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IMMUNE CORRELATES OF RESPONSE TO IMMUNE CHECKPOINT BLOCKADE IN ACUTE MYELOID LEUKAEMIA

ABSTRACT: Immunological classifiers that predict patient outcome and therapeutic responses have been constructed through targeted immune gene expression profiling of pre-treatment bone marrow samples from patients with acute myeloid leukaemia treated with pembrolizumab and hypomethylating agent azacytidine (clinicaltrials.gov identifier: NCT02845297).

ORGANISM(S): Homo sapiens

PROVIDER: GSE178926 | GEO | 2022/09/16

REPOSITORIES: GEO

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IMMUNE SENESCENCE PHENOTYPES PREDICT CHEMOTHERAPY RESISTANCE IN ACUTE MYELOID LEUKAEMIA

Project description:Immunological classifiers that predict patient outcome and therapeutic responses have been constructed through targeted immune gene expression profiling of diagnostic bone marrow samples from patients with acute myeloid leukaemia.

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IMMUNE LANDSCAPES PREDICT CHEMOTHERAPY RESISTANCE AND IMMUNOTHERAPY RESPONSE IN ACUTE MYELOID LEUKAEMIA

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Project description:DNA methyltransferase inhibitors have improved the prognosis of myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML). However, these agents must be administered intravenously or subcutaneously because they are degraded easily by cytidine deaminase (CDA). OR2100 (OR21), an oligonucleotide comprising decitabine nucleoside 5'-O-trisilylate, resists degradation by CDA. Direct duodenal administration led to high plasma concentrations of OR21 in a cynomolgus monkey model. Microarray analysis of MDS and AML cell lines revealed that OR21 enriched expression of genes associated with tumour suppression, cell differentiation, and immune system processes. Conversely, immune system process pathways were downregulated in azacytidine-resistant AML cells, indicating that these pathways play a pivotal role in the action of hypomethylating agents. Both in vivo and in vitro, OR21 showed anti-leukaemia effects against MDS and AML cells, and a better safety profile than decitabine. These results suggest that OR21 is a candidate drug for a phase 1 study as an alternative to DAC.

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Neoadjuvant anti-PD-1 immunotherapy promotes a survival benefit with intratumoral and systemic immune responses in recurrent glioblastoma

Project description:Glioblastoma is the most common primary malignant brain tumor in adults and associated with poor survival. Standard-of-care chemotherapy and radiation confer a median overall survival of under two years. The Ivy Foundation Early Phase Clinical Trials Consortium conducted a randomized, multi institution clinical trial to evaluate immune responses and survival following neoadjuvant and/or adjuvant therapy with pembrolizumab, a programmed cell death protein 1 (PD-1) monoclonal antibody, in 35 patients with recurrent, surgically resectable glioblastoma. Patients who were randomized to receive neoadjuvant pembrolizumab, with continued adjuvant therapy following surgery, had significantly extended overall survival compared to patients that were randomized to receive adjuvant, post-surgical PD-1 blockade alone (hazard ratio = 0.39; P = 0.04, log-rank test). Neoadjuvant PD-1 blockade was associated with upregulation of T cell and interferon-γ-related genes, but downregulation of cell cycle related genes within the tumor, which was not seen in patients that received adjuvant therapy alone. Focal induction of programmed death-ligand 1 (PD-L1) in the tumor microenvironment was observed more frequently in the neoadjuvant group than in tumors obtained from patients treated only in the adjuvant setting. Similarly, neoadjuvant pembrolizumab was associated with clonal T cell expansion and the overlap of T cell receptors between tumor and blood, decreased PD-1 expression in T cells and a decreasing peripheral monocytic population. These findings suggest that the neoadjuvant administration of PD-1 blockade enhances the local and systemic anti-tumor immune response and may represent a more efficacious approach to the treatment of this uniformly lethal brain tumor. This trial was registered with ClinicalTrials.gov under the identifier NCT02852655 (https://clinicaltrials.gov/ct2/show/NCT02852655).

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2019-11-01 | GSE124549 | GEO

Ablation of MYB-dependent leukaemia phenotype in MLL-driven AML correlates with increased expression of MAFB

Project description:The transcription factor MYB plays a pivotal role in haematopoietic homeostasis and its aberrant expression is involved in the genesis and maintenance of acute myeloid leukaemia (AML). Our previous work on CEBPA mutants has demonstrated that not all AML types display the same dependency on MYB expression, rather this depends on the nature of the driving mutations. However, whether this difference in MYB expression dependency is a general trend in AML still remains to be further elucidated. In this study, we investigate the importance of MYB in human leukaemia by performing siRNA-mediated knock-down in cell lines modelling AML driven by different genetic lesions. We show that the reduction in proliferation and the concomitant induction of myeloid commitment observed in MLL-driven leukaemia upon suppression of MYB expression is not seen in AML cells with a complex karyotype. By performing transcriptome analysis, we demonstrate that reduction of MYB in the cell line that responds to its manipulation leads to a strong activation of MAFB expression. Correlating with these observations, stratification of publicly available patient data reveals a reciprocal relationship between the expression of MYB and MAFB, highlighting a novel connection between those two factors in such AML.

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