Academic literature on the topic '18F-TEP'
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Journal articles on the topic "18F-TEP":
Perie, S., A. Burgess, L. Michaud, and J. Talbot. "L’utilité de la 18F-Choline TEP dans l’hyperparathyroïdie." Annales françaises d'Oto-rhino-laryngologie et de Pathologie Cervico-faciale 131, no. 4 (October 2014): A67. http://dx.doi.org/10.1016/j.aforl.2014.07.182.
Djelbani, S., A. Mekinian, M. O. Chanderis, O. Monssarat, G. Pop, I. Durieu, S. Georgin-Lavialle, et al. "Caractéristiques en TEP au 18F-FDG des mastocytoses systémiques." La Revue de Médecine Interne 34 (June 2013): A83. http://dx.doi.org/10.1016/j.revmed.2013.03.322.
Ait Sahel, O., S. Touil, Y. Benameur, S. Oueriagli, J. El Bakkali, A. Biyi, and A. Doudouh. "Métastase intramédullaire détectée par TEP/TDM au 18F-FDG." Médecine Nucléaire 44, no. 2 (March 2020): 107. http://dx.doi.org/10.1016/j.mednuc.2020.01.012.
Ayed, K., I. Yeddes, J. Charfi, M. Somai, I. Slim, I. Meddeb, and A. Mhiri. "La TEP-TDM au 18F-FDG dans l’ostéodystrophie rénale." Médecine Nucléaire 48, no. 2 (March 2024): 107. http://dx.doi.org/10.1016/j.mednuc.2024.01.143.
Schiazza, A., A. El Ouartassi, D. Chardin, N. Sapin, M. Koulibaly, C. Bayreuther Giordana, and J. Darcourt. "TEP-TDM à la 18F-FDOPA et syndromes cortico-basaux." Médecine Nucléaire 45, no. 4 (July 2021): 183–84. http://dx.doi.org/10.1016/j.mednuc.2021.06.025.
Collet, C., S. Schmitt, S. Lamandé-Langle, F. Chrétien, F. Maskali, S. Poussier, P. Y. Marie, G. Karcher, and Y. Chapleur. "Nouveaux dérivés [18F]fluoro-inositols : potentiels radiotraceurs pour l’imagerie TEP." Médecine Nucléaire 38, no. 3 (May 2014): 160. http://dx.doi.org/10.1016/j.mednuc.2014.03.116.
Cavet, M., F. Tenenbaum, C. Hignette, C. Modis, B. Richard, M. Faraggi, and B. Dousset. "Récidive d’une tumeur carcinoïde et TEP à la 18F-DOPA." Gastroentérologie Clinique et Biologique 34, no. 3 (March 2010): 213–17. http://dx.doi.org/10.1016/j.gcb.2009.06.018.
Ribeiro, M. J. Santiago, J. Vercouillie, V. Gissot, S. Maia, L. Barantin, Y. Peltier, J. P. Cottier, J. B. Deloye, N. Arlicot, and D. Guilloteau. "Le 18F-LBT-999, le nouveau traceur TEP du DAT ?" Médecine Nucléaire 42, no. 3 (May 2018): 137–38. http://dx.doi.org/10.1016/j.mednuc.2018.03.017.
Toledano, M. N., M. Soussan, S. Djelbani, and M. Hommada. "Endométriome ovarien simple et compliqué : aspect en TEP 18F-FDG." Médecine Nucléaire 42, no. 3 (May 2018): 156–57. http://dx.doi.org/10.1016/j.mednuc.2018.03.060.
Salomon, T., and B. Houdu. "Caractérisation des adénopathies médiastinales en TEP/TDM au 18F-FDG." Médecine Nucléaire 42, no. 4 (July 2018): 237–47. http://dx.doi.org/10.1016/j.mednuc.2018.06.001.
Dissertations / Theses on the topic "18F-TEP":
Hovhannisyan, Narinée. "[18F] Fludarabine pour l'imagerie TEP des lymphomes." Thesis, Normandie, 2018. http://www.theses.fr/2018NORMC412/document.
