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Jeffery, J. J.

Publications and source records attributed to Jeffery, J. J..

3 recordsLinked to original sources

Characterization and Calibration of the iQID Digital Autoradiography System for Direct Quantitative Imaging of Beta-Emitters in Tissue Samples

Autoradiography provides microscale mapping of radionuclide distributions, a promising approach to complement nuclear medicine imaging for small-scale radiopharmaceutical therapy (RPT) research. However, quantitative protocols for {beta}-emitters remain under-established compared to those for -emitters. In this work, the ionizing-radiation quantum imaging detector (iQID) digital autoradiography system was characterized and calibrated specifically for the theranostic {beta}-emitter 177Lu. Spatial resolution, detection efficiency, background and minimum detectable activity, and depth dependence were characterized and compared to Geant4 Monte Carlo simulations. A methodology for converting count rates to activity was established, yielding a high linear response (range from 0 to 300 Bq). To validate the system for realistic measurement scenarios, cross-modality benchmarking was performed using a custom stacked multi-layer virtual water phantom to compare iQID performance with preclinical {micro}SPECT/CT. The iQID system demonstrated an effective spatial resolution of [~]43 {micro}m for 177Lu and achieved total activity estimates of (0.194 {+/-} 0.022) MBq, agreeing within 2% with the dispensed reference (0.197 {+/-} 0.015) MBq. Crucially, iQID exhibited superior quantitative accuracy for small-scale features (0.8 mm to 2.5 mm diameters), resolving activity concentrations in regions where {micro}SPECT/CT performance was severely limited by partial volume effects. This study establishes a validated framework for quantitative 177Lu digital autoradiography, laying the groundwork for accurate activity estimation in ex vivo tissue samples.

cancer biology↗

Targeting both GD2 and B7-H3 using bispecific antibody improves tumor selectivity for GD2-positive tumors

ObjectivesDisialoganglioside 2 (GD2), overexpressed by cancers such as melanoma and neuroblastoma, is a tumor antigen for targeted therapy. The delivery of conventional IgG antibody technologies targeting GD2 is limited clinically by its co-expression on nerves that contributes to toxicity presenting as severe neuropathic pain. To improve the tumor selectivity of current GD2-targeting approaches, a next-generation bispecific antibody targeting GD2 and B7-H3 (CD276) was generated. MethodsDifferential expression of human B7-H3 (hB7-H3) was transduced into GD2+ B78 murine melanoma cells and confirmed by flow cytometry. We assessed the avidity and selectivity of our GD2-B7-H3 targeting bispecific antibodies (INV34-6, INV33-2, and INV36-6) towards GD2+/hB7-H3- B78 cells relative to GD2+/hB7-H3+ B78 cells using flow cytometry and competition binding assays, comparing results an anti-GD2 antibody (dinutuximab, DINU). The bispecific antibodies, DINU, and a non-targeted bispecific control (bsAb CTRL) were conjugated with deferoxamine for radiolabeling with Zr-89 (t1/2 = 78.4 h). Using positron emission tomography (PET) studies, we evaluated the in vivo avidity and selectivity of the GD2-B7-H3 targeting bispecific compared to bsAb CTRL and DINU using GD2+/hB7-H3+ and GD2+/hB7-H3- B78 tumor models. ResultsFlow cytometry and competition binding assays showed that INV34-6 bound with high avidity to GD2+/hB7-H3+ B78 cells with high avidity but not GD2+/hB7-H3+ B78 cells. In comparison, no selectivity between cell types was observed for DINU. PET in mice bearing the GD2+/hB7-H3- and GD2+/hB7-H3+ B78 murine tumor showed similar biodistribution in normal tissues for [89Zr]Zr-Df-INV34-6, [89Zr]Zr-Df-bsAb CTRL, and [89Zr]Zr-Df-DINU. Importantly, [89Zr]Zr-Df-INV34-6 tumor uptake was selective to GD2+/hB7-H3+ B78 over GD2+/hB7-H3- B78 tumors, and substantially higher to GD2+/hB7-H3+ B78 than the non-targeted [89Zr]Zr-Df-bsAb CTRL control. [89Zr]Zr-Df-DINU displayed similar uptake in both GD2+ tumor models, with uptake comparable to [89Zr]Zr-Df-INV34-6 in the GD2+/hB7-H3+ B78 model. ConclusionThe GD2-B7-H3 targeting bispecific antibodies successfully improved selectivity to cells expressing both antigens. This approach should address the severe toxicities associated with GD2-targeting therapies by reducing off-tumor GD2 binding in nerves. Continued improvements in bispecific antibody technologies will continue to transform the therapeutic biologics landscape. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/595624v2_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@11afee9org.highwire.dtl.DTLVardef@1558607org.highwire.dtl.DTLVardef@1d23d6eorg.highwire.dtl.DTLVardef@1bf1d63_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

Profound immunomodulatory effects of 225Ac-NM600 drive enhanced anti-tumor responsein prostate cancer

An immunosuppressive tumor microenvironment has hampered the efficacy of immunotherapy in prostate cancer. However, radiation-induced immunological effects can partly mediate anti-tumor effects by promoting a pro-inflammatory environment potentially responsive to immunotherapy. Herein, we examined the immunomodulatory properties of a radiopharmaceutical therapy (RPT) with NM600 radiolabeled with either a beta or alpha emitter in two prostate cancer models. 225Ac-NM600, but not 177Lu-NM600, promoted significant anti-tumor effects and improved overall survival. Immunomodulatory effects were dose, radionuclide, and tumor type-dependent. 225Ac-NM600 elicited an array of immunomodulatory effects such as increased CD8/Treg ratio, activation of effector and memory T cells, abrogation of infiltrating suppressor cells (e.g., Tregs and MDSCs), and increased levels of Th1 cytokine and pro-inflammatory chemokines. Importantly, we demonstrate the need to carefully characterize the immune responses elicited by RPT both pre-clinically and clinically to maximize tumor control and avoid potential counterproductive immunosuppressive effects. TeaserTargeted alpha therapy can create a pro-inflammatory tumor micro-environment that partly explains stronger anti-tumor responses in prostate cancer

immunology↗