ArticleeLife2024
Chromosomal instability induced in cancer can enhance macrophage-initiated immune responses that include anti-tumor IgG.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- SGO1 and SGO2 are Associated With Disease Progression and an Immunosuppressive Microenvironment in Papillary Renal Cell Carcinoma.Cancer medicine · 2026Article
- Sustained interferon exposure creates a hyper-metastatic subset of melanoma cells.bioRxiv : the preprint server for biology · 2026Article
- The chromosomal instability associated gene C2orf76 exerts dual roles in colorectal cancer through pyroptosis and chemotherapy response.Frontiers in oncology · 2026Article
- CD47 monoclonal antibodies differ in their capacity to induce immune response.European journal of microbiology & immunology · 2025Article
- Modeling and targeting general and chromosome-specific aneuploidy in cancer.Genes & development · 2025Review
- Evaluating Gene Fusions as Prognostic Biomarkers and Therapeutic Targets in Immune Checkpoint Blockade-Treated Advanced Melanoma: A Retrospective Analysis.Cancer research communications · 2025Article
- Clustered macrophages cooperate to eliminate tumors via coordinated intrudopodia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genomic instability as a driver and suppressor of anti-tumor immunity.Frontiers in immunology · 2024Review
- Chromosomal instability as an architect of the cancer stemness landscape.Frontiers in cell and developmental biology · 2024Review
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Authors and funding
11 authors.
Funding
Abstract
Solid tumors generally exhibit chromosome copy number variation, which is typically caused by chromosomal instability (CIN) in mitosis. The resulting aneuploidy can drive evolution and associates with poor prognosis in various cancer types as well as poor response to T-cell checkpoint blockade in melanoma. Macrophages and the SIRPα-CD47 checkpoint are understudied in such contexts. Here, CIN is induced in poorly immunogenic B16F10 mouse melanoma cells using spindle assembly checkpoint MPS1 inhibitors that generate persistent micronuclei and diverse aneuploidy while skewing macrophages toward a tumoricidal 'M1-like' phenotype based on markers and short-term anti-tumor studies. Mice bearing CIN-afflicted tumors with wild-type CD47 levels succumb similar to controls, but long-term survival is maximized by SIRPα blockade on adoptively transferred myeloid cells plus anti-tumor monoclonal IgG. Such cells are the initiating effector cells, and survivors make de novo anti-cancer IgG that not only promote phagocytosis of CD47-null cells but also suppress tumor growth. CIN does not affect the IgG response, but pairing CIN with maximal macrophage anti-cancer activity increases durable cures that possess a vaccination-like response against recurrence.
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