We retrospectively evaluated the usefulness of combined measurement of L-methyl-[11C]methionine (MET) and 3′-deoxy-3′-[18F]fluorothymidine (FLT) positron emission tomography (Family pet) in the differential diagnosis between recurrent gliomas and necrotic lesions. analysis showed that the areas beneath the curves had been high however, not different between MET- and FLT-PET. Family pet research using MET and FLT are of help in the differentiation of recurrent glioma from treatment-induced necrotic lesion. Nevertheless, there is absolutely no complementary info in the differentiation with simultaneous measurements of MET- and FLT-Family pet. degradation also make MET-PET less ideal for routine medical make use of. A fluorinated thymidine analog, 3′-deoxy-3′-[18F]fluorothymidine (FLT), offers emerged as a promising Family pet tracer for analyzing tumor proliferating activity in a variety of malignant mind tumors [18,19,20]. FLT can be phosphorylated by thymidine kinase-1 (TK1), a theory enzyme in the salvage pathway of DNA synthesis, and trapped in the cellular material. Phosphorylated FLT shows up resistant to degradation and would work for imaging with Family pet. The use of FLT phosphorylation as Apremilast inhibition a marker of cellular proliferation is founded on the assumption that cellular FLT trapping can be a representation of thymidine incorporation into DNA [21,22]. As FLT uptake in the standard brain cells is quite low, FLT-PET offers a low-background mind image and therefore is considered to be an ideal PET tracer for the imaging of brain tumors. FLT-PET has been found useful for noninvasive grading of newly diagnosed gliomas [7,18,19,20,21,23]. However, there is some data on the value of FLT-PET in the evaluation of recurrent brain tumors [24,25]. A recent study shows that FLT-PET has a high sensitivity but a low specificity, which has a limited role in the diagnosis of recurrent gliomas [25]. This retrospective study was conducted to evaluate the usefulness of combined use of MET-PET and FLT-PET in the differential diagnosis between recurrent gliomas and treatment-induced necrotic lesions. 2. Results and Discussion 2.1. Results 2.1.1. Visual Assessment Of Apremilast inhibition 21 lesions, 15 were recurrent tumors (initial diagnosis; eight glioblastomas, three anaplastic oligoastrocytomas, two anaplastic astrocytomas, one gliosarcoma, and one gliomatosis cerebri) and six were necrotic lesions by the final diagnosis. All lesions Apremilast inhibition showed moderate to strong enhancement effect on T1-weighted MR image after gadolinium administration. All 15 recurrent gliomas showed increased uptake on FLT- and MET-PET (Figure 1A). Of the six necrotic lesions, all showed increased uptake on FLT-PET and five lesions showed increased uptake on MET-PET (Figure 1B). The MET uptake of one necrotic lesion (Case 19) was faint compared to the normal brain parenchyma (L/N ratio of 1 1.25). Open in a separate window Figure 1 (A) Imaging of a 22 year-old female (case 9) with glioblastoma, previously treated with tumor resection followed by conventional radiotherapy and temozolomide. T1-weighted contrast enhanced MR image showing irregular enhancement in the right occipital lobe. MET-PET and FLT-PET show intense uptake of tracer in the lesion. Recurrent glioblastoma was pathologically confirmed by surgery; (B) Imaging of 61 year-old female (case 21) with glioblastoma, previously treated with tumor resection followed by conventional radiotherapy and temozolomide. T1-weighted contrast enhanced MR image showing enhanced mass in the left temporal lobe. MET-PET shows mild uptake of tracer and FLT-PET shows faint uptake of tracer in the lesion. Necrosis and gliosis dominant tissue was pathologically confirmed by surgery. 2.1.2. Semi-Quantitative Analysis The average SUVmax of 15 recurrent gliomas (4.59 Goserelin Acetate 1.64) was higher than that of six necrotic lesions (3.51 0.83) on MET-PET but this was not statistically significant (= 0.063). The average L/N ratio of recurrent gliomas (3.36 1.06) was significantly higher than that Apremilast inhibition of.