Although PET using [18F]FDG has proved to be useful for diagnosis and therapy monitoring in patients with lymphoma, the specificity of [18F]FDG uptake has been critically questioned because of its dependence on glucose metabolism, which may indiscriminately increase in benign conditions such as inflammatory or infectious processes. Considering these drawbacks, an adenine nucleoside analogue was developed as a novel PET imaging probe ([18F]fludarabine). An efficient and fully automated radiosynthesis has been implemented and, subsequently preclinical studies in xenograft murine models (follicular cell lines: RL7 and DOHH-2, multiple myeloma (MM): RPMI8226, central nervous system (CNS) lymphoma: MC116) were conducted with this novel 18F-radiopharmaceutical in parallel with [18F]FDG. The pattern of the radioactivity distribution in selected organs confirmed the tumor-specific targeting. In a follicular lymphoma model, we evaluated its robustness during rituximab therapy and demonstrated - the treatment did not interfere with its uptake - a stronger correlation between quantitative values extracted from this 18F-radiopharmaceutical and histology when compared to [18F]FDG-PET. Accordingly, this PET tool may be considered as a promising approach for detecting the persistence of residual disease during or after rituximab-like treatment. Furthermore, its behaviour in turpentine-induced inflammatory process showed significantly weaker uptake in inflammation when compared to [18F]FDG. In MM, the role of [18F]FDG-PET remains limited because of its lack of sensitivity for detecting diffuse bone marrow involvement, small skull lesions due to the physiological [18F]FDG uptake in brain. Our data suggested that [18F]fludarabine-PET might represent an alternative and perhaps more specific modality for MM imaging. In our latest study, on xenograft brain tumors, this novel PET probe revealed significantly divergent responses between CNS lymphoma and glioblastoma (GBM), while [18F]FDG demonstrated overlap between the groups. A first in man study, was undertaken, for an initial diagnosis, where 10 untreated patients were enrolled with either B-cell chronic lymphocytic leukemia (CLL) or diffuse large B-cell lymphoma (DLBCL). Successive partial body scans were acquired for 250 min after i.v. injection with an activity of 4 MBq/kg. The results with conventional modalities (CT and/or [18F]FDG-PET) have also been investigated. The study was also designed to estimate its radiation dose for major organs. In DLBCL patients, increased uptake was observed in sites considered abnormal by CT and [18F]FDG; in two patients discrepancies were observed in comparison with [18F]FDG. In CLL patients, the uptake coincided with sites expected to be involved and displayed a significant uptake in hematopoietic bone marrow. No uptake was observed, whatever the disease group, in the cardiac muscle and brain. Moreover, its mean effective dose was below the effective dose reported for [18F]FDG. In conclusion, these preclinical and clinical findings revealed a great specificity of this 18F-radiopharmaeutical for lymphoma tissues. Furthermore, it might well be a robust tool for correctly quantifying the disease, even with inflammatory processes, thus avoiding the false-positive results, and an innovative approach for imaging lymphoid neoplasms with low mitotic activity
Vanhoutte, Matthieu. "Caractérisation par imagerie TEP 18F-FDG de la maladie d’Alzheimer à début précoce." Thesis, Lille 2, 2018. http://www.theses.fr/2018LIL2S026/document.
Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia, characterized at 95% by late-onset forms (LOAD) which present episodic memory impairments and progress slowly. However, 5% of AD patients have an early-onset form (EOAD) of the disease whose onset begins before 65. Although the lesion substratum is similar between EOAD and LOAD, EOAD has more severe neuritic plaque deposits, neurofibrillary tangles and brain atrophy. Moreover, EOAD is more heterogeneous than LOAD, because even if most of the impairments are about episodic memory there is a high proportion of atypical forms impaired in language, visuospatial or executive functions. Although many 18F-FDG PET studies allowed to metabolically characterize EOAD compared to LOAD or healthy controls group, very few differentiated typical from atypical forms. In this thesis, we examined 18F-FDG PET data, complemented by structural MRI, in order to improve characterization and comprehension of typical and atypical forms of EOAD. Following a first harmonization work between 18F-FDG PET reconstructions from both GE and Siemens scanners used for the acquisition of patient data, our second aim was to study at baseline on the whole brain hypometabolic patterns characterizing the clinical forms of EOAD and their correlations with neuropsychological performance. This work showed that each clinical form of EOAD was characterized by specific hypometabolic patterns highly correlated with clinical symptoms and neuropsychological performance of the associated cognitive domain. Then, we focused on the 3-year hypometabolism progression on the cortical surface according typical or atypical forms of EOAD. Although similar patterns of hypometabolism evolution between typical and atypical forms were observed in parietal cortices, atypical only showed a more severe reduction of metabolism in lateral orbitofrontal cortices associated with more severe cognitive declines. Temporally, the results suggest that hypometabolism in typical forms would progress according to an anterior-to-posterior axis coherently with Braak and Braak stages, whereas in atypical forms hypometabolism would progress according a posterior-to-anterior axis. Taken together, results consolidate the hypothesis of a different tau distribution in terms of burden and temporal evolution between both forms of EOAD. Our last goal was to determine the discriminative power of 18F-FDG PET data, alone or combined to structural MRI data, in order to automatically classify in a supervised manner EOAD patients into typical or atypical form. We applied machine learning algorithms combined to cross-validation methods to assess influence of some components on classification performances. Maximum balanced accuracies equal to 80.8% in monomodal 18F-FDG PET and 92.4% in multimodal 18F-FDG PET/T1 MRI were obtained, validating 18F-FDG PET as a sensible biomarker of EOAD and highlighting the incontestable contribution of multimodality. In conclusion, our works allowed a better characterization and comprehension of clinical forms of EOAD, paving the way to personalized patient management and more effective treatments for these distinct clinical forms
Nioche, Christophe. "Caractérisation des tumeurs gliales en TEP/TDM à la 18F-Dopa et en IRM de perfusion." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112100.
