response decreased gradually in former smokers, a subset of individuals had detectable proliferation for many years and may benefit from targeted chemoprevention. Bronchial epithelial proliferation, measured by Ki-67, may provide a useful biomarker in the assessment of lung cancer risk and in the response to chemopreventive interventions.</description><identifier>ISSN: 0027-8874</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/93.14.1081</identifier><identifier>PMID: 11459869</identifier><identifier>CODEN: JNCIEQ</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Biomarkers, Tumor - analysis ; Biopsy ; Cell Division ; Epithelial Cells - immunology ; Epithelial Cells - pathology ; Female ; Humans ; Immunohistochemistry ; Ki-67 Antigen - analysis ; Lung - immunology ; Lung - pathology ; Male ; Medical sciences ; Metaplasia ; Middle Aged ; Pneumology ; Smoking - adverse effects ; Smoking Cessation ; Time Factors ; Tumors of the respiratory system and mediastinum</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2001-07, Vol.93 (14), p.1081-1088</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Jul 18, 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-5f5265f4ff7ad495d8a2ab8754db1425c6fb4ecf2880e9eb42688fd45f64a38a3</citedby><cites>FETCH-LOGICAL-c495t-5f5265f4ff7ad495d8a2ab8754db1425c6fb4ecf2880e9eb42688fd45f64a38a3</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=13376799$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11459869$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, J. Jack</creatorcontrib><creatorcontrib>Liu, Diane</creatorcontrib><creatorcontrib>Lee, Jin Soo</creatorcontrib><creatorcontrib>Kurie, Jonathan M.</creatorcontrib><creatorcontrib>Khuri, Fadlo R.</creatorcontrib><creatorcontrib>Ibarguen, Heladio</creatorcontrib><creatorcontrib>Morice, Rodolfo C.</creatorcontrib><creatorcontrib>Walsh, Garrett</creatorcontrib><creatorcontrib>Ro, Jae Y.</creatorcontrib><creatorcontrib>Broxson, Anita</creatorcontrib><creatorcontrib>Hong, Waun Ki</creatorcontrib><creatorcontrib>Hittelman, Walter N.</creatorcontrib><title>Long-Term Impact of Smoking on Lung Epithelial Proliferation in Current and Former Smokers</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>JNCI J Natl Cancer Inst</addtitle><description>Background: Lung cancer risk remains elevated for many years after quitting smoking. To assess using proliferation indices in bronchial tissues as an intermediate endpoint biomarker in lung cancer chemoprevention trials, we determined the relationship between the extent, intensity, and cessation of tobacco smoking and proliferative changes in bronchial epithelial biopsy specimens. Methods: Bronchial biopsy specimens were obtained from up to six epithelial sites in 120 current smokers (median pack-years, 42) and 207 former smokers (median pack-years, 40; median quit-years, 8.1). Sections from the paraffin-embedded specimens were stained with hematoxylin–eosin to determine the metaplasia index and with an antibody to Ki-67 to determine the proliferative (labeling) index for the basal and parabasal (Ki-67 PLI) layers. All statistical tests were two-sided. Results: Biopsy sites with metaplasia had statistically significantly higher Ki-67-labeling indices than those without metaplasia (P<.001) in both current and former smokers. Increased proliferation was observed in multiple biopsy sites, with the average Ki-67 PLI of the subject strongly correlating with the metaplasia index (r = .72 for current smokers; P<.001), even in sites without metaplasia (r = .23 for current smokers; P<.001). In current smokers, the Ki-67 PLI was associated with the number of packs smoked/day (P = .02) but not with smoking years or pack-years. In subjects who had quit smoking, the Ki-67 PLI dropped statistically significantly within 1 year (P = .008) but remained detectable for more than 20 years, even in the absence of squamous metaplasia. Conclusion: Smoking appears to elicit a dose-related proliferative response in the bronchial epithelia of active smokers. Although the proliferative response decreased gradually in former smokers, a subset of individuals had detectable proliferation for many years and may benefit from targeted chemoprevention. Bronchial epithelial proliferation, measured by Ki-67, may provide a useful biomarker in the assessment of lung cancer risk and in the response to chemopreventive interventions.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biopsy</subject><subject>Cell Division</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - pathology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Ki-67 Antigen - analysis</subject><subject>Lung - immunology</subject><subject>Lung - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metaplasia</subject><subject>Middle Aged</subject><subject>Pneumology</subject><subject>Smoking - adverse effects</subject><subject>Smoking Cessation</subject><subject>Time Factors</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>0027-8874</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkFtrFDEYhoModq1eeydB0Lvp5ny41KW1hUEL1gO9CZmZpGY7k6zJDOi_N-suFszNS_I930t4AHiJ0RlGmq63sQ9rTc8wq3eFH4EVZgI1BCP-GKwQIrJRSrIT8KyULapHE_YUnGDMuFZCr8Btm-Jdc-PyBK-mne1nmDz8PKX7EO9girBdap7vwvzDjcGO8DqnMXiX7RzqNES4WXJ2cYY2DvAi5cnlv-sul-fgibdjcS-OeQq-XJzfbC6b9tOHq827tumZ5nPDPSeCe-a9tEN9GZQltlOSs6HDjPBe-I653hOlkNOuY0Qo5QfGvWCWKktPwdtD7y6nn4srs5lC6d042ujSUozECGsicQVf_wdu05Jj_Zsh1RgliqMKrQ9Qn1Mp2Xmzy2Gy-bfByOydm71zUxMzs3deN14da5ducsMDf5RcgTdHwJbejj7b2lAeOEqlkHrPNQculNn9-je3-d4ISSU3l99vjWi_tu-_kWvzkf4Bu5KZIg</recordid><startdate>20010718</startdate><enddate>20010718</enddate><creator>Lee, J. Jack</creator><creator>Liu, Diane</creator><creator>Lee, Jin Soo</creator><creator>Kurie, Jonathan M.