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We report our fluorine-18-fluorodeoxyglucose positron emission tomography/computed tomography (18FFDG PET/CT) findings in a 51 years old female presenting with B symptoms, respectively fever, night sweats and malaise, that underwent an 18F-FDG PET/CT examination to exclude underlying lymphomatous disease. Whereas 18F-FDG PET scan findings were negative, CT put to evidence the presence of multiple small lesions suggestive for multifocal hamartoma. On a subsequently performed magnetic resonance imaging (MRI) of the spleen, multiple infracentimetric foci were visualized displaying characteristic findings for hamartoma. During a follow-up period of two years no change in size or characteristics of these lesions occurred. CONCLUSION: The normal :F-FDG PET/CT findings suggested that, at least in this patient, splenic hamartoma may display a similar :F-FDG avidity when compared to normal splenic tissue. Alternatively, due to the infra-centrimeric size of the hamartoma and spill-over from :F-FDG activity from neighbouring normal tissue, the true 18F-FDG avidity of the hamartomas present might also be overestimated.

In GEP‐NETs, especially the catecholamine and serotonin biosynthetic pathways are upregulated. Therefore, increased biosynthesis of these specific amines in GEP‐NETs enables imaging with specific amine precursors. For the catecholamine pathway, 6‐18F ‐l‐3,4‐dihydroxyphenylalanine (18F‐DOPA) is available, while for the serotonin pathway, carbon‐11‐labeled 5‐hydroxy‐l‐tryptophan ([11C]‐5‐HTP) is available as tracer. 11C‐5‐HTP PET and 18F‐DOPA PET are excellent functional imaging techniques for evaluating patients with proven pancreatic islet cell tumors and carcinoids. For both tracers, the combination with CT further improves the detection rate of NET, which shows that performing PET scans with these tracers in PET/CT scanners is beneficial for patients.Since well‐differentiated GEP‐NETs generally have a low glucose metabolism, 18F‐fluorodexyglucose (18F‐FDG) PET scanning has limited value for the primary staging of patients with well‐differentiated GEP‐NETs. However, in patients with rapidly progressive disease, dedifferentiation of GEP‐NET tumors can lead to a higher glucose metabolism in tumor cells. In these patients, 18F‐FDG PET can be of benefit for tumor staging. Also, 18F‐FDG PET can be of value when other malignancies are suspected in patients with GEP‐NETs, since these patients experience a higher incidence of these malignancies compared to the general population.Nowadays, (GEP)‐NETs can also be imaged with 68Ga‐labeled analogues of somatostatin, which are also PET tracers. Advantages of 68Ga‐labeled somatostatin analogues are the relatively easy generator‐based synthesis and the possibility to evaluate whether peptide (somatostatin) receptor radionuclide therapy (PRRT) for NETs can be considered.

Medullary thyroid cancer (MTC) is a neuroendocrine tumor originating from the calcitonin‐secreting C cells. Surgery, consisting of a total thyroidectomy and an extensive lymph node dissection, is the only effective treatment in MTC; however, metastases are frequently found in the regional cervical lymph. The biochemical marker for MTC is calcitonin, and this is frequently used for the detection of persistent/residual/metastatic tumor. The value of 111In‐labeled somatostatin receptor scintigraphy (SRS) in patients with MTC is limited, with sensitivity ranging between 0 and 75%. Other scintigraphic imaging techniques such as 18F‐FDG PET, 18F‐DOPA PET, and PET imaging with 68Ga‐labeled DOTA peptides combined with CT imaging are upcoming. Treatment of patients with metastatic disease with the current available somatostatin analogues, octreotide and lanreotide, does not seem to have an effect on survival but may be considered to control flushing and diarrhea in some patients. Experience with peptide receptor radionuclide therapy is limited in this patient group and disappointing. New therapies in the treatment of metastatic MTC use target tyrosine kinase receptors inhibitors belonging to the same family group of proteins as RET.

In breast cancer CA 15.3 is considered the tumour marker of choice. CA 15.3 is directly related to the disease extent and to hormone status (estrogen receptor ER+/ ER-, progesterone receptor PR+/PR-). This study was designed to assess the impact of disease extent, hormone receptor and HER2-status, and circulating blood volume on the area-under the ROC-curve of CA 15.3 to separate FDG PET positive from negative findings. Patients, methods: We retrospectively evaluated 379 FDG PET/CT examinations performed in 80 patients with breast cancer. Blood volumes were derived using the formulas by Nadler and multiplied by their corresponding CA 15.3 measurement. Results: ROC-curve analysis revealed an AUC of 0.695 (p = 0.0001) for CA 15.3 to separate FDG PET positive from negative findings. AUC measurements to separate normal scan findings from loco-regional disease and metastatic disease were 0.527 (p = 0.587) and 0.732 (p = 0.0001), respectively. AUC measurements for CA 15.3 to separate positive from negative FDG PET findings, in ER+ and ER-patients, were respectively 0.772 (p = 0.0001) and 0.596 (p = 0.143). AUC measurements for CA 15.3 to separate positive from negative FDG PET findings, in PR+ and PR-patients, were respectively 0.675 (p = 0.0001) and 0.694 (p = 0.0001). In HER2-positive and -negative patients, the AUC measurements were respectively 0.594 (p = 0.178) and 0.701 (p = 0.0001) to separate positive from negative FDG PET findings. Conclusion: The AUC for CA 15.3 measurements to separate FDG PET positive from negative findings in breast cancer patients with suspected recurrence proved to be directly related to the extent of the recurrent disease and hormone receptor status and inversely related to HER2-status. Correcting CA 15.3 measurements for blood volumes did not impact the AUC.

Tumor hypoxia and tumor metabolism are linked through the activation of metabolic genes following hypoxia-inducible factor 1 (HIF-1) activation. This raises the question of whether this relationship can be exploited to improve 2-deoxy-2-[F-18]fluoro-D-glucose positron emission tomography ([F-18]FDG-PET). To do this, [F-18]FDG uptake was investigated after chemical induction of hypoxia and chemical activation of HIF-1 in an in vitro and an in vivo model of a human colorectal carcinoma. [F-18]FDG uptake, HIF-1 alpha protein levels, and messenger ribonucleic acid expression of glucose transporter 1 (GLUT1), hexokinase 2, HIF-1 alpha, and carbonic anhydrase IX (CA IX) were determined in HT29 cells after treatment with 200 mu M CoCl2 and 500 mu M dimethyloxalylglycine (DMOG). In an HT29 xenograft, the distribution of endogenous and exogenous markers of hypoxia was investigated using immunohistochemistry, and tumor [F-18]FDG uptake was determined after treatment with a single dose of 5 mg/kg hydralazine and 8 mg DMOG. Treatment of HT29 cells with CoCl2 and DMOG induced functional HIF-1 and resulted in increased [(18) F]FDG uptake. In an HT29 xenograft, a similar spatial distribution of pimonidazole, CA IX, and GLUT1 was found, and treatment with DMOG resulted in significant increases in maximum and mean standardized uptake values using [(18) F]FDG-PET. Chemical activation of HIF-1 can increase in vitro and in vivo [(18) F]FDG uptake. Imaging after pharmacologic HIF-1 activation might increase tumor [(18) F]FDG uptake when using [(18) F]FDG-PET.