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Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer
The FDG uptake in lung cancer is considered to reflect the degree of malignancy, while alterations of some tumor suppressor genes are considered to be related to the malignant biological behavior of tumors. The aim of this study is to examine the relationship between FDG-PET and alterations in the t...
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Published in: | Annals of nuclear medicine 2003-05, Vol.17 (3), p.189-196 |
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creator | Sasaki, Masayuki Sugio, Kenji Kuwabara, Yasuo Koga, Hirofumi Nakagawa, Makoto Chen, Tao Kaneko, Koichiro Hayashi, Kazutaka Shioyama, Yoshiyuki Sakai, Shuji Honda, Hiroshi |
description | The FDG uptake in lung cancer is considered to reflect the degree of malignancy, while alterations of some tumor suppressor genes are considered to be related to the malignant biological behavior of tumors. The aim of this study is to examine the relationship between FDG-PET and alterations in the tumor suppression genes of lung cancer.
We examined 28 patients with primary lung cancer who underwent FDG-PET before surgery consisting of 17 patients with adenocarcinoma, 10 with squamous cell carcinoma and 1 with large cell carcinoma. The FDG-PET findings were evaluated based on the standardized uptake value (SUV). Alterations in the tumor suppressor genes, Rb, p16, p27 and p53, were evaluated immunohistochemically.
The FDG uptake in lung cancer with alteration in each tumor suppressor gene tended to be higher than in those genes without alterations, although the differences were not significant. In 15 tumors with alterations in either tumor suppressor genes, the FDG uptake was 6.83 +/- 3.21. On the other hand, the mean FDG uptake was 1.95 in 2 tumors without alterations in any genes. The difference in the FDG uptake between the 2 groups was statistically significant (p < 0.001).
In conclusion, the presence of abnormalities in the tumor suppressor genes, which results in an accelerated cell proliferation, is thus considered to increase the FDG uptake in lung cancer. |
doi_str_mv | 10.1007/BF02990021 |
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We examined 28 patients with primary lung cancer who underwent FDG-PET before surgery consisting of 17 patients with adenocarcinoma, 10 with squamous cell carcinoma and 1 with large cell carcinoma. The FDG-PET findings were evaluated based on the standardized uptake value (SUV). Alterations in the tumor suppressor genes, Rb, p16, p27 and p53, were evaluated immunohistochemically.
The FDG uptake in lung cancer with alteration in each tumor suppressor gene tended to be higher than in those genes without alterations, although the differences were not significant. In 15 tumors with alterations in either tumor suppressor genes, the FDG uptake was 6.83 +/- 3.21. On the other hand, the mean FDG uptake was 1.95 in 2 tumors without alterations in any genes. The difference in the FDG uptake between the 2 groups was statistically significant (p < 0.001).
In conclusion, the presence of abnormalities in the tumor suppressor genes, which results in an accelerated cell proliferation, is thus considered to increase the FDG uptake in lung cancer.</description><identifier>ISSN: 0914-7187</identifier><identifier>EISSN: 1864-6433</identifier><identifier>DOI: 10.1007/BF02990021</identifier><identifier>PMID: 12846540</identifier><language>eng</language><publisher>Japan: Springer Nature B.V</publisher><subject>Abnormalities ; Adenocarcinoma ; Adult ; Aged ; Cancer ; Carcinoma - diagnostic imaging ; Carcinoma - metabolism ; Cell proliferation ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Evaluation ; Female ; Fluorodeoxyglucose F18 - pharmacokinetics ; Gene Expression Regulation, Neoplastic ; Genes ; Genes, Tumor Suppressor ; Humans ; Lung cancer ; Lung Neoplasms - diagnostic imaging ; Lung Neoplasms - metabolism ; Male ; Malignancy ; Microfilament Proteins - metabolism ; Middle Aged ; Muscle Proteins ; p53 Protein ; Radiopharmaceuticals - pharmacokinetics ; Retinoblastoma Protein - metabolism ; Squamous cell carcinoma ; Statistical analysis ; Tomography, Emission-Computed - methods ; Tumor suppression ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - metabolism ; Tumor Suppressor Proteins - metabolism ; Tumors</subject><ispartof>Annals of nuclear medicine, 2003-05, Vol.17 (3), p.189-196</ispartof><rights>Springer 2003</rights><rights>Springer 2003.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-ff1e0c5fae7450fbe5dd8ce49b6eff70d6eba72ce68305871fd154eaf2f7ae373</citedby><cites>FETCH-LOGICAL-c456t-ff1e0c5fae7450fbe5dd8ce49b6eff70d6eba72ce68305871fd154eaf2f7ae373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12846540$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sasaki, Masayuki</creatorcontrib><creatorcontrib>Sugio, Kenji</creatorcontrib><creatorcontrib>Kuwabara, Yasuo</creatorcontrib><creatorcontrib>Koga, Hirofumi</creatorcontrib><creatorcontrib>Nakagawa, Makoto</creatorcontrib><creatorcontrib>Chen, Tao</creatorcontrib><creatorcontrib>Kaneko, Koichiro</creatorcontrib><creatorcontrib>Hayashi, Kazutaka</creatorcontrib><creatorcontrib>Shioyama, Yoshiyuki</creatorcontrib><creatorcontrib>Sakai, Shuji</creatorcontrib><creatorcontrib>Honda, Hiroshi</creatorcontrib><title>Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer</title><title>Annals of nuclear medicine</title><addtitle>Ann Nucl Med</addtitle><description>The FDG uptake in lung cancer is considered to reflect the degree of malignancy, while alterations of some tumor suppressor genes are considered to be related to the malignant biological behavior of tumors. The aim of this study is to examine the relationship between FDG-PET and alterations in the tumor suppression genes of lung cancer.