MRI provides morphological information about tumour, but also provides information regarding the micro-vascularization of the tumour. In PET/CT, the accumulation of 18F-FDopa in tumour cells results from the metabolic activity greater than that of healthy tissues. We studied 28 gliomas for which we analysed data from MRI and PET/CT. A registration method has been developed to combine information from both PET and MRI and to extract volumes of interest consistent with the information included in the two modalities. In these volumes, the tumour compartment and normal tissue compartment were identified using a Gaussian mixture model. Parameters from PET or MRI data were then calculated in these compartments. ROC analyses combined with linear discriminant analyses were used to assess whether joint observation of standardized uptake value (SUVmax ) and relative Cerebral Blood Volume (rCBV) or of relative rk1 and rCBV could distinguish between low grade and high grade tumours. We found that using this joint analysis, 82.4% of high-grade tumors and 70.0% of low-grade tumors were correctly classified (AUC of 0.88 for [SUVmax , rCBV] and of 0.92 for [rk1 , rCBV]). Considering the [SUVmax , rCBV] combined information, the sensitivity for detecting high-grade tumors was 95% with a specificity of 60%. The negative predictive value was 52% for a positive predictive value of 95%. Similarly, considering the [rk1 , rCBV] combined information, we also a specificity of 60% associated with a 95% sensitivity for detecting high-grade tumors, with a negative predictive value of 60% and positive predictive value of 95%. Our work shows that joint analysis of microvascular and metabolic information is possible by combining PET and MR imaging data. However, we found that, in our patient population, the microvascular information given by MR did not bring information more discriminating than the metabolic information derived from PET only
Palard, Xavier. "Quantification multiparamétrique par TEP à la 18F-Choline et IRM dans le cancer de la prostate." Thesis, Rennes 1, 2018. http://www.theses.fr/2018REN1B058.
Research question: Do the functional parameters derived by 18F-Choline (FCH) Positon Emission Tomography (PET) and Magnetic Resonance Imaging (MRI) add informations to characterize the aggressiveness of prostate cancer? Objectives: The first objective of this work was (i) to enhance a potential link between quantitative parameters extracted by FCH PET and clinicopathological parameters in prostate cancer. Then, after this preliminary study, in order to optimize the quantification of the FCH influx with a kinetic analysis, the second objective was (ii) to optimize the exam protocol of the FCH PET early acquisition. Finally, the last objective was (iii) to enhance a potential link between quantitative parameters extracted by FCH PET and quantitative parameters extracted by multiparametric MRI in prostate cancer. Results: For the first step (i), we compared FCH PET quantitative parameters and clinicopathological parameters extracted from 61 patients referred to the nuclear medicine department to perform an FCH PET/ CT with newly histologically proven prostate cancer and before any treatment The FCH influx measured using kinetic analysis was higher for patients with a Gleason score ≥ 4+3 than for patients with a Gleason score < 4 + 3. Concerning the second step (ii), firstly, we compared the contrast to noise ratio of 77 prostatic cancer lesions at 5 minutes and 10 minutes post-injection in order to optimize the length of the early FCH PET acquisition. No significant difference was observed. Secondly, we sought to define an optimal time sampling of the early FCH PET acquisition comparing 7 different time samplings with a FCH influx as objective extracted from 37 prostatic cancer lesions. The 12x5”-8x30” time sampling was selected. For the last step of this work (iii), we compared FCH PET and multiparametric MRI quantitative parameters extracted from 14 prostatic cancer lesions. The FCH influx was moderately correlated to the vessel permeability measured by the volume transfert constant of gadolinium (r = 0.55). Conclusion: The FCH influx extracted from the early FCH PET acquisition using kinetic analysis seems to be linked to the tumoral differentiation of prostatic cancers. This FCH influx seems also linked to the vessel permeability. However, due to the moderate degree of correlation, these two imaging parameters reflect two different processes. To confirm the results obtained in this work, other studies are needed to enhance the role of the functional parameters derived by FCH PET and multiparametric MRI as biomarkers for prostate cancer
Rmeily-Haddad, Mireille. "Analyse temporelle de la fixation cérébrale du 18F-FDG en TEP : cartographies et application clinique potentielle." Amiens, 2009. http://www.theses.fr/2009AMIED009.
