Molecular mechanisms of [18F]fluorodeoxyglucose accumulation in liver cancer
To elucidate the molecular mechanisms underlying the insufficient sensitivity in the detection of hepatocellular carcinoma (HCC) by [18F] 2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET), the characteristics of glucose metabolism-related protein expression in HCC were examined in li...
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| Veröffentlicht in: | Oncology reports 2014-02, Vol.31 (2), p.701-706 |
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| creator | IZUISHI, KUNIHIKO YAMAMOTO, YUKA MORI, HIROHITO KAMEYAMA, RIKO FUJIHARA, SHINTARO MASAKI, TSUTOMU SUZUKI, YASUYUKI |
| description | To elucidate the molecular mechanisms underlying the insufficient sensitivity in the detection of hepatocellular carcinoma (HCC) by [18F] 2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET), the characteristics of glucose metabolism-related protein expression in HCC were examined in liver metastasis from colorectal cancer (Meta). Thirty-four patients (14 Meta and 20 HCC) who underwent FDG-PET and hepatectomy were studied. The relationships between the maximum standardized uptake value (SUV) in tumors and the mRNA expression of glucose metabolism-related proteins [hexokinase (HK), glucose transporter 1 (GLUT1), and glucose-6-phosphatase (G6Pase)] and proliferating cell nuclear antigen (PCNA) were examined in snap-frozen specimens with quantitative PCR. Tumor detection rates were lower in HCC (15/20) compared to Meta (13/14) patients. HK and GLUT1 expression was lower and G6Pase expression was higher in HCC compared to Meta. In particular, GLUT1 overexpression was 92-fold in Meta and 11-fold in HCC compared to the surrounding liver. The SUV correlated with GLUT1 and PCNA expression in HCC, but not Meta patients. Of note, four cases of poorly differentiated (P/D) HCC compared to moderately differentiated (M/D) HCC produced completely different results for FDG uptake (SUV, 14.4 vs. 4.0) and mRNA expression (G6Pase expression, 0.007 vs. 1.5). Variations in the expression of glucose metabolism-related enzymes between HCC and Meta patients are attributed to origin or degree of differentiation. Low FDG uptake in M/D HCC reflected low GLUT1 and high G6Pase expression, while high FDG accumulation in P/D HCC could reflect increased GLUT1 and decreased G6Pase expression. These results may explain why M/D HCC is not detected as sensitively by FDG-PET. |
| doi_str_mv | 10.3892/or.2013.2886 |
| format | Article |
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Thirty-four patients (14 Meta and 20 HCC) who underwent FDG-PET and hepatectomy were studied. The relationships between the maximum standardized uptake value (SUV) in tumors and the mRNA expression of glucose metabolism-related proteins [hexokinase (HK), glucose transporter 1 (GLUT1), and glucose-6-phosphatase (G6Pase)] and proliferating cell nuclear antigen (PCNA) were examined in snap-frozen specimens with quantitative PCR. Tumor detection rates were lower in HCC (15/20) compared to Meta (13/14) patients. HK and GLUT1 expression was lower and G6Pase expression was higher in HCC compared to Meta. In particular, GLUT1 overexpression was 92-fold in Meta and 11-fold in HCC compared to the surrounding liver. The SUV correlated with GLUT1 and PCNA expression in HCC, but not Meta patients. Of note, four cases of poorly differentiated (P/D) HCC compared to moderately differentiated (M/D) HCC produced completely different results for FDG uptake (SUV, 14.4 vs. 4.0) and mRNA expression (G6Pase expression, 0.007 vs. 1.5). Variations in the expression of glucose metabolism-related enzymes between HCC and Meta patients are attributed to origin or degree of differentiation. Low FDG uptake in M/D HCC reflected low GLUT1 and high G6Pase expression, while high FDG accumulation in P/D HCC could reflect increased GLUT1 and decreased G6Pase expression. These results may explain why M/D HCC is not detected as sensitively by FDG-PET.