Oral leukoplakias with different degrees of dysplasia: comparative study of hMLH1, p53, and AgNOR
J Oral Pathol Med (2011) 40: 305–311 Background: hMLH1 is one of the major proteins of the mammalian mismatch repair system. It has been suggested that the mismatch repair machinery could be linked to p53, a tumor suppressor protein. The AgNOR technique is used to assess cell proliferation. The aim...
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| creator | Caldeira, Patrícia Carlos Aguiar, Maria Cássia Ferreira Mesquita, Ricardo Alves do Carmo, Maria Auxiliadora Vieira |
| description | J Oral Pathol Med (2011) 40: 305–311
Background: hMLH1 is one of the major proteins of the mammalian mismatch repair system. It has been suggested that the mismatch repair machinery could be linked to p53, a tumor suppressor protein. The AgNOR technique is used to assess cell proliferation. The aim was to compare the immunoexpression of hMLH1 and p53, and AgNOR number in oral leukoplakias with different degrees of dysplasia.
Methods: Sixty‐two samples were evaluated by immunohistochemistry for hMLH1 and p53, and AgNOR technique, being 17 without dysplasia, 19 with mild dysplasia, 16 with moderate dysplasia, and 10 with severe dysplasia.
Results: hMLH1 immunoexpression showed decreasing indexes, while p53 and AgNOR showed increasing indexes from lesions with lower degrees of dysplasia to lesions with more severe dysplasia. An inverse correlation between hMLH1 and both p53 and AgNOR, and a direct correlation between p53 and AgNOR were observed.
Conclusions: Alterations in the immunoexpression pattern of hMLH1 and p53 seemed to be early events in oral carcinogenesis. During acquisition of a more dysplastic phenotype, keratinocytes may show diminished capacity of DNA repair and tumor suppression, as well as higher cellular proliferation, and these pathways can be somehow interconnected. |
| doi_str_mv | 10.1111/j.1600-0714.2010.01000.x |
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Background: hMLH1 is one of the major proteins of the mammalian mismatch repair system. It has been suggested that the mismatch repair machinery could be linked to p53, a tumor suppressor protein. The AgNOR technique is used to assess cell proliferation. The aim was to compare the immunoexpression of hMLH1 and p53, and AgNOR number in oral leukoplakias with different degrees of dysplasia.
Methods: Sixty‐two samples were evaluated by immunohistochemistry for hMLH1 and p53, and AgNOR technique, being 17 without dysplasia, 19 with mild dysplasia, 16 with moderate dysplasia, and 10 with severe dysplasia.
Results: hMLH1 immunoexpression showed decreasing indexes, while p53 and AgNOR showed increasing indexes from lesions with lower degrees of dysplasia to lesions with more severe dysplasia. An inverse correlation between hMLH1 and both p53 and AgNOR, and a direct correlation between p53 and AgNOR were observed.
Conclusions: Alterations in the immunoexpression pattern of hMLH1 and p53 seemed to be early events in oral carcinogenesis. During acquisition of a more dysplastic phenotype, keratinocytes may show diminished capacity of DNA repair and tumor suppression, as well as higher cellular proliferation, and these pathways can be somehow interconnected.</description><identifier>ISSN: 0904-2512</identifier><identifier>EISSN: 1600-0714</identifier><identifier>DOI: 10.1111/j.1600-0714.2010.01000.x</identifier><identifier>PMID: 21208285</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adaptor Proteins, Signal Transducing - biosynthesis ; Adult ; Aged ; Aged, 80 and over ; AgNOR ; Analysis of Variance ; Antigens, Nuclear - biosynthesis ; Carcinogenesis ; Case-Control Studies ; Cell Proliferation ; DNA Mismatch Repair ; DNA repair ; Dysplasia ; Female ; human MLH1 protein ; Humans ; Immunohistochemistry ; Keratinocytes ; Keratinocytes - metabolism ; Keratinocytes - pathology ; Leukokeratosis ; Leukoplakia, Oral - metabolism ; Leukoplakia, Oral - pathology ; Male ; Middle Aged ; mismatch repair ; Mouth Mucosa - cytology ; Mouth Mucosa - metabolism ; Mouth Mucosa - pathology ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; MutL Protein Homolog 1 ; Nuclear Proteins - biosynthesis ; oral leukoplakia ; p53 protein ; Statistics, Nonparametric ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - biosynthesis ; Tumors</subject><ispartof>Journal of oral pathology & medicine, 2011-04, Vol.40 (4), p.305-311</ispartof><rights>2011 John Wiley & Sons A/S</rights><rights>2011 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4390-4afc000e7ef2363a8405545624e2d3d072d3b6eec8a5283a93a7dbb96ca1b3873</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-0714.2010.01000.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-0714.2010.01000.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21208285$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Caldeira, Patrícia Carlos</creatorcontrib><creatorcontrib>Aguiar, Maria Cássia Ferreira</creatorcontrib><creatorcontrib>Mesquita, Ricardo Alves</creatorcontrib><creatorcontrib>do Carmo, Maria Auxiliadora Vieira</creatorcontrib><title>Oral leukoplakias with different degrees of dysplasia: comparative study of hMLH1, p53, and AgNOR</title><title>Journal of oral pathology & medicine</title><addtitle>J Oral Pathol Med</addtitle><description>J Oral Pathol Med (2011) 40: 305–311
Background: hMLH1 is one of the major proteins of the mammalian mismatch repair system. It has been suggested that the mismatch repair machinery could be linked to p53, a tumor suppressor protein. The AgNOR technique is used to assess cell proliferation. The aim was to compare the immunoexpression of hMLH1 and p53, and AgNOR number in oral leukoplakias with different degrees of dysplasia.