Verdurand, Mathieu. "Vers l'imagerie TEP de la neurotransmission sérotoninergique dans la maladie d'Alzheimer : du radiotraceur au modèle animal." Phd thesis, Université Claude Bernard - Lyon I, 2008. http://tel.archives-ouvertes.fr/tel-00348975.
Une première partie, méthodologique, a consisté à automatiser et à optimiser la radiosynthèse du [11C]PIB, un radiotraceur pouvant détecter l'accumulation des peptides amyloïdes dans le cerveau de patients atteints de la MA.
Dans une seconde partie, nous nous sommes intéressés à l'imagerie TEP de la neurotransmission sérotoninergique. Les antagonistes des récepteurs 5-HT6 ont démontré des propriétés procognitives et des études post-mortem ont montrées leur modification dans la MA. Cependant, aucun centre ne dispose encore d'un radiotraceur spécifique. Nous rapportons l'évaluation biologique d'un radiotraceur antagoniste des 5-HT6, le [18F]12ST05. D'autre part, une étude récente en imagerie TEP au [18F]MPPF, un antagoniste des récepteurs 5-HT1A, a révélé une diminution de sa fixation chez des patients Alzheimer alors qu'une augmentation pouvait être constatée chez des patients MCI. Nous sommes parvenus à reproduire une surexpression transitoire des 5-HT1A dans un modèle animal de la MA et nous proposons différents mécanismes compensatoires à l'origine de cette augmentation. Ces résultats apportent des hypothèses sur la nature des phénomènes compensatoires précoces stimulés et pourraient avoir des conséquences sur les thérapeutiques ciblant les 5-HT1A.
Didelot, Adrien. "Étude par la TEP au [18F]MPPF des récepteurs cérébraux sérotoninergiques 5-HT1A dans l’épilepsie du lobe temporal." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10104/document.
In patients suffering from epilepsy, no neuroimaging method has proved able to delineate the epileptogenic zone (EZ), which is defined by the area of cortex required to generate the epileptic seizures. About one third of patient suffering from temporal lobe epilepsies (TLE) are not seizure free after surgery after removal of the cortical area supposed to included the EZ according to the presurgical evaluation. Data from previous studies carried out in our departement suggested that decreases of the [18F]MPPF binding potential (BPND) correlated, at the group level, with cortical epileptogenicity. Our aim was to validate the relevance of [18F]MPPF PET at the individual level for identifying the EZ in TLE. In a first study, the [18F]MPPF PET of 42 patients suffering from TLE were visually and statistically analyzed and compared with [18F]FDG PET, which were performed in the same group of patients during their presurgical evaluation. In a second study, we developed a voxel based analysis of asymmetry index (AI) of [18F]MPPF binding and compared the sensibility and specificity of this method to those of conventional SPM analysis of [18F]MPPF PET data. This second study was carried out in 24 patients, who have been operated and remained seizure-free after surgery. Two statistical thresholds (p< 0.05 corrected at the voxel level and p< 0.05 corrected at the cluster level) were used for each method. In a last study, the correlation between the depressive symptoms and the BPND of [18F]MPPF was studied in 24 patients suffering from TLE. These three studies lead to the following conclusions: i) [18F]MPPF PET is more performant than [18F]FDG PET for identifying the epileptogenic lobe in patients suffering from TLE, ii) AI analysis with a statistical threshold of p< 0.05 corrected at the cluster is the method of analysis of [18F]MPPF PET that allowed EZ identification with the best sensitivity [96%] and specificity [88%] in TLE, iii) at the group level, depressive symptoms positively correlate with an increase of the BPND of [18F]MPPF BPND within the raphe nuclei and the insula controlateral to the EZ
Didelot, Adrien. "Étude par la TEP au [18F]MPPF des récepteurs cérébraux sérotoninergiques 5-HT1A dans l'épilepsie du lobe temporal." Phd thesis, Université Claude Bernard - Lyon I, 2010. http://tel.archives-ouvertes.fr/tel-00705810.
Awde, Ali Reda. "Evaluation de la protéine translocatrice TSPO comme cible pour l’imagerie moléculaire et la thérapie du glioblastome dans un modèle expérimental chez le rat." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05P647.
