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Chondrosarcoma of the mandible is rare, especially in children. The available literature consists mostly of a few case reports which are partly integrated in small studies. Growing this small pool of literature is helpful in solidifying knowledge about this disease and facilitating appropriate treatment for children. Therefore, we present such a case in a 12-year-old boy, exhibit comprehensive and relevant information concerning this entity, and discuss our findings in the context of other publications.

Recent clinical evidence suggests that positron emission tomography with fluorine-18 fluorodeoxyglucose (FDG-PET) is more accurate in detecting thyroid carcinomatous tissue at high than at low TSH levels. The aim of this study was to determine the influence of TSH on FDG uptake in human thyroid cells in vitro. Monolayers of human thyroid tissue were cultured after mechanical disintegration and enzymatic digestion of samples from patients undergoing surgery for nodular goitre. The purity of thyroid cell preparations was ascertained by immunohistochemical staining for the epithelial antigen KL-1, and their viability by measuring the synthesis of thyroglobulin in vitro. The cells were incubated with 0.8-1.5 MBq FDG/ml uptake medium for 1 h. FDG uptake in thyroid cells was quantified as percent of whole FDG activity per well (% ID) or as % ID in relation to total protein mass. This experimental protocol was subsequently varied to study the effect of incubation time, glucose dependency and TSH. Furthermore, radio-thin layer chromatography was used to identify intracellular FDG metabolites. FDG accumulated in the thyroid cells linearly with time, doubling roughly every 20 min. Uptake was competitively inhibited by unlabelled glucose and decreased to approximately 70% at 100 mg/dl glucose compared to the value measured in glucose-free medium. FDG was intracellularly trapped as FDG-6 phosphate and FDG-1,6-diphosphate. TSH significantly increased FDG uptake in vitro in a time- and concentration-dependent manner: Cells cultured at a TSH concentration of 50 micro U/ ml doubled FDG uptake compared to TSH-free conditions, and uptake after 72 h of TSH pre-incubation was approximately 300% of that without TSH pre-incubation. TSH stimulates FDG uptake by benign thyroid cells in a time- and concentration-dependent manner. This supports the clinical evidence that in well-differentiated thyroid carcinomas, most of which are still TSH-sensitive, FDG-PET is more accurate at high levels of TSH.

The radiopharmaceutical 3-[(123)I]iodo-alpha-methyl-L-tyrosine ([(123)I]IMT) can be used to study amino acid transport by single-photon emission tomography (SPET). In order to evaluate the potential contribution of [(123)I]IMT accumulation in macrophages to overall uptake values measured in neoplastic lesions in vivo, we studied the mechanisms governing the uptake of this tracer by human monocyte-macrophages (HMMs). HMMs were isolated from healthy human donors by density gradient centrifugation using Ficoll methods. The human glioblastoma cell line U-138 MG (GLIOs) was obtained from American Type Culture Collection. Using multiwell dishes, cells were incubated in phosphate buffered saline or an equivalent sodium-free buffer with 50 kBq [(131)I]IMT per well. [(131)I]IMT uptake was quantified as % injected dose per mass of protein within each culture well. Several natural and artificial amino acids were used as potential transport inhibitors both in sodium-containing and sodium-free medium. [(131)I]IMT uptake was significantly lower in HMMs than in GLIOs (34 +/- 2 %/mg (40 min) vs. 507 +/- 50 %/mg at 30 minutes of incubation, respectively; p < 0.01). Endotoxin (LPS) significantly increased [(131)I]IMT uptake in HMMs by a factor of approximately 2. Transport into non-stimulated HMMs was exclusively sodium-independent and inhibitable by BCH, but not by MeAIB. Under LPS stimulation exclusively, there was in addition also a sodium-dependent inhibition of [(131)I]IMT uptake by L-arginine and MeAIB, albeit to a minor extent. [(131)I]IMT accumulation in HMMs is mainly mediated via an L-like amino acid transport system and increases on HMM activation by LPS. LPS may induce an additional Na(+)-dependent transport system in HMMs. The considerably lower [(131)I]IMT uptake in HMMs than in GLIOs suggests that overall uptake values of this tracer measured by SPET in tumors are not significantly affected by [(123)I]IMT accumulation in macrophages within the neoplastic lesion.

Unlabelled: The contribution of (18)F-FDG uptake by endothelial cells to uptake values measured by PET in various tissues is as yet unclear. We therefore sought to characterize (18)F-FDG uptake in an in vitro model of human endothelial cells., Methods: Commercially obtained human umbilical vein endothelial cells (HUVECs) were seeded in 6-multiwell plates 48-96 h before incubation with 1-2 MBq (18)F-FDG per well. Radioactivity measurements were performed after washing and mechanical dissolvation of the cellular monolayers. Cellular (18)F-FDG uptake was referred to protein concentration. This experimental protocol was subsequently varied to study the effect of different parameters of interest. Furthermore, radio-thin-layer chromatography was used to identify intracellular (18)F-FDG metabolites. (18)F-FDG uptake in HUVECs was compared with that by a human monocyte-macrophage (HMM) preparation and by glioblastoma cells (GLIOs) under identical experimental conditions., Results: (18)F-FDG accumulated in HUVECs in a time-dependent manner and was trapped mainly as (18)F-FDG-6-phosphate and (18)F-FDG-1,6-diphosphate. Unlabeled glucose and cytochalasin B competitively inhibited (18)F-FDG uptake, whereas phlorizin had no significant effect. Glucose deprivation significantly enhanced (18)F-FDG uptake by a factor of 2.7, whereas sodium depletion had no significant influence. HUVECs treated with vascular endothelial growth factor (VEGF) showed a significant 82% increase in (18)F-FDG accumulation after a 2-h exposure to 50 ng/mL VEGF. (18)F-FDG uptake in HUVECs was significantly higher than that in HMMs and in the range of the uptake values measured in GLIOs., Conclusion: (18)F-FDG accumulates in HUVECs by mechanisms analogous to those in neoplastic cells or neurons. VEGF significantly stimulates endothelial (18)F-FDG uptake. The observed differences in (18)F-FDG uptake between HUVECs, HMMs, and GLIOs are difficult to extrapolate to in vivo conditions but stimulate further studies on the contribution of endothelial (18)F-FDG uptake to the overall uptake of that tracer in neoplastic or vascular lesions.

The fact that fluorine-18 fluorodeoxyglucose ([(18)F]FDG) accumulates in inflammatory lesions as well as in tumours reduces the diagnostic specificity of positron emission tomography (PET) in oncology. The aim of this study was to characterise the uptake of [(18)F]FDG in isolated human monocyte-macrophages (HMMs) in vitro in comparison with that in human glioblastoma (GLI) and pancreatic carcinoma cells (PAN). The purity of HMM preparations was determined by immunohistochemical staining and their functional integrity was assessed by long-term incubation with iodine-131 acetylated bovine serum albumin. [(18)F]FDG uptake in HMMs was quantified as percent of whole [(18)F]FDG activity per well (% ID) or as % ID in relation to total protein mass. [(18)F]FDG uptake in HMMs significantly increased with culture duration, yielding 7.5%+/-0.9% (% ID/100 micro g) at day 14. Stimulation by lipopolysaccharide further enhanced [(18)F]FDG uptake in HMMs by a factor of 2. [(18)F]FDG uptake significantly decreased with increasing glucose concentration in the medium. Radio-thin layer chromatography of intracellular metabolites revealed that [(18)F]FDG was trapped by HMMs mainly as [(18)F]FDG-6-phosphate and [(18)F]FDG-1,6-diphosphate. [(18)F]FDG uptake was in the range of uptake values measured in GLI and PAN. By accumulating [(18)F]FDG in a manner analogous to uptake by tumour cells, activated HMMs may contribute to the [(18)F]FDG uptake values measured by PET in neoplasms.

High-density lipoprotein (HDL) cholesteryl esters (CE) are taken up by many cells without parallel uptake of HDL apolipoproteins. This selective uptake of HDL CE was investigated in human monocyte-derived macrophages (HMM). HDL3 (d = 1.125-1.21 g/ml) was labeled in its apolipoprotein A-I moiety with 125I and in its CE moiety with [3H]cholesteryl oleyl ether. Cultured human monocyte-macrophages were incubated in the presence of doubly labeled HDL3 followed by determination of tracer uptake. HMM took up HDL3 particles as indicated by the uptake of HDL3 apolipoproteins. Uptake of HDL3-associated CE tracer was in significant excess of that due to HDL3 particle uptake indicating selective uptake of CE. Increased cell cholesterol due to preincubation with acetylated low-density lipoprotein (LDL) down-regulated selective uptake by HMM. According to several experimental approaches, selective uptake of HDL3 CE was independent from cell-secreted products, LDL receptor-mediated endocytosis or HDL3 retroendocytosis. The intracellular catabolism of HDL3 CE was investigated with HDL3 labeled in its CE moiety with [3H]cholesteryl oleate. The lysosomal inhibitor chloroquine had no effect on CE hydrolysis indicating that CE selectively taken up is hydrolyzed independently from lysosomes. In conclusion, HMM selectively take up HDL3-associated CE. The cellular mechanism of selective uptake is independent from endocytosis or retroendocytosis. Intracellularly, HDL3 CE selectively taken up are catabolized independently from lysosomes.