Methods: Sixty‐two samples were evaluated by immunohistochemistry for hMLH1 and p53, and AgNOR technique, being 17 without dysplasia, 19 with mild dysplasia, 16 with moderate dysplasia, and 10 with severe dysplasia.
Results: hMLH1 immunoexpression showed decreasing indexes, while p53 and AgNOR showed increasing indexes from lesions with lower degrees of dysplasia to lesions with more severe dysplasia. An inverse correlation between hMLH1 and both p53 and AgNOR, and a direct correlation between p53 and AgNOR were observed.
Conclusions: Alterations in the immunoexpression pattern of hMLH1 and p53 seemed to be early events in oral carcinogenesis. During acquisition of a more dysplastic phenotype, keratinocytes may show diminished capacity of DNA repair and tumor suppression, as well as higher cellular proliferation, and these pathways can be somehow interconnected.</description><subject>Adaptor Proteins, Signal Transducing - biosynthesis</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>AgNOR</subject><subject>Analysis of Variance</subject><subject>Antigens, Nuclear - biosynthesis</subject><subject>Carcinogenesis</subject><subject>Case-Control Studies</subject><subject>Cell Proliferation</subject><subject>DNA Mismatch Repair</subject><subject>DNA repair</subject><subject>Dysplasia</subject><subject>Female</subject><subject>human MLH1 protein</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Keratinocytes</subject><subject>Keratinocytes - metabolism</subject><subject>Keratinocytes - pathology</subject><subject>Leukokeratosis</subject><subject>Leukoplakia, Oral - metabolism</subject><subject>Leukoplakia, Oral - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>mismatch repair</subject><subject>Mouth Mucosa - cytology</subject><subject>Mouth Mucosa - metabolism</subject><subject>Mouth Mucosa - pathology</subject><subject>Mouth Neoplasms - metabolism</subject><subject>Mouth Neoplasms - pathology</subject><subject>MutL Protein Homolog 1</subject><subject>Nuclear Proteins - biosynthesis</subject><subject>oral leukoplakia</subject><subject>p53 protein</subject><subject>Statistics, Nonparametric</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - biosynthesis</subject><subject>Tumors</subject><issn>0904-2512</issn><issn>1600-0714</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kFtv0zAYhi0EYmXwF5DvuFk6H-MEiYtpgnZTtyLE6c76En_Z3KZNFies_fdz6FZLPsjv81ryQwjlbMrjOF9NecpYwgxXU8HibZyMTXevyOQYvCYTljOVCM3FCXkXwooxbqTib8mJ4IJlItMTAssOalrjsG7aGtYeAn30_T11vqqww21PHd51iIE2FXX7EKHg4TMtm00LHfT-H9LQD24_5vc3izk_o62WZxS2jl7c3S5_vCdvKqgDfnjeT8mvb19_Xs6TxXJ2dXmxSEolc5YoqMr4BzRYCZlKyBTTWulUKBROOmbiWqSIZQZaZBJyCcYVRZ6WwAuZGXlKPh3ebbvmYcDQ240PJdY1bLEZgs2jlJQrpSP58Zkcig0623Z-A93evliJwJcD8Ohr3B9zzuxo367sKNmOku1o3_63b3f2evl9PMV-cuj70OPu2IdubVMjjbZ_bmc2m_1OtZnP7F_5BBMnhUM</recordid><startdate>201104</startdate><enddate>201104</enddate><creator>Caldeira, Patrícia Carlos</creator><creator>Aguiar, Maria Cássia Ferreira</creator><creator>Mesquita, Ricardo Alves</creator><creator>do Carmo, Maria Auxiliadora Vieira</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>201104</creationdate><title>Oral leukoplakias with different degrees of dysplasia: comparative study of hMLH1, p53, and AgNOR</title><author>Caldeira, Patrícia Carlos ; Aguiar, Maria Cássia Ferreira ; Mesquita, Ricardo Alves ; do Carmo, Maria Auxiliadora Vieira</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4390-4afc000e7ef2363a8405545624e2d3d072d3b6eec8a5283a93a7dbb96ca1b3873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adaptor Proteins, Signal Transducing - biosynthesis</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>AgNOR</topic><topic>Analysis of Variance</topic><topic>Antigens, Nuclear - biosynthesis</topic><topic>Carcinogenesis</topic><topic>Case-Control Studies</topic><topic>Cell Proliferation</topic><topic>DNA Mismatch Repair</topic><topic>DNA repair</topic><topic>Dysplasia</topic><topic>Female</topic><topic>human MLH1 protein</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Keratinocytes</topic><topic>Keratinocytes - metabolism</topic><topic>Keratinocytes - pathology</topic><topic>Leukokeratosis</topic><topic>Leukoplakia, Oral - metabolism</topic><topic>Leukoplakia, Oral - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>mismatch repair</topic><topic>Mouth Mucosa - cytology</topic><topic>Mouth Mucosa - metabolism</topic><topic>Mouth Mucosa - pathology</topic><topic>Mouth Neoplasms - metabolism</topic><topic>Mouth Neoplasms - pathology</topic><topic>MutL Protein Homolog 1</topic><topic>Nuclear Proteins - biosynthesis</topic><topic>oral leukoplakia</topic><topic>p53 protein</topic><topic>Statistics, Nonparametric</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - biosynthesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Caldeira, Patrícia Carlos</creatorcontrib><creatorcontrib>Aguiar, Maria Cássia Ferreira</creatorcontrib><creatorcontrib>Mesquita, Ricardo Alves</creatorcontrib><creatorcontrib>do Carmo, Maria Auxiliadora Vieira</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of oral pathology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Caldeira, Patrícia Carlos</au><au>Aguiar, Maria Cássia Ferreira</au><au>Mesquita, Ricardo Alves</au><au>do Carmo, Maria Auxiliadora Vieira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oral leukoplakias with different degrees of dysplasia: comparative study of hMLH1, p53, and AgNOR</atitle><jtitle>Journal of oral pathology & medicine</jtitle><addtitle>J Oral Pathol Med</addtitle><date>2011-04</date><risdate>2011</risdate><volume>40</volume><issue>4</issue><spage>305</spage><epage>311</epage><pages>305-311</pages><issn>0904-2512</issn><eissn>1600-0714</eissn><abstract>J Oral Pathol Med (2011) 40: 305–311
Background: hMLH1 is one of the major proteins of the mammalian mismatch repair system. It has been suggested that the mismatch repair machinery could be linked to p53, a tumor suppressor protein. The AgNOR technique is used to assess cell proliferation. The aim was to compare the immunoexpression of hMLH1 and p53, and AgNOR number in oral leukoplakias with different degrees of dysplasia.
Methods: Sixty‐two samples were evaluated by immunohistochemistry for hMLH1 and p53, and AgNOR technique, being 17 without dysplasia, 19 with mild dysplasia, 16 with moderate dysplasia, and 10 with severe dysplasia.
Results: hMLH1 immunoexpression showed decreasing indexes, while p53 and AgNOR showed increasing indexes from lesions with lower degrees of dysplasia to lesions with more severe dysplasia. An inverse correlation between hMLH1 and both p53 and AgNOR, and a direct correlation between p53 and AgNOR were observed.
Conclusions: Alterations in the immunoexpression pattern of hMLH1 and p53 seemed to be early events in oral carcinogenesis. During acquisition of a more dysplastic phenotype, keratinocytes may show diminished capacity of DNA repair and tumor suppression, as well as higher cellular proliferation, and these pathways can be somehow interconnected.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21208285</pmid><doi>10.1111/j.1600-0714.2010.01000.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - biosynthesis Adult Aged Aged, 80 and over AgNOR Analysis of Variance Antigens, Nuclear - biosynthesis Carcinogenesis Case-Control Studies Cell Proliferation DNA Mismatch Repair DNA repair Dysplasia Female human MLH1 protein Humans Immunohistochemistry Keratinocytes Keratinocytes - metabolism Keratinocytes - pathology Leukokeratosis Leukoplakia, Oral - metabolism Leukoplakia, Oral - pathology Male Middle Aged mismatch repair Mouth Mucosa - cytology Mouth Mucosa - metabolism Mouth Mucosa - pathology Mouth Neoplasms - metabolism Mouth Neoplasms - pathology MutL Protein Homolog 1 Nuclear Proteins - biosynthesis oral leukoplakia p53 protein Statistics, Nonparametric Tumor suppressor genes Tumor Suppressor Protein p53 - biosynthesis Tumors |
| title | Oral leukoplakias with different degrees of dysplasia: comparative study of hMLH1, p53, and AgNOR |
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