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Conditioning of LCs in situ by the epidermal microenvironment is likely to be more important.
The cytokine microenvironment is likely to reduce the surface RANKL on KO immune cells.
The cellular crosstalk in the tumor microenvironment is likely to play a role in promoting lymphangiogenesis and thus lymphatic metastasis.
Thus, recruitment of MSCs to cancer microenvironment is likely mediated by the interaction of cytokines/chemokines and their specific receptors.
Our work suggests that targeting the stromal microenvironment is likely to be an important strategy for future anti-inflammatory therapies.
However, targeting the crosstalk between cancer cells and components of the microenvironment is likely to provide much more profound clinical benefits.
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A significant alteration of chemokine signaling within the tumor microenvironment was likely to result in BMDC recruitment.
Additional factors within the tumor microenvironment are likely to be involved in the transcriptional regulation of autophagy genes.
Therefore, a number of factors including the microenvironment are likely to determine whether CD26 enhances or diminishes invasion.
Specific aspects of both breast cancer cells and the bone microenvironment are likely important contributors to the development of bone metastasis [ 5, 6].
Besides the specific stromal cell types, other factors from within the tumour microenvironment are likely to play significant roles in promoting cancer stemness and malignant behaviour through β-catenin nuclear accumulation and signalling.
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