In France alone, there are 3000 new cases of glioblastoma multiforme (GBM) per year and therefore GBM is the most common and aggressive form of the primary tumor in the central nervous system (CNS). The clinical prognosis for glioblastoma patients is extremely poor with a median survival period that rarely exceeds 15 months post-diagnosis. Since the study performed by Stupp and colleagues in 2005, the standard treatment for newly diagnosed glioblastoma consists of surgical removal of the tumor, followed by radiotherapy and concomitant chemotherapy with temozolomide. The 18 kDa Translocator Protein (TSPO), previously known as the peripheral benzodiazepine receptor (PBR) is a mitochondrial membrane protein known to be implicated in cholesterol transport, protein import, transport of porphyrin, cell proliferation and apoptosis through its interaction with VDAC (Voltage-Dependent Anion Channel) in the mitochondrial permeability transition pore (PTPM). Previous studies have reported overexpression of TSPO in brain tumors, suggesting that this protein may represent a molecular target for the therapy of GBM. In particular, Erucylphosphohomocholine (ErPC3, erufosine), an alkylphosphocholine, seems to be a promising agent in the treatment of glioblastoma. Previous studies have reported its ability to induce apoptosisin otherwise highly apoptosis resistant glioma cell lines and ErPC3 induced apoptosis seems to require the presence TSPO. [18F]DPA-714, a new TSPO radioligand for positron emission tomography (PET) imaging, was developed at the CEA and validated in different models of neuroinflammation. The hypotheses underlying this thesis are: 1) that the overexpression of TSPO in GBM can be detected by PET imaging using [18F]DPA-714 and 2) that the targeting of TSPO, via specific ligands or via ErPC3, can induce apoptosis in GBM. The objectives of the thesis were: 1) to evaluate the expression of TSPO in a panel of rodent and human glioma cell lines and 2) to characterize, in vitro and in vivo, the anti-neoplastic effect of TSPO ligands (PK11195 and RO5-4864) or ErPC3 in glioma cell lines as well as 3) to develop a preclinical model for in vivo PET imaging using [18F]DPA-714 to monitor treatment efficacy of selected ligands. In this thesis, we demonstrated the feasibility of using PET imaging with [18F]DPA-714 to characterize 9L glioma in an orthotopic rat model and to evaluate the effect of ErPC3 treatment, which could provide a new approach to molecular imaging of GBM. We confirmed the pro-apoptotic effect of ErPC3 in the rat 9L glioma cells in vitro and in vivo, and found an infiltration of microglia/macrophages (CD11b-positive) and astrocytes (GFAP-positive) in the tumor area of animals treated with ErPC3. These results open interesting perspectives for clinical research in the treatment of GBM
Tiss, Amal. "Joint Reconstruction of Longitudinal Positron Emission Tomography Studies for Tau Protein Imaging." Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS387.pdf.
The accumulation of the paired helical filament tau protein leads to the cognitive decline seen in Alzheimer’s disease (AD). The Positron Emission Tomography tracer, [18F]-AV-1451, permits the observation of PHF tau in vivo. To determine the rate of tau deposition in the brain, the conventional approach involves scanning the subject two times (2-3 years apart) and reconstructing the images separately. Region-specific rates of accumulation are derived from the difference image which suffers from an increased intensity variation making this approach inadequate for clinical trial looking at the effect of a candidate drug on tau because the increased variation leads to a higher sample size required. We propose a joint longitudinal image reconstruction where the tau deposition difference image is reconstructed directly from measurements leading to a lower intensity variation. This approach introduces a linear temporal dependency and accounts for spatial alignment, and the different injected doses. We validate the reconstruction method by simulating higher tau accumulation in real data at different intensity levels. We additionally reconstruct the data from 123 subjects: 109 healthy subjects, 10 suffering from mild cognitive impairment, and 4 diagnosed with AD. The joint reconstruction shows better contrast in the difference image obtained by the numerical simulations and a drastically reduced variance in the change of the Standard Uptake Value Ratio among subjects. The decreased variance of our method leads to a smaller sample size for a potential clinical trial evaluating the effect of a candidate drug against AD
Book chapters on the topic "18F-TEP":
"Tomographie par émission de positons au [18F]- déoxyglucose (TEP-scan)." In Méga Guide STAGES IFSI, 134–35. Elsevier, 2015. http://dx.doi.org/10.1016/b978-2-294-74529-4.00032-x.
Alexandre, J., A. Balian, L. Bensoussan, A. Chaïb, G. Gridel, K. Kinugawa, F. Lamazou, et al. "Tomographie par émission de positons au [18F]-déoxyglucose (TEP-scan)." In Le tout en un révisions IFSI, 127–28. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70633-2.50032-9.