Published online Aug 21, 2019. doi: 10.3748/wjg.v25.i31.4383
Peer-review started: April 25, 2019
First decision: May 24, 2019
Revised: June 7, 2019
Accepted: July 19, 2019
Article in press: July 19, 2019
Published online: August 21, 2019
Processing time: 118 Days and 21.4 Hours
Systemic inflammation is a marker of poor prognosis preoperatively present in around 20%-40% of colorectal cancer patients. The hallmarks of systemic inflammation include an increased production of proinflammatory cytokines and acute phase proteins that enter the circulation. While the low-level systemic inflammation is often clinically silent, its consequences are many and may ultimately lead to chronic cancer-associated wasting, cachexia. In this review, we discuss the pathogenesis of cancer-related systemic inflammation, explore the role of systemic inflammation in promoting cancer growth, escaping antitumor defense, and shifting metabolic pathways, and how these changes are related to less favorable outcome.
Core tip: Increasing evidence indicates that systemic inflammation has wide-ranging effects on colorectal cancer (CRC) pathogenesis, spanning from supporting primary tumor growth by promoting tumor cell proliferation to helping angiogenesis by enhancing the availability of pro-angiogenic molecules, to suppressing anti-tumor immunity by recruiting anti-inflammatory cell types, and to shaping pre-metastatic niches to promote subsequent metastasis. Systemic inflammatory biomarkers, such as circulating acute phase proteins, cytokines, exosomes, and leukocytes, may help to classify CRC patients into useful prognostic categories. However, further larger-scale studies are needed to determine optimal marker combinations for selecting patients to receive specific treatments.