Alfredo Quiñones‐Hinojosa

This study identifies therapeutic options, biomarkers, and resistance mechanisms for high-grade gliomas using genomic, transcriptomic profiling, and drug testing in patient-derived models.

This study identifies cholesterol dependency as a therapeutic target in glioblastoma, showing that combined treatment with clemastine and bexarotene induces metabolic collapse and enhances antitumor immunity.

This study identifies ATAT1 as a therapeutic target in glioblastoma by showing its role in promoting tumor invasion, proliferation, and resistance, with potential for combination therapies.

This study identifies YAP's role in controlling cell migration and invasion via a Rho-GTPase switch, with implications for glioblastoma progression.

This paper develops a 3D GBM model with pericytes to study TMZ resistance, finding that pericytes increase TMZ resistance in GBM spheroids by upregulating CCL5.

This study develops a PD-L1-targeting CAR T cell therapy, MC9999, which effectively eradicates glioblastoma and immunosuppressive cells in the tumor microenvironment through intracranial delivery.

This paper develops a PD-L1-targeting CAR T-cell therapy (MC9999) that effectively attacks both tumor and immunosuppressive cells in solid tumors.

This paper develops a mathematical model of GBM tumor growth and evaluates BMP4 as a differentiation therapy through virtual clinical trials, finding that continuous BMP4 delivery during radiotherapy is more effective than a single dose.

The paper profiles the SHANK3 transcriptome using cDNA-capture and long-read sequencing, revealing complex transcript variants altered in Shank3 mutants and ASD brains, improving variant detection in neuropsychiatric disorders.

The paper characterizes GSC-derived GBM organoids, revealing an immune-like molecular program and identifying SATB2+ and HOPX+ progenitor populations that contribute to GBM progression.

The paper shows that higher TREM2 expression in gliomas correlates with poor prognosis, but TREM2 deficiency does not improve outcomes in pre-clinical models, as it impairs myeloid cell phagocytosis and MHCII-dependent CD4+ T cell responses.

The paper characterizes human microglia transcriptomes and identifies gene expression signatures linked to age, sex, and APOE-ε4, revealing immunometabolic pathway perturbations in neurodegeneration.