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Background: Publicly available data are essential for the progress of medical image analysis, in particular for crafting machine learning models. Glioma is the most common group of primary brain tumors, and magnetic resonance imaging (MRI) is a widely used modality in their diagnosis and treatment. However, the availability and quality of public datasets for glioma MRI are not well known., Methods: In this review, we searched for public datasets of glioma MRI using Google Dataset Search, The Cancer Imaging Archive, and Synapse., Results: A total of 28 datasets published between 2005 and May 2024 were found, containing 62 019 images from 5515 patients. We analyzed the characteristics of these datasets, such as the origin, size, format, annotation, and accessibility. Additionally, we examined the distribution of tumor types, grades, and stages among the datasets. The implications of the evolution of the World Health Organization (WHO) classification on tumors of the brain are discussed, in particular the 2021 update that significantly changed the definition of glioblastoma., Conclusions: Potential research questions that could be explored using these datasets were highlighted, such as tumor evolution through malignant transformation, MRI normalization, and tumor segmentation. Interestingly, only 2 datasets among the 28 studied reflect the current WHO classification. This review provides a comprehensive overview of the publicly available datasets for glioma MRI currently at our disposal, providing aid to medical image analysis researchers in their decision-making on efficient dataset choice., Competing Interests: All research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© The Author(s) 2025. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.)

Humanized mice, defined as mice with human immune systems, have become an emerging model to study human hematopoiesis, infectious disease, and cancer. Here, we describe the techniques to generate humanized NSGF6 mice using adult human CD34 + hematopoietic stem and progenitor cells (HSPCs). We describe steps for constructing and monitoring the engraftment of humanized mice. We then detail procedures for tissue processing and immunophenotyping by flow cytometry to evaluate the multilineage hematopoietic differentiation. For complete details on the use and execution of this protocol, please refer to Yu et al. 1 ., Competing Interests: Declaration of interests C.I.Y., R.M., J.B., and K.P. filed a patent on novel humanized mouse models via genetic editing of NSG mouse. K.P. is a stockholder in Cue Biopharma and Guardian Bio, scientific advisor to Cue Biopharma and Guardian Bio, and co-founder of Guardian Bio. K.P. declares unrelated funding support from Guardian Bio (current) and Merck (past). J.B. is associated with Immunai., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Pre-clinical use of humanized mice transplanted with CD34 + hematopoietic stem and progenitor cells (HSPCs) is limited by insufficient engraftment with adult non-mobilized HSPCs. Here, we developed a novel immunodeficient mice based on NOD-SCID- Il2γc -/- (NSG) mice to support long-term engraftment with human adult HSPCs. As both Flt3L and IL-6 are critical for many aspects of hematopoiesis, we knock-out mouse Flt3 and knock-in human IL6 gene. The resulting mice showed an increase in the availability of mouse Flt3L to human cells and a dose-dependent production of human IL-6 upon activation. Upon transplantation with low number of human HSPCs from adult bone marrow, these humanized mice demonstrated a significantly higher engraftment with multilineage differentiation of human lymphoid and myeloid cells, and tissue colonization at one year after adult HSPC transplant. Thus, these mice enable studies of human hematopoiesis and tissue colonization over time and may facilitate building autologous models for immuno-oncology studies., Competing Interests: C.Y., R.M., J.B., and K.P filed a patent on novel humanized mouse models via genetic editing of NSG mouse. K.P. is a stockholder in Cue Biopharma and Guardian Bio, scientific advisor to Cue Biopharma and Guardian Bio and co-founder of Guardian Bio. K.P. declares unrelated funding support from Guardian Bio (current) and MERCK (past). J.B. is associated with Immunai., (© 2024 The Author(s).)

