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TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens
In several tumors the transketolase activity, controlled inter alia by enzymes of the pentose phosphate pathway which is an alternative, energy generating reaction-cascade to glycolysis, has been correlated with proliferation. The increase of thiamine-dependent transketolase enzyme reactions is indu...
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Published in: | Diagnostic pathology 2008-08, Vol.3 (1), p.35-35, Article 35 |
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description | In several tumors the transketolase activity, controlled inter alia by enzymes of the pentose phosphate pathway which is an alternative, energy generating reaction-cascade to glycolysis, has been correlated with proliferation. The increase of thiamine-dependent transketolase enzyme reactions is induced especially through upregulated transketolase-like enzyme 1 (TKTL1)-activity; that shows TKTL1 to be a causative enzyme for tumors enhanced, anaerobic glucose degradation. We investigated TKTL1-expression in 88 human, formalin-fixed non-small cell lung cancer tissues and 24 carcinomas of the breast by immunohistochemical stainings applying a 0 to 3 staining-score system (3 = strongest expression). For means of validation we additionally stained 40 NSCLC fixed and paraffin-embedded utilizing the HOPE-technique; showing comparable results to the formalin-fixed, paraffin-embedded specimens (not shown). Potential correlations with age, sex, TNM-classification parameters and tumor grading as well as tumor transcription factor 1 (TTF1) and surfactant protein A (SPA) expression were investigated. 40.9% of the analyzed lung tumors expressed TKTL1 weakly (Score 1), 38.6% moderately (score 2) and 17.1% strongly (score 3). 3 tumors were diagnosed TKTL1-negative (3.4%; score 0). All breast cancer specimen stainings were positive and scored 1: 32%; scored 2: 36%; scored 3: 32%. Alveolar macrophages and Alveolar Epithelial Cells Type II were also found to be TKTL1-positive.None of the listed clinical parameters could be found to show a significant correlation to TKTL1 signal appearance. Although we describe the expression of TKTL1 in lung cancers, we need to state that up till now there is no scientific indication for any treatment regimens based upon these findings. |
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The increase of thiamine-dependent transketolase enzyme reactions is induced especially through upregulated transketolase-like enzyme 1 (TKTL1)-activity; that shows TKTL1 to be a causative enzyme for tumors enhanced, anaerobic glucose degradation. We investigated TKTL1-expression in 88 human, formalin-fixed non-small cell lung cancer tissues and 24 carcinomas of the breast by immunohistochemical stainings applying a 0 to 3 staining-score system (3 = strongest expression). For means of validation we additionally stained 40 NSCLC fixed and paraffin-embedded utilizing the HOPE-technique; showing comparable results to the formalin-fixed, paraffin-embedded specimens (not shown). Potential correlations with age, sex, TNM-classification parameters and tumor grading as well as tumor transcription factor 1 (TTF1) and surfactant protein A (SPA) expression were investigated. 40.9% of the analyzed lung tumors expressed TKTL1 weakly (Score 1), 38.6% moderately (score 2) and 17.1% strongly (score 3). 3 tumors were diagnosed TKTL1-negative (3.4%; score 0). All breast cancer specimen stainings were positive and scored 1: 32%; scored 2: 36%; scored 3: 32%. Alveolar macrophages and Alveolar Epithelial Cells Type II were also found to be TKTL1-positive.None of the listed clinical parameters could be found to show a significant correlation to TKTL1 signal appearance. Although we describe the expression of TKTL1 in lung cancers, we need to state that up till now there is no scientific indication for any treatment regimens based upon these findings.