Researchers investigated whether bone marrow-derived cells contribute to colitis-associated colon cancer.
By Pooja Toshniwal PahariaAug 29 2023Reviewed by Lily Ramsey, LLM In a recent study published in the Journal of Experimental Medicine, researchers investigated whether bone marrow-derived cells with heterozygous loss of Dnmt3a , the most common genetic alteration in clonal hematopoiesis , contribute to colitis-associated colon cancer pathogenesis.
Understanding the causal association between clonal hematopoiesis and aggressive tumor phenotypes is crucial for optimal therapeutic approaches and improved survival rates. To investigate the impact of Dnmt3a+/Δ within hematopoietic organs characteristic of clonal hematopoiesis on colitis-associated colon cancer development, murine animals were sacrificed for colon assessment ten weeks after initiating dextran sulfate sodium and azoxymethane treatment.
Animals diagnosed with hematopoietic diseases using flow cytometry and complete blood counts were excluded from the analysis. Transcriptome profiling of colon tumors identified signatures of increased colitis-associated colon tumor formation among mice with Dnmt3a-driven experimental clonal hematopoiesis, with an enrichment of genes related to carcinogenesis, including angiogenesis.
Axitinib treatment eliminated the colon cancer-promoting effects of Dnmt3a+/Δ bone marrow directly by decreased tumor vascular density and indirectly by normalizing aberrant Dnmt3a-CH hematopoiesis, with a decrease in circulating myeloid cells and an increase in T lymphocytes among Dnmt3a+/Δ BM chimeras.
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