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1.
J Nucl Med ; 56(11): 1681-9, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26359256

RESUMO

UNLABELLED: Our objective was to determine whether early change in standardized uptake values (SUVs) of 3'deoxy-3'-(18)F-fluorothymidine ((18)F-FLT) using PET with CT could predict pathologic complete response (pCR) of primary breast cancer to neoadjuvant chemotherapy (NAC). The key secondary objective was to correlate SUV with the proliferation marker Ki-67 at baseline and after NAC. METHODS: This prospective, multicenter phase II study did not specify the therapeutic regimen, thus, NAC varied among centers. All evaluable patients underwent (18)F-FLT PET/CT at baseline (FLT1) and after 1 cycle of NAC (FLT2); 43 patients were imaged at FLT1, FLT2, and after NAC completion (FLT3). The percentage change in maximum SUV (%ΔSUVmax) between FLT1 and FLT2 and FLT3 was calculated for the primary tumors. The predictive value of ΔSUVmax for pCR was determined using receiver-operating-characteristic curve analysis. The correlation between SUVmax and Ki-67 was also assessed. RESULTS: Fifty-one of 90 recruited patients (median age, 54 y; stage IIA-IIIC) met the eligibility criteria for the primary objective analysis, with an additional 22 patients totaling 73 patients for secondary analyses. A pCR in the primary breast cancer was achieved in 9 of 51 patients. NAC resulted in a significant reduction in %SUVmax (mean Δ, 39%; 95% confidence interval, 31-46). There was a marginal difference in %ΔSUVmax_FLT1-FLT2 between pCR and no-pCR patient groups (Wilcoxon 1-sided P = 0.050). The area under the curve for ΔSUVmax in the prediction of pCR was 0.68 (90% confidence interval, 0.50-0.83; Delong 1-sided P = 0.05), with slightly better predictive value for percentage mean SUV (P = 0.02) and similar prediction for peak SUV (P = 0.04). There was a weak correlation with pretherapy SUVmax and Ki-67 (r = 0.29, P = 0.04), but the correlation between SUVmax and Ki-67 after completion of NAC was stronger (r = 0.68, P < 0.0001). CONCLUSION: (18)F-FLT PET imaging of breast cancer after 1 cycle of NAC weakly predicted pCR in the setting of variable NAC regimens. Posttherapy (18)F-FLT uptake correlated with Ki-67 on surgical specimens. These results suggest some efficacy of (18)F-FLT as an indicator of early therapeutic response of breast cancer to NAC and support future multicenter studies to test (18)F-FLT PET in a more uniformly treated patient population.


Assuntos
Neoplasias da Mama/diagnóstico por imagem , Neoplasias da Mama/tratamento farmacológico , Didesoxinucleosídeos , Terapia Neoadjuvante/métodos , Compostos Radiofarmacêuticos , Neoplasias da Mama/patologia , Didesoxinucleosídeos/efeitos adversos , Feminino , Humanos , Processamento de Imagem Assistida por Computador , Antígeno Ki-67 , Pessoa de Meia-Idade , Tomografia por Emissão de Pósitrons , Valor Preditivo dos Testes , Estudos Prospectivos , Curva ROC , Compostos Radiofarmacêuticos/efeitos adversos , Resultado do Tratamento
2.
Mol Imaging Biol ; 6(1): 7-11, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15018823

RESUMO

Systemic lupus erythematosus (SLE) and lymphoma are disease entities that often have similar presenting signs and symptoms that can complicate or delay definitive diagnosis. 2-Deoxy-2-[(18)F]fluoro-D-glucose positron emission tomography (FDG-PET) has become a valuable tool in the diagnosis, staging, and evaluation of response to therapy in lymphoma patients. However, its utility in patients with SLE has been limited to the central nervous system. Significant FDG uptake has not been previously reported in lymphadenopathy associated with SLE. The case presented is an example of histologically proven benign adenopathy in a 16-year-old female with SLE that was hypermetabolic on FDG-PET imaging. It highlights the importance of recognizing that widespread inflammatory adenopathy in SLE can mimic the pattern of FDG uptake seen with lymphoma at PET imaging.


Assuntos
Fluordesoxiglucose F18 , Lúpus Eritematoso Sistêmico/complicações , Doenças Linfáticas/diagnóstico por imagem , Compostos Radiofarmacêuticos , Tomografia Computadorizada de Emissão , Adolescente , Diagnóstico Diferencial , Feminino , Humanos , Doenças Linfáticas/complicações
3.
J Alzheimers Dis ; 18(2): 419-27, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19625742

RESUMO

Over the past several decades, there has been extensive research devoted toward determining the cause of Alzheimer's disease. Numerous biochemical, histological, and imaging investigations have elegantly characterized the neuropathologic and functional changes associated with AD. Proponents of one theory or another can find supporting data among the myriad of studies in the literature. This paper attempts to summarize some of the major conclusions and controversies in imaging literature (especially, magnetic resonance imaging and nuclear medicine) in relation to pathogenesis theories of Alzheimer's disease. In spite of considerable progress, the primary cause of Alzheimer's disease remains elusive.


Assuntos
Doença de Alzheimer/patologia , Peptídeos beta-Amiloides/metabolismo , Encéfalo/metabolismo , Diagnóstico por Imagem , Doenças Neurodegenerativas/patologia , Proteínas tau/metabolismo , Animais , Encéfalo/patologia , Mapeamento Encefálico , Humanos
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