Portal:CPTAC/Hallmark/Inflammation

From WikiPathways

(Difference between revisions)
Jump to: navigation, search
Current revision (23:33, 4 December 2018) (view source)
(Added descriptive summary)
 
(One intermediate revision not shown.)
Line 1: Line 1:
 +
Inflammation can contribute to multiple hallmarks by supplying bioactive molecules to the tumor microenvironment, including growth factors that sustain proliferative signaling, survival factors that limit cell death, proangiogenic factors, extracellular matrix-modifying enzymes that facilitate angiogenesis, invasion, and metastasis, and inductive signals that lead to activation of EMT and other hallmark-facilitating programs. Also, inflammatory cells can release chemicals, for example reactive oxygen species, that are actively mutagenic for nearby cancer cells, accelerating their genetic evolution toward states of heightened malignancy. (Adapted from [https://www.ncbi.nlm.nih.gov/pubmed/21376230 Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011])
*[[Pathway:WP530]] Cytokines and Inflammatory Response
*[[Pathway:WP530]] Cytokines and Inflammatory Response
*[[Pathway:WP3929]] Chemokine signaling pathway
*[[Pathway:WP3929]] Chemokine signaling pathway
 +
*[[Pathway:WP364]] IL-6 signaling pathway
 +
*[[Pathway:WP195]] IL-1 signaling pathway

Current revision

Inflammation can contribute to multiple hallmarks by supplying bioactive molecules to the tumor microenvironment, including growth factors that sustain proliferative signaling, survival factors that limit cell death, proangiogenic factors, extracellular matrix-modifying enzymes that facilitate angiogenesis, invasion, and metastasis, and inductive signals that lead to activation of EMT and other hallmark-facilitating programs. Also, inflammatory cells can release chemicals, for example reactive oxygen species, that are actively mutagenic for nearby cancer cells, accelerating their genetic evolution toward states of heightened malignancy. (Adapted from Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011)