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Aim: The aim of this study was to develop a dual-modality positron emission tomography/magnetic resonance (PET/MR) imaging probe by radiolabeling gadolinium-containing AGuIX derivatives with the positron-emitter Gallium-68 (68Ga). Materials & methods: AGuIX@NODAGA nanoparticles were labeled with 68Ga at high efficiency. Tumor accumulation in an appropriate disease model was assessed by ex vivo biodistribution and in vivo PET/MR imaging. Results: 68Ga-AGuIX@NODAGA was proven to passively accumulate in U87MG human glioblastoma tumor xenografts. Metabolite assessment in serum, urine and tumor samples showed that 68Ga-AGuIX@NODAGA remains unmetabolized up to at least 60 min postinjection. Conclusion: This study demonstrates that 68Ga-AGuIX@NODAGA can be used as a dual-modality PET/MR imaging agent with passive accumulation in the diseased area, thus showing great potential for PET/MR image-guided radiation therapy.

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The SRT provides images of higher resolution, higher contrast, and lower bias than FBP, by increasing slightly the noise in the reconstructed images. Furthermore, it eliminates streak artifacts outside the object boundary. Unlike other analytic algorithms, the reconstruction time of SRT is comparable with that of FBP. The source code for SRT will become available in a future release of STIR.

The beneficial effects of checkpoint blockade in tumor immunotherapy are limited to patients with increased tumor-infiltrating lymphocytes (TILs). Delineation of the regulatory networks that orchestrate the presence of TILs holds great promise for the design of effective immunotherapies. Podoplanin/gp38 (PDPN)-expressing lymph node stromal cells (LNSCs) are present in tumor stroma; however, their effect in the regulation of TILs remains elusive. Herein we demonstrate that intratumor injection of ex-vivo-isolated PDPN LNSCs into melanoma-bearing mice induces elimination of TILs and promotes tumor growth. In support, PDPN LNSCs exert their function through direct inhibition of CD4 T cell proliferation in a cell-to-cell contact independent fashion. Mechanistically, we demonstrate that PDPN LNSCs mediate T cell growth arrest and induction of apoptosis to activated CD69CD4 T cells. Importantly, LTbR-Ig-mediated blockade of PDPN LNSCs expansion and function significantly attenuates melanoma tumor growth and enhances the infiltration and proliferation of CD4 TILs. Overall, our findings decipher a novel role of PDPN-expressing LNSCs in the elimination of CD4 TILs and propose a new target for tumor immunotherapy.

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Lung cancer is the leading cause of cancer-related deaths worldwide, and elucidation of its complicated pathobiology has been traditionally targeted by studies incorporating genomic as well other high-throughput approaches. Recently, a collection of methods used for cancer imaging, supplemented by quantitative aspects leading towards imaging biomarker assessment termed “radiomics”, has introduced a novel dimension in cancer research. Integration of genomics and radiomics approaches, where identifying the biological basis of imaging phenotypes is feasible due to the establishment of associations between molecular features at the genomic–transcriptomic–proteomic level and radiological features, has recently emerged termed radiogenomics. This review article aims to briefly describe the main aspects of radiogenomics, while discussing its basic limitations related to lung cancer clinical applications for clinicians, researchers and patients.

A high regularization level at 52 iteration updates and 30 min acquisition time were found to optimize most of the figures of merit investigated.