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Biology subjects

Baus, V.

Publications and source records attributed to Baus, V..

3 recordsLinked to original sources

Humanized glioblastoma patient-derived orthotopic xenografts recreate a locally immunosuppressed human immune ecosystem amenable to immunotherapeutic modulation

Immune-based strategies have so far failed to demonstrate clinical benefit in glioblastoma (GBM), largely due to the profound immunosuppressive tumor microenvironment (TME). To achieve more predictive preclinical insights, advanced in vivo models that faithfully recapitulate the human brain immune landscape are urgently needed. Here, we established GBM patient-derived orthotopic xenografts (PDOXs) across diverse mouse strains, including humanized models. Humanization was achieved through transplantation of CD34+ hematopoietic stem cells (HU-CD34+) or peripheral blood mononuclear cells (HU-PBMC). Both models successfully reconstituted human T-cells systemically, with stronger engraftment in HU-CD34+ mice. We observed selective infiltration and spatial organization to intracranial GBM tumors, including exhausted, memory-like, and regulatory CD4+ T-cell phenotypes, TIM-3+ immunosuppressive-like myeloid cells and intratumoral B cells. Mouse microglia-derived tumor-associated macrophages (TAMs) remained the dominant immunosuppressive immune population. Anti-PD-1 therapy, but not anti-GITR, modestly modulated the infiltration dynamics, demonstrating the susceptibility of the reconstructed adaptive immunity to immunotherapeutic intervention. These findings position humanized GBM PDOXs as a relevant preclinical platform to interrogate tumor-immune interactions and evaluate immunotherapeutic strategies in a human context. Key pointsO_LIGBM PDOXs developed in HU-CD34+ and HU-PBMC mice faithfully reconstitute systemic and local human adaptive immunity. C_LIO_LIHuman immune components undergo selective infiltration, spatial organization and transition towards exhausted CD4+ T-cells and immunosuppressive CD11c+ myeloid cells. C_LIO_LIAnti-PD-1, but not anti-GITR, locally promote human immune infiltration into intracranial GBM tumors, while sparing systemic compartments. C_LIO_LIHumanized GBM PDOXs provide a powerful preclinical platform to test novel immunotherapeutic strategies. C_LI Study importanceImmune checkpoint blockade has shown limited efficacy in GBM, reflecting the highly immunosuppressive and lymphocyte-poor nature of the TME. Conventional syngeneic and GEMM models fail to recapitulate these features, contributing to the translational disconnect between preclinical success and clinical failure. Humanized mice provide a solution to interrogate human-specific immunity in vivo, but their use in GBM has remained limited. Here, we provide the first comparison of GBM PDOX modeling in two complementary modes of humanization based on CD34+ HSCs and PBMCs. We systematically profile systemic and intratumoral compartments, showing that these models faithfully reconstitute human adaptive immunity and capture the interplay with the murine brain TME. Furthermore, we demonstrate clinically-relevant responses upon treatment with checkpoint antibodies targeting PD-1 and GITR, showing modulation of human immune subsets without altering murine TAM immunosuppression, underscoring the translational value of the system. This study establishes humanized GBM PDOXs as a versatile platform for dissecting tumor-immune interactions in the brain and for preclinical evaluation and development of novel immunotherapies. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/689484v2_ufig1.gif" ALT="Figure 1"> View larger version (74K): org.highwire.dtl.DTLVardef@1b684e1org.highwire.dtl.DTLVardef@1cdfbbdorg.highwire.dtl.DTLVardef@4a570borg.highwire.dtl.DTLVardef@98b112_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Adenoviral Delivery of the CIITA Transgene Induces T-Cell-Mediated Killing in Glioblastoma Organoids

The immunosuppressive nature of the tumor microenvironment poses a significant challenge to effective immunotherapies against glioblastoma (GB). Boosting the immune response is critical for a successful therapy. Here, we adopted a cancer gene therapy approach to induce T-cell mediated killing of the tumor through increased activation of the immune system. Patient-based 3D GB models were infected with a replication-deficient adenovirus (AdV) armed with the Class II Major Histocompatibility Complex (MHC-II) Transactivator CIITA gene (Ad-CIITA). Successful induction of surface MHC-II was achieved in infected GB cell lines and primary human GB organoids. Infection with an AdV carrying a mutant form of CIITA with a single amino acid substitution resulted in cytoplasmic accumulation of CIITA without subsequent MHC-II expression. Co-culture of infected tumor cells with either PBMCs or isolated T-cells led to dramatic breakdown of GB organoids. Intriguingly, both wild-type and mutant Ad-CIITA but not unarmed AdV, triggered immune-mediated tumor cell death in the co-culture system, suggesting an at least partially MHC-II-independent process. We further show that the observed cancer cell killing requires the presence of either CD8+ or CD4+ T-cells and the direct contact between GB and immune cells. We did not however detect evidence of activation of canonical T-cell mediated cell death pathways. While the precise mechanism remains to be determined, these findings highlight the potential of AdV-mediated CIITA delivery to enhance T-cell-mediated immunity against GB.

cancer biology↗

Primary and recurrent glioma patient-derived orthotopic xenografts (PDOX) represent relevant patient avatars for precision medicine

Patient-derived cancer models are essential tools for studying tumor biology and preclinical interventions. Here, we show that glioma patient-derived orthotopic xenografts (PDOXs) enable long-term propagation of patient tumors and represent clinically relevant patient avatars. We created a large collection of PDOXs from primary and recurrent gliomas with and without mutations in IDH1, which retained histopathological, genetic, epigenetic and transcriptomic features of patient tumors with no mouse-specific clonal evolution. Longitudinal PDOX models recapitulate the limited genetic evolution of gliomas observed in patient tumors following treatment. PDOX-derived standardized tumor organoid cultures enabled assessment of drug responses, which were validated in mice. PDOXs showed clinically relevant responses to Temozolomide and to targeted treatments such as EGFR and CDK4/6 inhibitors in (epi)genetically defined groups, according to MGMT promoter and EGFR/CDK status respectively. Dianhydrogalactitol, a bifunctional alkylating agent, showed promising potential against glioblastoma. Our study underlines the clinical relevance of glioma PDOX models for translational research and personalized treatment studies.

cancer biology↗