Multimodality imaging using proton magnetic resonance spectroscopic imaging and ^(18)F-fluorodeoxyglucose-positron emission tomography in local prostate cancer

AIM To assess the relationship using multimodality imaging between intermediary citrate/choline metabolism as seen on proton magnetic resonance spectroscopic imaging(1H-MRSI) and glycolysis as observed on ^(18)F-fluorodeoxyglucose positron emission tomography/computed tomography(^(18)F-FDG-PET/CT) in prostate cancer(PCa) patients. METHODS The study included 22 patients with local PCa who were referred for endorectal magnetic resonance imaging/1HMRSI(April 2002 to July 2007) and ^(18)F-FDG-PET/CT and then underwent prostatectomy as primary or salvage treatment. Whole-mount step-section pathology was used as the standard of reference. We assessed the relationships between PET parameters [standardized uptake value(SUVmax and SUVmean)] and MRSI parameters [choline + creatine/citrate(CC/Cmax and CC/Cmean) and total number of suspicious voxels] using spearman's rank correlation, and the relationships of PET and 1H-MRSI index lesion parameters to surgical Gleason score.RESULTS Abnormal intermediary metabolism on 1H-MRSI was present in 21/22 patients, while abnormal glycolysis on ^(18)F-FDG-PET/CT was detected in only 3/22 patients. Specifically, index tumor localization rates were 0.95(95%CI: 0.77-1.00) for 1H-MRSI and 0.14(95%CI: 0.03-0.35) for ^(18)F-FDG-PET/CT. Spearman rank correlations indicated little relationship(ρ =-0.36-0.28) between 1H-MRSI parameters and ^(18)F-FDG-PET/CT parameters. Both the total number of suspicious voxels(ρ = 0.55, P = 0.0099) and the SUVmax(ρ = 0.46, P = 0.0366) correlated weakly with the Gleason score. No significant relationship was found between the CC/Cmax, CC/Cmean or SUVmean and the Gleason score(P = 0.15-0.79). CONCLUSION The concentration of intermediary metabolites detected by 1H MRSI and glycolytic flux measured ^(18)F-FDG PET show little correlation. Furthermore, only few tumors were FDG avid on PET, possibly because increased glycolysis represents a late and rather ominous event in the progression of PCa.

Genome-wide Studies Reveal Genetic Risk Factors for Hepatic Fat Content

Genetic susceptibility to metabolic associated fatty liver disease(MAFLD)is complex and poorly characterized.Accurate characterization of the genetic background of hepatic fat content would provide insights into disease etiology and causality of risk factors.We performed genome-wide association study(GWAS)on two noninvasive definitions of hepatic fat content:magnetic resonance imaging proton density fat fraction(MRI-PDFF)in 16,050 participants and fatty liver index(FLI)in 388,701 participants from the United Kingdom(UK)Biobank(UKBB).Heritability,genetic overlap,and similarity between hepatic fat content phenotypes were analyzed,and replicated in 10,398 participants from the University Medical Center Groningen(UMCG)Genetics Lifelines Initiative(UGLI).Meta-analysis of GWASs of MRI-PDFF in UKBB revealed five statistically significant loci,including two novel genomic loci harboring CREB3L1(rs72910057-T,P=5.40E−09)and GCM1(rs1491489378-T,P=3.16E−09),respectively,as well as three previously reported loci:PNPLA3,TM6SF2,and APOE.GWAS of FLI in UKBB identified 196 genome-wide significant loci,of which 49 were replicated in UGLI,with top signals in ZPR1(P=3.35E−13)and FTO(P=2.11E−09).Statistically significant genetic correlation(rg)between MRI-PDFF(UKBB)and FLI(UGLI)GWAS results was found(rg=0.5276,P=1.45E−03).Novel MRI-PDFF genetic signals(CREB3L1 and GCM1)were replicated in the FLI GWAS.We identified two novel genes for MRI-PDFF and 49 replicable loci for FLI.Despite a difference in hepatic fat content assessment between MRI-PDFF and FLI,a substantial similar genetic architecture was found.FLI is identified as an easy and reliable approach to study hepatic fat content at the population level.