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FOXO1 dependent transcription network is a targetable vulnerability of Mantle Cell Lymphomas [ChIP-Seq]

ABSTRACT: ChIP-seq analysis of CCMCL1 MCL cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE182687 | GEO | 2023/05/25

REPOSITORIES: GEO

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FOXO1 dependent transcription network is a targetable vulnerability of Mantle Cell Lymphomas [RNA-Seq]

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FOXO1 dependent transcription network is a targetable vulnerability of Mantle Cell Lymphomas

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ibrutinib resistance mantle cell lymphoma [ChIP-seq]

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Project description:Successful cancer therapy is contingent on identifying cancer-specific aberrant phenotypes and their associated vulnerabilities. We recently reported that a subset of almost every cancer type contains a genome-wide defect in RNA Polymerase II-mediated transcription elongation (TEdef), which impairs the expression of long genes and confers resistance to anti-tumor immune attack. Using a combination of computational analysis and laboratory experiments, we report that tumor cells with TEdef have widespread overexpression of the components of the protein homeostasis machinery (mostly composed of short genes), including protein folding and clearance. Accordingly, TEdef cells were characterized by abnormally high levels of insoluble protein aggregates in the cytoplasm and autophagy influx. We present evidence that TEdef cells exhibit impaired clearance of misfolded protein aggregates through the ubiquitin-proteasome system, and thus rely on autophagy for their degradation. As such, while these cells were highly resistant to proteasome inhibitors, they were acutely sensitive to inhibitors of autophagy in vitro and in vivo. This study reveals a major aberrant phenotype that is observed in ∼15-25% of all cancers and characterizes a unique cellular vulnerability that can be readily exploited in the clinic to improve treatment efficacy.

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Mantle Cell Lymphoma

2013-06-25 | GSE36000 | GEO

Mantle Cell Lymphoma

Project description:Gene expression analyis of primary MCL including IGHV mutated and unmutated cases Gene set analysis was perfomed in MCL samples, comparing IGHV mutated cases vs. IGHV unmutated cases In total 38 MCL samples were processed with the HU133plus 2.0 microarray. Twenty four cases had a IGHV mutations and 14 were unmutated.

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Project description:Mantle cell lymphoma (MCL) accumulates in lymphoid organs but disseminates early on in extranodal tissues. Although proliferation remains located in lymphoid organs only, suggesting a major role of the tumor ecosystem, few studies have assessed MCL microenvironment. We therefore cocultured primary circulating MCL cells from 21 patients several weeks ex vivo with stromal or lymphoid-like (CD40L) cells to determine which interactions could support proliferation of MCL cells. We showed that coculture with lymphoid-like cells, but not stromal cells, induced cell-cycle progression, which was amplified by MCL-specific cytokines (IGF-1, BAFF, IL-6, IL-10). Of interest, we showed that our model recapitulated the MCL in situ molecular signatures i.e., proliferation, NFkB and survival signatures. We further demonstrated that proliferating MCL harbored an imbalance in Bcl-2 family expression leading to a consequent loss of mitochondrial priming. Interestingly, this loss of priming was overcome by the Type II anti-CD20 antibody obinutuzumab, which counteracted Bcl-xL induction through NFkB inhibition. Finally, we showed that the mitochondrial priming directly correlated with the sensitivity toward venetoclax and alkylating drugs. By identifying the microenvironment as the major support for proliferation and drug resistance in MCL, our results highlight a selective approach to target the lymphoma niche.

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