AI Article Synopsis
- Aging increases the risk of cancer by affecting how the immune system works, especially in lung tumors.
- Older immune cells lead to the buildup of certain cells that produce IL-1⍺, which makes cancer grow faster.
- By blocking IL-1R1 signaling early on, scientists found they could slow down cancer growth in the lungs, colon, and pancreas, and learned how aging is linked to worse cancer outcomes in humans.
Article Abstract
Age is a major risk factor for cancer, but how aging impacts tumor control remains unclear. In this study, we establish that aging of the immune system, regardless of the age of the stroma and tumor, drives lung cancer progression. Hematopoietic aging enhances emergency myelopoiesis, resulting in the local accumulation of myeloid progenitor-like cells in lung tumors. These cells are a major source of interleukin (IL)-1⍺, which drives the enhanced myeloid response. The age-associated decline of DNA methyltransferase 3A enhances IL-1⍺ production, and disrupting IL-1 receptor 1 signaling early during tumor development normalized myelopoiesis and slowed the growth of lung, colonic, and pancreatic tumors. In human tumors, we identified an enrichment for IL-1⍺-expressing monocyte-derived macrophages linked to age, poorer survival, and recurrence, unraveling how aging promotes cancer and offering actionable therapeutic strategies.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7616710 | PMC |
| http://dx.doi.org/10.1126/science.adn0327 | DOI Listing |
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