We examined 28 patients with primary lung cancer who underwent FDG-PET before surgery consisting of 17 patients with adenocarcinoma, 10 with squamous cell carcinoma and 1 with large cell carcinoma. The FDG-PET findings were evaluated based on the standardized uptake value (SUV). Alterations in the tumor suppressor genes, Rb, p16, p27 and p53, were evaluated immunohistochemically.
The FDG uptake in lung cancer with alteration in each tumor suppressor gene tended to be higher than in those genes without alterations, although the differences were not significant. In 15 tumors with alterations in either tumor suppressor genes, the FDG uptake was 6.83 +/- 3.21. On the other hand, the mean FDG uptake was 1.95 in 2 tumors without alterations in any genes. The difference in the FDG uptake between the 2 groups was statistically significant (p < 0.001).
In conclusion, the presence of abnormalities in the tumor suppressor genes, which results in an accelerated cell proliferation, is thus considered to increase the FDG uptake in lung cancer.</description><subject>Abnormalities</subject><subject>Adenocarcinoma</subject><subject>Adult</subject><subject>Aged</subject><subject>Cancer</subject><subject>Carcinoma - diagnostic imaging</subject><subject>Carcinoma - metabolism</subject><subject>Cell proliferation</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>Evaluation</subject><subject>Female</subject><subject>Fluorodeoxyglucose F18 - pharmacokinetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genes, Tumor Suppressor</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - diagnostic imaging</subject><subject>Lung Neoplasms - metabolism</subject><subject>Male</subject><subject>Malignancy</subject><subject>Microfilament Proteins - metabolism</subject><subject>Middle Aged</subject><subject>Muscle Proteins</subject><subject>p53 Protein</subject><subject>Radiopharmaceuticals - pharmacokinetics</subject><subject>Retinoblastoma Protein - metabolism</subject><subject>Squamous cell carcinoma</subject><subject>Statistical analysis</subject><subject>Tomography, Emission-Computed - methods</subject><subject>Tumor suppression</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Tumors</subject><issn>0914-7187</issn><issn>1864-6433</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqF0V1rFDEUBuBQlHatvfEHlGBBW3E0J99zWVu3CgVB6vWQyZwsW2cz02Tmov_erF0oCLU3ySE8vHDyEvIG2CdgzHz-smS8rhnjsEcWYLWstBTiBVmwGmRlwJoD8irn2yKssnyfHAC3UivJFmR13k-Y3LQeYqZDoNO8GRLN8zgmzLmMK4yY6enP9iMdQZeDG-piR0clzv4OLtJ19Aldxo4uL6_oPE7uN5ZH2s9xRb2LHtNr8jK4PuPR7j4kv5Zfby6-Vdc_rr5fnF9XXio9VSEAMq-CQyMVCy2qrrMeZd1qDMGwTmPrDPeorWDKGggdKIku8GAcCiMOyfuH3DENdzPmqdmss8e-dxGHOTc140JoYaHId_-VRigGCuSzkAMvqtYFnvwDb4c5xbJuw401XJb_38a9fVKBYrIWarvGhwfk05BzwtCMab1x6b4B1mxLbx5LL_h4lzi3G-we6a5l8Qc4aKMo</recordid><startdate>20030501</startdate><enddate>20030501</enddate><creator>Sasaki, Masayuki</creator><creator>Sugio, Kenji</creator><creator>Kuwabara, Yasuo</creator><creator>Koga, Hirofumi</creator><creator>Nakagawa, Makoto</creator><creator>Chen, Tao</creator><creator>Kaneko, Koichiro</creator><creator>Hayashi, Kazutaka</creator><creator>Shioyama, Yoshiyuki</creator><creator>Sakai, Shuji</creator><creator>Honda, Hiroshi</creator><general>Springer Nature B.V</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>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7QO</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030501</creationdate><title>Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer</title><author>Sasaki, Masayuki ; Sugio, Kenji ; Kuwabara, Yasuo ; Koga, Hirofumi ; Nakagawa, Makoto ; Chen, Tao ; Kaneko, Koichiro ; Hayashi, Kazutaka ; Shioyama, Yoshiyuki ; Sakai, Shuji ; Honda, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-ff1e0c5fae7450fbe5dd8ce49b6eff70d6eba72ce68305871fd154eaf2f7ae373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Abnormalities</topic><topic>Adenocarcinoma</topic><topic>Adult</topic><topic>Aged</topic><topic>Cancer</topic><topic>Carcinoma - diagnostic imaging</topic><topic>Carcinoma - metabolism</topic><topic>Cell