68 Ga-DOTATATE PET/CT targeting somatostatin receptors is commonly utilized in the imaging of neuroendocrine tumors. However, other malignancies such as lymphomas (both Hodgkin and non-Hodgkin) also have expression of somatostatin receptors, albeit to a lesser degree compared with the neuroendocrine tumors, and thus can be positive on a 68 Ga-DOTATATE PET/CT. We describe an atypical presentation of an aggressive large B-cell lymphoma mimicking a metastatic neuroendocrine tumor at initial presentation with high somatostatin receptor expression demonstrated on the 68 Ga-DOTATATE PET/CT and a rapidly progressing course on the subsequent 18 F-FDG PET/CT.
View Article and Find Full Text PDFMethods that enable monitoring of therapeutic efficacy of autologous chimeric antigen receptor (CAR) T-cell therapy will be clinically useful. The aim of this study is to demonstrate the feasibility of blood-derived cell-free DNA (cfDNA) to predict CAR T-cell therapy response in patients with refractory B-cell lymphomas. Whole blood was collected before and throughout CAR T-cell therapy until day 154.
View Article and Find Full Text PDFStandardized uptake values (SUVs) of F-fluorodeoxyglucose positron emission tomography (FDG PET) are widely used to help characterize pulmonary nodules. The purpose of this study is to assess the accuracy of the SUV corrected by blood glucose levels (SUV), compared to four other commonly used semi-quantitative methods: maximal SUV normalized to body weight (SUV), ratio of SUV of nodule to cerebellum (SUV), SUV normalized to body surface area (SUV) and SUV normalized to body mass index (SUV). 52 patients with lung nodules had FDG PET scans, consecutively imaged between 7/1/2015 and 6/7/2016.
View Article and Find Full Text PDFAn unmet need for the clinical management of chronic kidney disease is a predictive tool of kidney function during the first decade of the disease, when there is silent loss of glomerular function. The objective of this study was to demonstrate receptor-mediated binding of tilmanocept to CD206 within the kidney and provide evidence of kinetic sensitivity of this binding to renal function. Rats were positioned in a PET scanner with the liver and kidneys within the field of view.
View Article and Find Full Text PDFFluorine-19 MRI is an emerging cellular imaging approach, enabling lucid, quantitative "hot-spot" imaging with no background signal. The utility of F-MRI to detect inflammation and cell therapy products in vivo could be expanded by improving the intrinsic sensitivity of the probe by molecular design. We describe a metal chelate based on a salicylidene-tris(aminomethyl)ethane core, with solubility in perfluorocarbon (PFC) oils, and a potent accelerator of the F longitudinal relaxation time ( T).
View Article and Find Full Text PDFBackground: A single center, prospective tissue-based study was conducted to investigate an association between neutrophil extracellular traps (NETs) and venous thromboembolic disease in patients with malignancy.
Methods: Plasma was collected from 65 patients in which 27 were cancer patients and 38 were age-matched non-cancer patients. Plasma NETs, circulating free DNA (cfDNA), DNase-1, endonuclease-G, endonuclease activity and thrombin-antithrombin III (TAT) complex levels was quantified.
An expanded CUG repeat transcript (CUG(exp)) is the causative agent of myotonic dystrophy type 1 (DM1) by sequestering muscleblind-like 1 protein (MBNL1), a regulator of alternative splicing. On the basis of a ligand (1) that was previously reported to be active in an in vitro assay, we present the synthesis of a small library containing 10 dimeric ligands (4-13) that differ in length, composition, and attachment point of the linking chain. The oligoamino linkers gave a greater gain in affinity for CUG RNA and were more effective when compared to oligoether linkers.
View Article and Find Full Text PDFMyotonic dystrophy type 1 (DM1) is caused by an expanded CUG repeat (CUG(exp)) that sequesters muscleblind-like 1 protein (MBNL1), a protein that regulates alternative splicing. CUG(exp) RNA is a validated drug target for this currently untreatable disease. Herein, we develop a bioactive small molecule (1) that targets CUG(exp) RNA and is able to inhibit the CUG(exp)·MBNL1 interaction in cells that model DM1.
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