Michel Mittelbronn

Circulating immune profiling reveals impaired monocyte states and trajectories driving immunosuppression in glioblastoma

Advancing CNS tumor diagnostics with expanded DNA methylation-based classification

AMP-activated protein kinase mediates adaptation of glioblastoma cells to conditions of the tumor microenvironment

Fusobacterium nucleatum interacts with cancer-associated fibroblasts to promote colorectal cancer.

Advancing CNS tumor diagnostics with expanded DNA methylation-based classification

AMP-activated protein kinase mediates adaptation of glioblastoma cells to conditions of the tumor microenvironment.

Park7 deletion leads to sex-specific transcriptome changes involving NRF2-CYP1B1 axis in mouse midbrain astrocytes.

Microglia aggregates define distinct immune and neurodegenerative niches in Alzheimer's disease hippocampus.

Advancing sarcoma diagnostics with expanded DNA methylation-based classification

Integrative multi-omics combined with functional pharmacological profiling in patient-derived organoids identifies personalized therapeutic vulnerabilities of adult high-grade gliomas

Modulation of the ACOD1/itaconate pathway differentially affects atherosclerosis severity across genetic models and sexes.

GPC5 expression highlights astrocytic heterogeneity and divergent hippocampal responses in Alzheimer’s and Parkinson’s Dementia

Transcriptional Dysregulation in the Hippocampus of a murine model for Parkinson’s Disease Cognition Impairment is Driven by Sex, Age, and Alpha-synuclein overexpression

ARHGAP12 and ARHGAP29 exert distinct regulatory effects on switching between two cell morphological states through GSK-3 activity.

Author Correction: Propagative α-synuclein seeds as serum biomarkers for synucleinopathies.

Supplementary Table S3 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 4 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Supplementary Table S1 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Supplementary Table S4 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 1 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 7 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Supplementary Table S2 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Supplementary Methods and Figures from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 3 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 2 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 5 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Figure 6 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses

Glioblastoma-instructed microglia transition to heterogeneous phenotypic states with phagocytic and dendritic cell-like features in patient tumors and patient-derived orthotopic xenografts

A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation

A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation.