Kinase Signaling in Colitis-Associated Colon Cancer and Inflammatory Bowel Disease

Author:

Temby Michelle1,Boye Theresa L.2,Hoang Jacqueline1,Nielsen Ole H.2ORCID,Gubatan John1ORCID

Affiliation:

1. Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94305-5101, USA

2. Department of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, 2730 Herlev, Denmark

Abstract

Colorectal cancer is a known complication of chronic inflammation of the colon (“colitis-associated colon cancer”). Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Patients with IBD are at increased risk of colon cancer compared to the general population. Kinase signaling pathways play critical roles in both the inflammation and regulating cellular processes such as proliferation and survival that contribute to cancer development. Here we review the interplay of kinase signaling pathways (mitogen-activated protein kinases, cyclin-dependent kinases, autophagy-activated kinases, JAK-STAT, and other kinases) and their effects on colitis-associated colon cancer. We also discuss the role of JAK-STAT signaling in the pathogenesis of IBD and the therapeutic landscape of JAK inhibitors for the treatment of IBD.

Funder

Chan Zuckerberg Biohub Physician Scientist Scholar Award, NIH NIDDK LRP Award

Doris Duke Physician Scientist Fellowship Award

Stanford MCHRI Pediatric IBD and Celiac Disease Research Award

Publisher

MDPI AG

Subject

Molecular Biology,Biochemistry

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