proliferation</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>Evaluation</topic><topic>Female</topic><topic>Fluorodeoxyglucose F18 - pharmacokinetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genes, Tumor Suppressor</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - diagnostic imaging</topic><topic>Lung Neoplasms - metabolism</topic><topic>Male</topic><topic>Malignancy</topic><topic>Microfilament Proteins - metabolism</topic><topic>Middle Aged</topic><topic>Muscle Proteins</topic><topic>p53 Protein</topic><topic>Radiopharmaceuticals - pharmacokinetics</topic><topic>Retinoblastoma Protein - metabolism</topic><topic>Squamous cell carcinoma</topic><topic>Statistical analysis</topic><topic>Tomography, Emission-Computed - methods</topic><topic>Tumor suppression</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - 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Academic</collection><jtitle>Annals of nuclear medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sasaki, Masayuki</au><au>Sugio, Kenji</au><au>Kuwabara, Yasuo</au><au>Koga, Hirofumi</au><au>Nakagawa, Makoto</au><au>Chen, Tao</au><au>Kaneko, Koichiro</au><au>Hayashi, Kazutaka</au><au>Shioyama, Yoshiyuki</au><au>Sakai, Shuji</au><au>Honda, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer</atitle><jtitle>Annals of nuclear medicine</jtitle><addtitle>Ann Nucl Med</addtitle><date>2003-05-01</date><risdate>2003</risdate><volume>17</volume><issue>3</issue><spage>189</spage><epage>196</epage><pages>189-196</pages><issn>0914-7187</issn><eissn>1864-6433</eissn><abstract>The FDG uptake in lung cancer is considered to reflect the degree of malignancy, while alterations of some tumor suppressor genes are considered to be related to the malignant biological behavior of tumors. The aim of this study is to examine the relationship between FDG-PET and alterations in the tumor suppression genes of lung cancer.
We examined 28 patients with primary lung cancer who underwent FDG-PET before surgery consisting of 17 patients with adenocarcinoma, 10 with squamous cell carcinoma and 1 with large cell carcinoma. The FDG-PET findings were evaluated based on the standardized uptake value (SUV). Alterations in the tumor suppressor genes, Rb, p16, p27 and p53, were evaluated immunohistochemically.
The FDG uptake in lung cancer with alteration in each tumor suppressor gene tended to be higher than in those genes without alterations, although the differences were not significant. In 15 tumors with alterations in either tumor suppressor genes, the FDG uptake was 6.83 +/- 3.21. On the other hand, the mean FDG uptake was 1.95 in 2 tumors without alterations in any genes. The difference in the FDG uptake between the 2 groups was statistically significant (p < 0.001).
In conclusion, the presence of abnormalities in the tumor suppressor genes, which results in an accelerated cell proliferation, is thus considered to increase the FDG uptake in lung cancer.</abstract><cop>Japan</cop><pub>Springer Nature B.V</pub><pmid>12846540</pmid><doi>10.1007/BF02990021</doi><tpages>8</tpages></addata></record> |
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subjects | Abnormalities Adenocarcinoma Adult Aged Cancer Carcinoma - diagnostic imaging Carcinoma - metabolism Cell proliferation Cyclin-Dependent Kinase Inhibitor p16 - metabolism Evaluation Female Fluorodeoxyglucose F18 - pharmacokinetics Gene Expression Regulation, Neoplastic Genes Genes, Tumor Suppressor Humans Lung cancer Lung Neoplasms - diagnostic imaging Lung Neoplasms - metabolism Male Malignancy Microfilament Proteins - metabolism Middle Aged Muscle Proteins p53 Protein Radiopharmaceuticals - pharmacokinetics Retinoblastoma Protein - metabolism Squamous cell carcinoma Statistical analysis Tomography, Emission-Computed - methods Tumor suppression Tumor suppressor genes Tumor Suppressor Protein p53 - metabolism Tumor Suppressor Proteins - metabolism Tumors |
title | Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer |
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