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2013.2886</identifier><identifier>PMID: 24297035</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>18-fluorodeoxyglucose ; Aged ; Cancer therapies ; Carcinoma, Hepatocellular - diagnosis ; Carcinoma, Hepatocellular - diagnostic imaging ; Carcinoma, Hepatocellular - surgery ; Cellular proteins ; Chemotherapy ; Colorectal cancer ; Development and progression ; Female ; Fluorodeoxyglucose F18 - chemistry ; Gene expression ; Genetic aspects ; Glucose ; Glucose - metabolism ; Glucose Transporter Type 1 - analysis ; Glucose Transporter Type 1 - genetics ; Glucose Transporter Type 2 - analysis ; glucose transporter-1 ; Glucose-6-Phosphatase - genetics ; Glucose-6-Phosphatase - metabolism ; Glucose-6-Phosphate - analogs & derivatives ; Glucose-6-Phosphate - chemistry ; Growth factors ; Health aspects ; Hepatectomy ; hepatocellular carcinoma ; Hepatoma ; Hexokinase - analysis ; Hexokinase - genetics ; Humans ; Kinases ; Liver - diagnostic imaging ; Liver - metabolism ; Liver - pathology ; Liver cancer ; liver metastasis ; Liver Neoplasms - diagnosis ; Liver Neoplasms - diagnostic imaging ; Liver Neoplasms - surgery ; Male ; Medical imaging ; Metabolism ; Metastasis ; Phosphorylation ; positron emission tomography ; Positron-Emission Tomography - methods ; Proliferating Cell Nuclear Antigen - genetics ; Properties ; Protein expression ; Proteins ; Radiopharmaceuticals ; RNA, Messenger - biosynthesis ; Studies ; Tumors ; Variance analysis</subject><ispartof>Oncology reports, 2014-02, Vol.31 (2), p.701-706</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c552t-ba49caf409e015ef900a7381e0799f29c324e0c5f7b1060a63f32de04115f3f33</citedby><cites>FETCH-LOGICAL-c552t-ba49caf409e015ef900a7381e0799f29c324e0c5f7b1060a63f32de04115f3f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24297035$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>IZUISHI, KUNIHIKO</creatorcontrib><creatorcontrib>YAMAMOTO, YUKA</creatorcontrib><creatorcontrib>MORI, HIROHITO</creatorcontrib><creatorcontrib>KAMEYAMA, RIKO</creatorcontrib><creatorcontrib>FUJIHARA, SHINTARO</creatorcontrib><creatorcontrib>MASAKI, TSUTOMU</creatorcontrib><creatorcontrib>SUZUKI, YASUYUKI</creatorcontrib><title>Molecular mechanisms of [18F]fluorodeoxyglucose accumulation in liver cancer</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>To elucidate the molecular mechanisms underlying the insufficient sensitivity in the detection of hepatocellular carcinoma (HCC) by [18F] 2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET), the characteristics of glucose metabolism-related protein expression in HCC were examined in liver metastasis from colorectal cancer (Meta). Thirty-four patients (14 Meta and 20 HCC) who underwent FDG-PET and hepatectomy were studied. The relationships between the maximum standardized uptake value (SUV) in tumors and the mRNA expression of glucose metabolism-related proteins [hexokinase (HK), glucose transporter 1 (GLUT1), and glucose-6-phosphatase (G6Pase)] and proliferating cell nuclear antigen (PCNA) were examined in snap-frozen specimens with quantitative PCR. Tumor detection rates were lower in HCC (15/20) compared to Meta (13/14) patients. HK and GLUT1 expression was lower and G6Pase expression was higher in HCC compared to Meta. In particular, GLUT1 overexpression was 92-fold in Meta and 11-fold in HCC compared to the surrounding liver. The SUV correlated with GLUT1 and PCNA expression in HCC, but not Meta patients. Of note, four cases of poorly differentiated (P/D) HCC compared to moderately differentiated (M/D) HCC produced completely different results for FDG uptake (SUV, 14.4 vs. 4.0) and mRNA expression (G6Pase expression, 0.007 vs. 1.5). Variations in the expression of glucose metabolism-related enzymes between HCC and Meta patients are attributed to origin or degree of differentiation. Low FDG uptake in M/D HCC reflected low GLUT1 and high G6Pase expression, while high FDG accumulation in P/D HCC could reflect increased GLUT1 and decreased G6Pase expression. These results may explain why M/D HCC is not detected as sensitively by FDG-PET.</description><subject>18-fluorodeoxyglucose</subject><subject>Aged</subject><subject>Cancer therapies</subject><subject>Carcinoma, Hepatocellular - diagnosis</subject><subject>Carcinoma, Hepatocellular - diagnostic imaging</subject><subject>Carcinoma, Hepatocellular - surgery</subject><subject>Cellular proteins</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Development and progression</subject><subject>Female</subject><subject>Fluorodeoxyglucose F18 - chemistry</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose Transporter Type 1 - analysis</subject><subject>Glucose Transporter Type 1 - genetics</subject><subject>Glucose Transporter Type 2 - analysis</subject><subject>glucose