INTRODUCTION: Glucose transporters and hexokinases determine the kinetics of 2-deoxy-2-[(18)F]fluoro-D: -glucose (FDG). However, the genes controlling these proteins are not independent and may be modulated from other biological processes, e.g., like angiogenesis and proliferation. The impact of cell-proliferation-related genes on the FDG kinetics was assessed in colorectal tumors in this study. METHODS: Patients with primary colorectal tumors (n = 25) were examined with positron emission tomography and FDG within 2 days prior to surgery. Tissue specimens were obtained from the colorectal tumor and the normal colon by surgery and gene expression was assessed using gene arrays. RESULTS: Overall, an increase of the expression of proliferation associated genes was observed by a factor of 2-5.3 for the colorectal tumors as compared with the normal colon. Correlation analysis revealed an impact of cdk2 on K1, thus directing to a modulation of the FDG uptake into the cells. The correlations were generally higher for the FDG influx as compared with the standardized uptake value (SUV). The influx was mainly correlated with proliferation inhibiting genes (cyclin G2, cdk inhibitor 1 C, cdk inhibitor 2B). It was possible to predict the expression of cyclin D2 using a multiple linear regression function and the parameters of the FDG kinetics with r = 0.67. Using a group based analysis it was possible to demonstrate, that tumors with an SUV >12 are associated with a high expression of cyclin D2 in the colorectal tumors. If the gene expression data for cyclin D1, cyclin G2, cdk2, cdk6 and cdk inhibtor 2B were used, the overall FDG uptake as measured by the SUV could be predicted with r = 0.75. CONCLUSIONS: The results suggest that the FDG kinetics is modulated by proliferation associated genes. Especially K1, the parameter for the FDG transport into the cells, is modulated by cdk2. Tumors with a SUV exceeding 12 have usually a higher expression of cyclin D2. The parameters of the FDG kinetics can be used to predict the expression of proliferation associated genes individually.
INTRODUCTION: Glucose transporters and hexokinases determine the kinetics of 2-deoxy-2-[(18)F]fluoro-D: -glucose (FDG). However, the genes controlling these proteins are not independent and may be modulated from other biological processes, e.g., like angiogenesis and proliferation. The impact of cell-proliferation-related genes on the FDG kinetics was assessed in colorectal tumors in this study. METHODS:Patients with primary colorectal tumors (n = 25) were examined with positron emission tomography and FDG within 2 days prior to surgery. Tissue specimens were obtained from the colorectal tumor and the normal colon by surgery and gene expression was assessed using gene arrays. RESULTS: Overall, an increase of the expression of proliferation associated genes was observed by a factor of 2-5.3 for the colorectal tumors as compared with the normal colon. Correlation analysis revealed an impact of cdk2 on K1, thus directing to a modulation of the FDG uptake into the cells. The correlations were generally higher for the FDG influx as compared with the standardized uptake value (SUV). The influx was mainly correlated with proliferation inhibiting genes (cyclin G2, cdk inhibitor 1 C, cdk inhibitor 2B). It was possible to predict the expression of cyclin D2 using a multiple linear regression function and the parameters of the FDG kinetics with r = 0.67. Using a group based analysis it was possible to demonstrate, that tumors with an SUV >12 are associated with a high expression of cyclin D2 in the colorectal tumors. If the gene expression data for cyclin D1, cyclin G2, cdk2, cdk6 and cdk inhibtor 2B were used, the overall FDG uptake as measured by the SUV could be predicted with r = 0.75. CONCLUSIONS: The results suggest that the FDG kinetics is modulated by proliferation associated genes. Especially K1, the parameter for the FDG transport into the cells, is modulated by cdk2. Tumors with a SUV exceeding 12 have usually a higher expression of cyclin D2. The parameters of the FDG kinetics can be used to predict the expression of proliferation associated genes individually.
Authors: Ludwig G Strauss; Leyun Pan; Dirk Koczan; Sven Klippel; Krzysztof Mikolajczyk; Cyrill Burger; Uwe Haberkorn; Klaus Schönleben; Hans-Jürgen Thiesen; Antonia Dimitrakopoulou-Strauss Journal: IEEE Trans Med Imaging Date: 2007-06 Impact factor: 10.048
Authors: A Dimitrakopoulou-Strauss; L G Strauss; M Schwarzbach; C Burger; T Heichel; F Willeke; G Mechtersheimer; T Lehnert Journal: J Nucl Med Date: 2001-05 Impact factor: 10.057
Authors: Andrei Pugachev; Shutian Ruan; Sean Carlin; Steven M Larson; Jose Campa; C Clifton Ling; John L Humm Journal: Int J Radiat Oncol Biol Phys Date: 2005-06-01 Impact factor: 7.038
Authors: Vicky Goh; Steve Halligan; Frances Daley; David M Wellsted; Thomas Guenther; Clive I Bartram Journal: Radiology Date: 2008-09-23 Impact factor: 11.105
Authors: Andreas K Buck; Gisela Halter; Holger Schirrmeister; Jörg Kotzerke; Imke Wurziger; Gerhard Glatting; Torsten Mattfeldt; Bernd Neumaier; Sven N Reske; Martin Hetzel Journal: J Nucl Med Date: 2003-09 Impact factor: 10.057
Authors: Ludwig G Strauss; Dirk Koczan; Sven Klippel; Leyun Pan; Stefan Willis; Christos Sachpekidis; Antonia Dimitrakopoulou-Strauss Journal: Am J Nucl Med Mol Imaging Date: 2013-09-19
Authors: G P Ralli; R D Carter; F M Buffa; J D Fenwick; D R McGowan; W-C Cheng; D Liu; E J Teoh; N Patel; F Gleeson; A L Harris; S R Lord Journal: Breast Cancer Res Date: 2022-05-17 Impact factor: 8.408