In an effort to improve HLA-"humanized" mouse models for type 1 diabetes (T1D) therapy development, we previously generated directly in the NOD strain CRISPR/Cas9-mediated deletions of various combinations of murine MHC genes. These new models improved upon previously available platforms by retaining β2-microglobulin functionality in FcRn and nonclassical MHC class I formation. As proof of concept, we generated H2-Db/H2-Kd double knockout NOD mice expressing human HLA-A*0201 or HLA-B*3906 class I variants that both supported autoreactive diabetogenic CD8+ T cell responses. In this follow-up work, we now describe the creation of 10 new NOD-based mouse models expressing various combinations of HLA genes with and without chimeric transgenic human TCRs reactive to proinsulin/insulin. The new TCR-transgenic models develop differing levels of insulitis mediated by HLA-DQ8-restricted insulin-reactive T cells. Additionally, these transgenic T cells can transfer insulitis to newly developed NSG mice lacking classical murine MHC molecules, but expressing HLA-DQ8. These new models can be used to test potential therapeutics for a possible capacity to reduce islet infiltration or change the phenotype of T cells expressing type 1 diabetes patient-derived β cell autoantigen-specific TCRs., (Copyright © 2023 by The American Association of Immunologists, Inc.)

Pre-clinical use of humanized mice transplanted with CD34 + hematopoietic progenitor cells (HPCs) is limited by insufficient engraftment with adult HPCs. Here, we developed a novel immunodeficient mice based in NOD-SCID- Il2γc -/- (NSG) mice to support long-term engraftment with human adult HPCs and tissue colonization with human myeloid cells. As both Flt3L and IL-6 are critical for many aspects of hematopoiesis, we knock-out mouse Flt3 and knock-in human IL6 gene. The resulting mice showed an increase in the availability of mouse Flt3L to human cells, and a dose-dependent production of human IL-6 upon activation. Upon transplantation with low number of human HPCs from adult bone marrow, these humanized mice demonstrated a significantly higher engraftment with multilineage differentiation of human lymphoid and myeloid cells. Furthermore, higher frequencies of human lymphoid and myeloid cells were detected in tissues at one year after adult HPC transplant. Thus, these mice enable studies of human hematopoiesis and tissue colonization over time., Summary: Pre-clinical use of humanized mice is limited by insufficient engraftment with adult hematopoietic progenitor cells (HPCs). Here, we developed a novel immunodeficient mice which support long-term engraftment with adult bone marrow HPCs and facilitate building autologous models for immuno-oncology studies.

Metastasis of melanoma significantly worsens prognosis; thus, therapeutic interventions that prevent metastasis could improve patient outcomes. Here, we show using humanized mice that colonization of distant visceral organs with melanoma is dependent upon a human CD33+CD11b+CD117+ progenitor cell subset comprising <4% of the human CD45+ leukocytes. Metastatic tumor-infiltrating CD33+ cells from patients and humanized (h)NSG-SGM3 mice showed converging transcriptional profiles. Single-cell RNA-seq analysis identified a gene signature of a KIT/CD117-expressing CD33+ subset that correlated with decreased overall survival in a TCGA melanoma cohort. Thus, human CD33+CD11b+CD117+ myeloid cells represent a novel candidate biomarker as well as a therapeutic target for metastatic melanoma., Competing Interests: Disclosures:   C.I. Yu reported a patent to humanized mouse model for cancer metastasis pending. P. Metang reported “other” from University of Texas Southwestern Medical Center outside the submitted work. J. Banchereau reported grants from Merck during the conduct of the study; grants from Sanofi, personal fees from Cue Biopharma, personal fees from Neovacs, personal fees from Ascend Pharma, and personal fees from Georgiamune outside the submitted work; in addition, J. Banchereau had a patent to humanized mouse model for cancer metastasis pending. K. Palucka reported grants from Merck, “other” from Merck, personal fees from Cue Biopharma, and personal fees from Sobi outside the submitted work; in addition, K. Palucka had a patent on humanized mice to study metastasis pending. No other disclosures were reported., (© 2021 Yu et al.)