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    Keywords: brain ; RECEPTOR ; CANCER ; EXPRESSION ; BLOOD ; Germany ; LUNG ; MODEL ; imaging ; lung cancer ; LUNG-CANCER ; POPULATION ; GENE ; GENE-EXPRESSION ; TISSUE ; PATIENT ; CONTRAST ; gene expression ; metastases ; PARAMETERS ; SCINTIGRAPHY ; PET ; SOMATOSTATIN ; QUANTITATIVE ASSESSMENT ; RE ; SOMATOSTATIN ANALOG ; GA-68-DOTATOC ; LOSSES ; uptake ; FDG ; viability ; DOTATOC ; EMISSION-TOMOGRAPHY ; F-18-FDG PET ; kinetic modelling ; kinetic parameters ; non-small cell lung tumours ; TC-99M DEPREOTIDE
    Abstract: Purpose: Dynamic PET studies with Ga-68-DOTATOC were performed in patients with non-small cell lung cancer (NSCLC) to assess the somatostatin receptor 2 (SSTR2) expression. Furthermore, dynamic F-18-fluorodeoxyglucose (FDG) studies were performed in the same patients to compare the SSTR2 expression with the tumour viability. Methods: The study population comprised nine patients, examined with both tracers on two different days within 1 week. Standardised uptake values (SUVs) were calculated and a two-tissue compartment model was applied to the data. Furthermore, a non-compartment model based on the fractal dimension (FD) was applied to the data. Results: The DOTATOC uptake was generally lower than the FDG uptake. Moderately enhanced DOTATOC uptake was noted in seven of the nine tumours. All kinetic parameters exceptk (4) were lower for DOTATOC than for FDG. The mean SUV was 2.018 for DOTATOC, in comparison to 5.683 for FDG. In particular,k (3) was highly variable for DOTATOC and showed an overlap with the normal lung tissue. The fractional blood volumeV (B) was relatively low for both tracers, not exceeding 0.3. The highest significant logarithmic correlation was found for the FD of the two tracers (r=0.764,p=0.017). The logarithmic correlation for SUVs was also significant (r=0.646,p=0.060), as was that forV (B) (r=0.629,p=0.069). In contrast, none of the eight metastases which were positive on FDG PET showed any DOTATOC uptake. Conclusion: The results demonstrated moderate Ga-68-DOTATOC uptake in primary NSCLC but did not provide any evidence for SSTR2 expression in metastases. This may be caused by loss of the gene expression in metastases as compared with the primary tumours
    Type of Publication: Journal article published
    PubMed ID: 16570185
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