</description><identifier>ISSN: 1746-1596</identifier><identifier>EISSN: 1746-1596</identifier><identifier>DOI: 10.1186/1746-1596-3-35</identifier><identifier>PMID: 18700018</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Care and treatment ; Gene expression ; Genetic aspects ; Health aspects ; Lung cancer, Non-small cell ; Physiological aspects ; Short Report</subject><ispartof>Diagnostic pathology, 2008-08, Vol.3 (1), p.35-35, Article 35</ispartof><rights>COPYRIGHT 2008 BioMed Central Ltd.</rights><rights>Copyright © 2008 Schultz et al; licensee BioMed Central Ltd. 2008 Schultz et al; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b580t-6e66a78052035792bb8dc871216328710ed32464e8d2b5e4e99f8e1f1dd5d6293</citedby><cites>FETCH-LOGICAL-b580t-6e66a78052035792bb8dc871216328710ed32464e8d2b5e4e99f8e1f1dd5d6293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2526982/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2526982/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18700018$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schultz, Holger</creatorcontrib><creatorcontrib>Kähler, Daniel</creatorcontrib><creatorcontrib>Branscheid, Detlev</creatorcontrib><creatorcontrib>Vollmer, Ekkehard</creatorcontrib><creatorcontrib>Zabel, Peter</creatorcontrib><creatorcontrib>Goldmann, Torsten</creatorcontrib><title>TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens</title><title>Diagnostic pathology</title><addtitle>Diagn Pathol</addtitle><description>In several tumors the transketolase activity, controlled inter alia by enzymes of the pentose phosphate pathway which is an alternative, energy generating reaction-cascade to glycolysis, has been correlated with proliferation. The increase of thiamine-dependent transketolase enzyme reactions is induced especially through upregulated transketolase-like enzyme 1 (TKTL1)-activity; that shows TKTL1 to be a causative enzyme for tumors enhanced, anaerobic glucose degradation. We investigated TKTL1-expression in 88 human, formalin-fixed non-small cell lung cancer tissues and 24 carcinomas of the breast by immunohistochemical stainings applying a 0 to 3 staining-score system (3 = strongest expression). For means of validation we additionally stained 40 NSCLC fixed and paraffin-embedded utilizing the HOPE-technique; showing comparable results to the formalin-fixed, paraffin-embedded specimens (not shown). Potential correlations with age, sex, TNM-classification parameters and tumor grading as well as tumor transcription factor 1 (TTF1) and surfactant protein A (SPA) expression were investigated. 40.9% of the analyzed lung tumors expressed TKTL1 weakly (Score 1), 38.6% moderately (score 2) and 17.1% strongly (score 3). 3 tumors were diagnosed TKTL1-negative (3.4%; score 0). All breast cancer specimen stainings were positive and scored 1: 32%; scored 2: 36%; scored 3: 32%. Alveolar macrophages and Alveolar Epithelial Cells Type II were also found to be TKTL1-positive.None of the listed clinical parameters could be found to show a significant correlation to TKTL1 signal appearance. Although we describe the expression of TKTL1 in lung cancers, we need to state that up till now there is no scientific indication for any treatment regimens based upon these findings.</description><subject>Care and treatment</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Lung cancer, Non-small cell</subject><subject>Physiological aspects</subject><subject>Short Report</subject><issn>1746-1596</issn><issn>1746-1596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp1kk2LFDEQhhtR3HX16lECHjz1mu9OLsKw-LE4IMJ4Dumkus3SnYzJzKL_3rQzrDu4EpIKlTcPbyrVNC8JviREybek47IlQsuWtUw8as7vEo_v7c-aZ6XcYMyFoPhpc0ZUhzEm6rz5uvm8WRMUCkq3kOHnNkMp4FGIyKLJ5hHQNuVdSBGlAcUU2zLbaUIO6jLt44icjQ4yKltwYYZYnjdPBjsVeHGMF823D-83V5_a9ZeP11erddsLhXetBCltp3A1xESnad8r71RHKJGM1ojBM8olB-VpL4CD1oMCMhDvhZdUs4vm-sD1yd6YbQ6zzb9MssH8SaQ8GluNuwkM15jwgfd1Ws6kto5hzcWgeE-hx1BZ7w6s7b6fwTuIu2ynE-jpSQzfzZhuDRVUakUrYHUA9CH9B3B64tJslu8xy_cYZpiojDdHEzn92EPZmTmUpc42QtoX07Eq0qJTVfn6oBxtfV2IQ6pMt6jNiihOeKc5rqrLB1R1eJiDSxGGUPMPXXA5lZJhuPNPsFm67V_Hr-6X7a_82F7sN2vtzc0</recordid><startdate>20080812</startdate><enddate>20080812</enddate><creator>Schultz, Holger</creator><creator>Kähler, Daniel</creator><creator>Branscheid, Detlev</creator><creator>Vollmer, Ekkehard</creator><creator>Zabel, Peter</creator><creator>Goldmann, Torsten</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20080812</creationdate><title>TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens</title><author>Schultz, Holger ; Kähler, Daniel ; Branscheid, Detlev ; Vollmer, Ekkehard ; Zabel, Peter ; Goldmann, Torsten</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b580t-6e66a78052035792bb8dc871216328710ed32464e8d2b5e4e99f8e1f1dd5d6293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Care and treatment</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Lung cancer, Non-small cell</topic><topic>Physiological aspects</topic><topic>Short Report</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schultz, Holger</creatorcontrib><creatorcontrib>Kähler, Daniel</creatorcontrib><creatorcontrib>Branscheid, Detlev</creatorcontrib><creatorcontrib>Vollmer, Ekkehard</creatorcontrib><creatorcontrib>Zabel, Peter</creatorcontrib><creatorcontrib>Goldmann, Torsten</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Diagnostic pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schultz, Holger</au><au>Kähler, Daniel</au><au>Branscheid, Detlev</au><au>Vollmer, Ekkehard</au><au>Zabel, Peter</au><au>Goldmann, Torsten</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens</atitle><jtitle>Diagnostic pathology</jtitle><addtitle>Diagn Pathol</addtitle><date>2008-08-12</date><risdate>2008</risdate><volume>3</volume><issue>1</issue><spage>35</spage><epage>35</epage><pages>35-35</pages><artnum>35</artnum><issn>1746-1596</issn><eissn>1746-1596</eissn><abstract>In several tumors the transketolase activity, controlled inter alia by enzymes of the pentose phosphate pathway which is an alternative, energy generating reaction-cascade to glycolysis, has been correlated with proliferation. The increase of thiamine-dependent transketolase enzyme reactions is induced especially through upregulated transketolase-like enzyme 1 (TKTL1)-activity; that shows TKTL1 to be a causative enzyme for tumors enhanced, anaerobic glucose degradation. We investigated TKTL1-expression in 88 human, formalin-fixed non-small cell lung cancer tissues and 24 carcinomas of the breast by immunohistochemical stainings applying a 0 to 3 staining-score system (3 = strongest expression). For means of validation we additionally stained 40 NSCLC fixed and paraffin-embedded utilizing the HOPE-technique; showing comparable results to the formalin-fixed, paraffin-embedded specimens (not shown). Potential correlations with age, sex, TNM-classification parameters and tumor grading as well as tumor transcription factor 1 (TTF1) and surfactant protein A (SPA) expression were investigated. 40.9% of the analyzed lung tumors expressed TKTL1 weakly (Score 1), 38.6% moderately (score 2) and 17.1% strongly (score 3). 3 tumors were diagnosed TKTL1-negative (3.4%; score 0). All breast cancer specimen stainings were positive and scored 1: 32%; scored 2: 36%; scored 3: 32%. Alveolar macrophages and Alveolar Epithelial Cells Type II were also found to be TKTL1-positive.None of the listed clinical parameters could be found to show a significant correlation to TKTL1 signal appearance. Although we describe the expression of TKTL1 in lung cancers, we need to state that up till now there is no scientific indication for any treatment regimens based upon these findings.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>18700018</pmid><doi>10.1186/1746-1596-3-35</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Care and treatment Gene expression Genetic aspects Health aspects Lung cancer, Non-small cell Physiological aspects Short Report |
title | TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens |
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