transporter-1</subject><subject>Glucose-6-Phosphatase - genetics</subject><subject>Glucose-6-Phosphatase - metabolism</subject><subject>Glucose-6-Phosphate - analogs & derivatives</subject><subject>Glucose-6-Phosphate - chemistry</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Hepatectomy</subject><subject>hepatocellular carcinoma</subject><subject>Hepatoma</subject><subject>Hexokinase - analysis</subject><subject>Hexokinase - genetics</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver - diagnostic imaging</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver cancer</subject><subject>liver metastasis</subject><subject>Liver Neoplasms - diagnosis</subject><subject>Liver Neoplasms - diagnostic imaging</subject><subject>Liver Neoplasms - surgery</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Metabolism</subject><subject>Metastasis</subject><subject>Phosphorylation</subject><subject>positron emission tomography</subject><subject>Positron-Emission Tomography - methods</subject><subject>Proliferating Cell Nuclear Antigen - genetics</subject><subject>Properties</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Radiopharmaceuticals</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Studies</subject><subject>Tumors</subject><subject>Variance analysis</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpt0d9r1TAUB_AiipvTN5-lIAwf7PWcpGmbxzHcD7iyFwVBJOSmJ7sZaXJNWnH_vS2b-yEjDwnhc05-fIviLcKKd5J9imnFAPmKdV3zrNjHVmLFao7P5zUwrDgX3_eKVzlfAbAWGvmy2GM1ky1wsV-sv0RPZvI6lQOZrQ4uD7mMtvyB3clP66eYYk_xz_Wln0zMVGpjpmH2o4uhdKH07jel0uhgKL0uXljtM725nQ-Kbyefvx6fVeuL0_Pjo3VlhGBjtdG1NNrWIAlQkJUAuuUdErRSWiYNZzWBEbbdIDSgG2456wlqRGHnNT8oPtz03aX4a6I8qsFlQ97rQHHKCmsJrUDsFvr-P3oVpxTm2ymUnDWt4Ky7V5fak3LBxjFpszRVRzUK0TDJ2KxWT6h59DQ4EwNZN-8_Kjh8ULAl7cdtjn5a_i4_hh9voEkx50RW7ZIbdLpWCGpJWcWklpTVkvLM390-atoM1N_hf7HeH5x3OvSuj_nOxFRxrIBV0M79_gLUzatu</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>IZUISHI, KUNIHIKO</creator><creator>YAMAMOTO, YUKA</creator><creator>MORI, HIROHITO</creator><creator>KAMEYAMA, RIKO</creator><creator>FUJIHARA, SHINTARO</creator><creator>MASAKI, TSUTOMU</creator><creator>SUZUKI, YASUYUKI</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140201</creationdate><title>Molecular mechanisms of [18F]fluorodeoxyglucose accumulation in liver cancer</title><author>IZUISHI, KUNIHIKO ; YAMAMOTO, YUKA ; MORI, HIROHITO ; KAMEYAMA, RIKO ; FUJIHARA, SHINTARO ; MASAKI, TSUTOMU ; SUZUKI, YASUYUKI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-ba49caf409e015ef900a7381e0799f29c324e0c5f7b1060a63f32de04115f3f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>18-fluorodeoxyglucose</topic><topic>Aged</topic><topic>Cancer therapies</topic><topic>Carcinoma, Hepatocellular - diagnosis</topic><topic>Carcinoma, Hepatocellular - diagnostic imaging</topic><topic>Carcinoma, Hepatocellular - surgery</topic><topic>Cellular proteins</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Development and progression</topic><topic>Female</topic><topic>Fluorodeoxyglucose F18 - chemistry</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glucose Transporter Type 1 - analysis</topic><topic>Glucose Transporter Type 1 - genetics</topic><topic>Glucose Transporter Type 2 - analysis</topic><topic>glucose transporter-1</topic><topic>Glucose-6-Phosphatase - genetics</topic><topic>Glucose-6-Phosphatase - metabolism</topic><topic>Glucose-6-Phosphate - analogs & derivatives</topic><topic>Glucose-6-Phosphate - chemistry</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Hepatectomy</topic><topic>hepatocellular carcinoma</topic><topic>Hepatoma</topic><topic>Hexokinase - analysis</topic><topic>Hexokinase - genetics</topic><topic>Humans</topic><topic>Kinases</topic><topic>Liver - diagnostic imaging</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver cancer</topic><topic>liver metastasis</topic><topic>Liver Neoplasms - diagnosis</topic><topic>Liver Neoplasms - diagnostic imaging</topic><topic>Liver Neoplasms - surgery</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Metabolism</topic><topic>Metastasis</topic><topic>Phosphorylation</topic><topic>positron emission tomography</topic><topic>Positron-Emission Tomography - methods</topic><topic>Proliferating Cell Nuclear Antigen - genetics</topic><topic>Properties</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Radiopharmaceuticals</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Studies</topic><topic>Tumors</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>IZUISHI, KUNIHIKO</creatorcontrib><creatorcontrib>YAMAMOTO, YUKA</creatorcontrib><creatorcontrib>MORI, HIROHITO</creatorcontrib><creatorcontrib>KAMEYAMA, RIKO</creatorcontrib><creatorcontrib>FUJIHARA, SHINTARO</creatorcontrib><creatorcontrib>MASAKI, TSUTOMU</creatorcontrib><creatorcontrib>SUZUKI, YASUYUKI</creatorcontrib><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>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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>IZUISHI, KUNIHIKO</au><au>YAMAMOTO, YUKA</au><au>MORI, HIROHITO</au><au>KAMEYAMA, RIKO</au><au>FUJIHARA, SHINTARO</au><au>MASAKI, TSUTOMU</au><au>SUZUKI, YASUYUKI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular mechanisms of [18F]fluorodeoxyglucose accumulation in liver cancer</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>31</volume><issue>2</issue><spage>701</spage><epage>706</epage><pages>701-706</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>To elucidate the molecular mechanisms underlying the insufficient sensitivity in the detection of hepatocellular carcinoma (HCC) by [18F] 2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET), the characteristics of glucose metabolism-related protein expression in HCC were examined in liver metastasis from colorectal cancer (Meta). Thirty-four patients (14 Meta and 20 HCC) who underwent FDG-PET and hepatectomy were studied. The relationships between the maximum standardized uptake value (SUV) in tumors and the mRNA expression of glucose metabolism-related proteins [hexokinase (HK), glucose transporter 1 (GLUT1), and glucose-6-phosphatase (G6Pase)] and proliferating cell nuclear antigen (PCNA) were examined in snap-frozen specimens with quantitative PCR. Tumor detection rates were lower in HCC (15/20) compared to Meta (13/14) patients. HK and GLUT1 expression was lower and G6Pase expression was higher in HCC compared to Meta. In particular, GLUT1 overexpression was 92-fold in Meta and 11-fold in HCC compared to the surrounding liver. The SUV correlated with GLUT1 and PCNA expression in HCC, but not Meta patients. Of note, four cases of poorly differentiated (P/D) HCC compared to moderately differentiated (M/D) HCC produced completely different results for FDG uptake (SUV, 14.4 vs. 4.0) and mRNA expression (G6Pase expression, 0.007 vs. 1.5). Variations in the expression of glucose metabolism-related enzymes between HCC and Meta patients are attributed to origin or degree of differentiation. Low FDG uptake in M/D HCC reflected low GLUT1 and high G6Pase expression, while high FDG accumulation in P/D HCC could reflect increased GLUT1 and decreased G6Pase expression. These results may explain why M/D HCC is not detected as sensitively by FDG-PET.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24297035</pmid><doi>10.3892/or.2013.2886</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology reports, 2014-02, Vol.31 (2), p.701-706 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 18-fluorodeoxyglucose Aged Cancer therapies Carcinoma, Hepatocellular - diagnosis Carcinoma, Hepatocellular - diagnostic imaging Carcinoma, Hepatocellular - surgery Cellular proteins Chemotherapy Colorectal cancer Development and progression Female Fluorodeoxyglucose F18 - chemistry Gene expression Genetic aspects Glucose Glucose - metabolism Glucose Transporter Type 1 - analysis Glucose Transporter Type 1 - genetics Glucose Transporter Type 2 - analysis glucose transporter-1 Glucose-6-Phosphatase - genetics Glucose-6-Phosphatase - metabolism Glucose-6-Phosphate - analogs & derivatives Glucose-6-Phosphate - chemistry Growth factors Health aspects Hepatectomy hepatocellular carcinoma Hepatoma Hexokinase - analysis Hexokinase - genetics Humans Kinases Liver - diagnostic imaging Liver - metabolism Liver - pathology Liver cancer liver metastasis Liver Neoplasms - diagnosis Liver Neoplasms - diagnostic imaging Liver Neoplasms - surgery Male Medical imaging Metabolism Metastasis Phosphorylation positron emission tomography Positron-Emission Tomography - methods Proliferating Cell Nuclear Antigen - genetics Properties Protein expression Proteins Radiopharmaceuticals RNA, Messenger - biosynthesis Studies Tumors Variance analysis |
| title | Molecular mechanisms of [18F]fluorodeoxyglucose accumulation in liver cancer |
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