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        Sequential Use of 90Y Microspheres Radioembolization and 177Lu-Dotatate in Pluri-Metastatic Neuroendocrine Tumors: A Case Report

        Luca Filippi,Alida Ciorra,Barbara Sardella,Orazio Schillaci,Oreste Bagni 대한핵의학회 2014 핵의학 분자영상 Vol.48 No.4

        Abstract 90Y radioembolization and peptide-receptor radionuclidetherapy (PRRT) with177Lu-DOTATATE are both effectivetreatments for patients with inoperable neuroendocrinemetastatic tumors (NET). We report the case of a 72-year-oldman with severe functional syndrome due to a metastaticNET. 68Ga-DOTATOC positron-emission tomography (PET)revealed high somatostatin receptor expression in a gross livermetastasis, in one abdominal lymph node and in severals k e l e t a l l esions. The patient underwent l iverradioembolization with 90Y-resin microspheres followed byfour cycles of PRRT with177Lu-DOTATATE. After 3 months,a complete remission of the functional syndrome was observed. 68Ga-DOTATOC PET demonstrated a complete responsefor skeletal and lymph nodal lesions with a residualbulky mass in the liver. Therefore a further 90Yradioembolization was performed as consolidation treatmentfor the hepatic lesion. Six months after these combined treatments,68Ga-DOTATOC PET demonstrated complete metabolicresponse in liver and stable extrahepatic lesions. Nosignificant long-term adverse reactions were registered. Toour knowledge, the sequential use of 90Y radiembolizationbefore and after PRRT in a liver-dominant advanced NET hasnot been reported in the literature and this case suggests thatthese combined treatments can be safe and effective.

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        Imaging Findings of 18F-Choline and 18F-DOPA PET/MRI in a Case of Glioblastoma Multiforme Pseudoprogression: Correlation with Clinical Outcome

        Filippi Luca,Angela Spanu,Bagni Oreste,Orazio Schillaci,Barbara Palumbo 대한핵의학회 2022 핵의학 분자영상 Vol.56 No.5

        We describe the case of 74-year-old-male, previously treated with fronto-parietal craniotomy due to primary glioblastoma multiforme (GBM), followed by concurrent radiation therapy (RT) and temozolomide (TMZ) chemotherapy. Magnetic resonance imaging (MRI) of the brain, at 1 month after completing RT + TMZ, depicted partial response. Three months later, the patient was submitted to a further brain MRI, that resulted doubtful for therapy induced changes (i.e., pseudoprogression). The patient, who had been previously treated with prostatectomy for prostate cancer (PC), underwent a positron emission tomography/computed tomography (PET/CT) scan with 18F-choline for PC biochemical recurrence. 18F-choline whole body PET/CT resulted negative for PC relapse, while segmental brain PET, co-registered with MRI, demonstrated increased tracer uptake corresponding to tumor boundaries. In order to solve differential diagnosis between pseudoprogression and GBM recurrence, brain PET/CT with 18F-L-dihydroxy-phenil-alanine (18F-DOPA) was subsequently performed: fused axial PET/MRI images showed increased 18F-DOPA incorporation in the peri-tumoral edema, but not in tumor boundaries, consistent with the suspicion of GBM pseudoprogression, as then confirmed by clinical and radiological follow-up.

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        Acute Promyelocytic Leukemia After Radium-223 Exposure for Prostate Cancer in a Chemotherapy-Naïve Patient

        Perrone Salvatore,Ortu La Barbera Elettra,Ottone Tiziana,Capriata Marcello,Passucci Mauro,Filippi Luca,Bagni Oreste,Voso Maria Teresa,Cimino Giuseppe 대한핵의학회 2020 핵의학 분자영상 Vol.54 No.5

        223Ra-dichloride is a bone-seeking targeted alpha (α)-emitting approved for bonemetastases in prostate cancer. Here, we report a case of therapy-related acute promyelocytic leukemia (t-APL) following administration of 223Ra, showing some evidence of a causative relationship. A patient with metastatic prostate cancer received therapy with 223Ra, with 6 injections of the radiopharmaceutical at a standard dose of 55 kBq/kg at 4-week intervals for a cumulative administered activity of 26.3MBq. PET/CT with 18F-methylcholine repeated 1 month after the conclusion of 223Ra was negative. After 8 months, he developed pancytopenia and we made a diagnosis of therapy-related acute promyelocytic leukemia (t-APL). We then studied the genomic locations of the breakpoints in the PML and RARA genes, which were at nucleotide positions 1708-09 of PML intron 3, respectively, outside the previously reported Topo II-associated hotspot region. t-APL was cured with all-trans-retinoic acid (ATRA) and arsenic trioxide. The type of PML/RARA rearrangement we identified, in absence of other myelotoxic treatments, is suggestive of a possible direct causal relationship with exposure to 223Ra and warrants further investigations.

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