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tid Target Cancers General Effect on Target
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Type

Also called G-CSF
A cytokine that drives the generation of myeloid cell subsets including neutrophils, monocytes, macrophages, and dendritic cells in response to stress, infections, and cancers.
While too little GM-CSF prevents the appropriate production of innate immune cells and subsequent activation of adaptive anti-cancer immune responses, too much of GM-CSF can exhaust immune cells and promote cancer growth. The consequences of GM-CSF signaling in cancer progression are a function of the levels of GM-CSF, the cancer type, and the tumor microenvironment. In this review, we first discuss the secretion of GM-CSF, signaling downstream of the GM-CSF receptor, and GM-CSF’s role in modulating myeloid cell homeostasis.

GM-CSF expression is often elevated in various cancers and is generally associated with poorer prognosis due to its role in promoting an immunosuppressive tumor microenvironment and supporting tumor growth. Its ability to influence the behavior of immune cells, particularly macrophages, can contribute to tumor progression and metastasis.




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