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Chromosomal instability upregulates interferon in acute myeloid leukemia
Journal article   Peer reviewed

Chromosomal instability upregulates interferon in acute myeloid leukemia

Ning Jin, Robert F. Lera, Rachel E. Yan, Fen Guo, Kim Oxendine, Vanessa L. Horner, Yang Hu, Jun Wan, Ryan J. Mattison, Beth A. Weaver, …
Genes chromosomes & cancer, Vol.59(11), pp.627-638
11/2020
DOI: 10.1002/gcc.22880
PMCID: PMC7597364
PMID: 32557940
url
https://www.ncbi.nlm.nih.gov/pmc/articles/7597364View
Open Access

Abstract

Chromosome instability (CIN) generates genetic and karyotypic diversity that is common in hematological malignancies. Low to moderate levels of CIN are well tolerated and can promote cancer proliferation. However, high levels of CIN are lethal. Thus, CIN may serve both as a prognostic factor to predict clinical outcome and as a predictive biomarker. A retrospective study was performed to evaluate CIN in acute myeloid leukemia (AML). Chromosome mis-segregation frequency was correlated with clinical outcome in bone marrow core biopsy specimens from 17 AML cases. Additionally, we induced chromosome segregation errors in AML cell lines with AZ3146, an inhibitor of the Mps1 mitotic checkpoint kinase, to quantify the phenotypic effects of high CIN. We observed a broad distribution of chromosome mis-segregation frequency in AML bone marrow core specimens. High CIN correlated with complex karyotype in AML, as expected, although there was no clear survival effect. In addition to CIN, experimentally inducing chromosome segregation errors by Mps1 inhibition in AML cell lines causes DNA damage, micronuclei formation, and upregulation of interferon stimulated genes. High levels of CIN appear to be immunostimulatory, suggesting an opportunity to combine mitotic checkpoint inhibitors with immunotherapy in treatment of AML.
Genetics & Heredity Life Sciences & Biomedicine Oncology Science & Technology

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