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Mechanisms of immunoediting and immune evasion in AML1-ETO (AE) NrasG12D AML.

ABSTRACT: Immunoediting describes the dynamic sculpting of cancer cells to evade cancer immune control, thereby enabling the development of tumors in an immunocompetent host resulting in the outgrowth of cancer cells with reduced immunogenicity.

ORGANISM(S): Mus musculus

PROVIDER: GSE164951 | GEO | 2023/02/23

REPOSITORIES: GEO

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Mechanisms of immunoediting and immune evasion in MLL-AF9 AML.

Project description:Immunoediting describes the dynamic sculpting of cancer cells to evade cancer immune control, thereby enabling the development of tumors in an immunocompetent host resulting in the outgrowth of cancer cells with reduced immunogenicity.

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Mechanisms of immunoediting and immune evasion in AML1-ETO (AE) NrasG12D AML.

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [smartseq]

Project description:Immunoediting sculpts immunogenicity and thwarts host anti-tumor responses in tumor cells during tumorigenesis; however, it remains unknown whether metabolic programming of tumor cells can be guided by immunosurveillance. Here, we report that T cell-mediated immunosurveillance in early staged tumorigenesis instructs c-Myc upregulation and metabolic reprogramming in tumor cells. This previously unexplored tumor-immune interaction is controlled by a non-canonical IFNg-STAT3 signaling and supports tumor immune evasion. Our findings uncover that immunoediting instructs deregulated bioenergetic programs in tumor cells for empowering them to disarm the T cell-mediated immunosurveillance by imposing metabolic tug-of-war between tumor and infiltrating T cells and forming the suppressive tumor microenvironment.

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Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [WGS]

Project description:Glioblastoma multiforme (GBM) is an aggressive brain tumour. Current immunotherapy approaches have been unsuccessful, highlighting the need to determine underlying mechanisms of immune evasion. Here, we developed syngeneic immunocompetent mouse models of GBM to explore this. GBM stem cells (GSCs) were serially transplanted through immunocompetent hosts, which uncovered an acquired capability to escape immune clearance through an enhanced immunosuppressive tumour microenvironment. Mechanistically, this was not elicited via genetic selection of tumour subclones, but through an epigenetic immunoediting process wherein stable transcriptional and epigenetic changes in GSCs are enforced following immune attack. These include activation of interferon signalling modules, myeloid-affiliated transcription factors and chemokines, which leads to increased recruitment of tumour-associated macrophages. Furthermore, we identify similar epigenetic and transcriptional signatures in human mesenchymal subtype GSCs. We conclude that epigenetic immunoediting may drive an acquired immune evasion program in the most aggressive mesenchymal GBM subtype by reshaping the tumour immune microenvironment.

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