</creator><creator>Khuri, Fadlo R.</creator><creator>Ibarguen, Heladio</creator><creator>Morice, Rodolfo C.</creator><creator>Walsh, Garrett</creator><creator>Ro, Jae Y.</creator><creator>Broxson, Anita</creator><creator>Hong, Waun Ki</creator><creator>Hittelman, Walter N.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</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>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20010718</creationdate><title>Long-Term Impact of Smoking on Lung Epithelial Proliferation in Current and Former Smokers</title><author>Lee, J. Jack ; Liu, Diane ; Lee, Jin Soo ; Kurie, Jonathan M. ; Khuri, Fadlo R. ; Ibarguen, Heladio ; Morice, Rodolfo C. ; Walsh, Garrett ; Ro, Jae Y. ; Broxson, Anita ; Hong, Waun Ki ; Hittelman, Walter N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-5f5265f4ff7ad495d8a2ab8754db1425c6fb4ecf2880e9eb42688fd45f64a38a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biopsy</topic><topic>Cell Division</topic><topic>Epithelial Cells - immunology</topic><topic>Epithelial Cells - pathology</topic><topic>Female</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Ki-67 Antigen - analysis</topic><topic>Lung - immunology</topic><topic>Lung - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metaplasia</topic><topic>Middle Aged</topic><topic>Pneumology</topic><topic>Smoking - adverse effects</topic><topic>Smoking Cessation</topic><topic>Time Factors</topic><topic>Tumors of the respiratory system and mediastinum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, J. Jack</creatorcontrib><creatorcontrib>Liu, Diane</creatorcontrib><creatorcontrib>Lee, Jin Soo</creatorcontrib><creatorcontrib>Kurie, Jonathan M.</creatorcontrib><creatorcontrib>Khuri, Fadlo R.</creatorcontrib><creatorcontrib>Ibarguen, Heladio</creatorcontrib><creatorcontrib>Morice, Rodolfo C.</creatorcontrib><creatorcontrib>Walsh, Garrett</creatorcontrib><creatorcontrib>Ro, Jae Y.</creatorcontrib><creatorcontrib>Broxson, Anita</creatorcontrib><creatorcontrib>Hong, Waun Ki</creatorcontrib><creatorcontrib>Hittelman, Walter N.</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>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, J. Jack</au><au>Liu, Diane</au><au>Lee, Jin Soo</au><au>Kurie, Jonathan M.</au><au>Khuri, Fadlo R.</au><au>Ibarguen, Heladio</au><au>Morice, Rodolfo C.</au><au>Walsh, Garrett</au><au>Ro, Jae Y.</au><au>Broxson, Anita</au><au>Hong, Waun Ki</au><au>Hittelman, Walter N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-Term Impact of Smoking on Lung Epithelial Proliferation in Current and Former Smokers</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>JNCI J Natl Cancer Inst</addtitle><date>2001-07-18</date><risdate>2001</risdate><volume>93</volume><issue>14</issue><spage>1081</spage><epage>1088</epage><pages>1081-1088</pages><issn>0027-8874</issn><eissn>1460-2105</eissn><coden>JNCIEQ</coden><abstract>Background: Lung cancer risk remains elevated for many years after quitting smoking. To assess using proliferation indices in bronchial tissues as an intermediate endpoint biomarker in lung cancer chemoprevention trials, we determined the relationship between the extent, intensity, and cessation of tobacco smoking and proliferative changes in bronchial epithelial biopsy specimens. Methods: Bronchial biopsy specimens were obtained from up to six epithelial sites in 120 current smokers (median pack-years, 42) and 207 former smokers (median pack-years, 40; median quit-years, 8.1). Sections from the paraffin-embedded specimens were stained with hematoxylin–eosin to determine the metaplasia index and with an antibody to Ki-67 to determine the proliferative (labeling) index for the basal and parabasal (Ki-67 PLI) layers. All statistical tests were two-sided. Results: Biopsy sites with metaplasia had statistically significantly higher Ki-67-labeling indices than those without metaplasia (P<.001) in both current and former smokers. Increased proliferation was observed in multiple biopsy sites, with the average Ki-67 PLI of the subject strongly correlating with the metaplasia index (r = .72 for current smokers; P<.001), even in sites without metaplasia (r = .23 for current smokers; P<.001). In current smokers, the Ki-67 PLI was associated with the number of packs smoked/day (P = .02) but not with smoking years or pack-years. In subjects who had quit smoking, the Ki-67 PLI dropped statistically significantly within 1 year (P = .008) but remained detectable for more than 20 years, even in the absence of squamous metaplasia. Conclusion: Smoking appears to elicit a dose-related proliferative response in the bronchial epithelia of active smokers. Although the proliferative response decreased gradually in former smokers, a subset of individuals had detectable proliferation for many years and may benefit from targeted chemoprevention. Bronchial epithelial proliferation, measured by Ki-67, may provide a useful biomarker in the assessment of lung cancer risk and in the response to chemopreventive interventions.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>11459869</pmid><doi>10.1093/jnci/93.14.1081</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Biological and medical sciences Biomarkers, Tumor - analysis Biopsy Cell Division Epithelial Cells - immunology Epithelial Cells - pathology Female Humans Immunohistochemistry Ki-67 Antigen - analysis Lung - immunology Lung - pathology Male Medical sciences Metaplasia Middle Aged Pneumology Smoking - adverse effects Smoking Cessation Time Factors Tumors of the respiratory system and mediastinum |
| title | Long-Term Impact of Smoking on Lung Epithelial Proliferation in Current and Former Smokers |
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