TY - JOUR
T1 - Understanding the Complexity of the Tumor Microenvironment in K-ras Mutant Lung Cancer
T2 - Finding an Alternative Path to Prevention and Treatment
AU - Deng, Shanshan
AU - Clowers, Michael J.
AU - Velasco, Walter V.
AU - Ramos-Castaneda, Marco
AU - Moghaddam, Seyed Javad
N1 - Publisher Copyright:
© Copyright © 2020 Deng, Clowers, Velasco, Ramos-Castaneda and Moghaddam.
PY - 2020/1/22
Y1 - 2020/1/22
N2 - Kirsten rat sarcoma viral oncogene (K-ras) is a well-documented, frequently mutated gene in lung cancer. Since K-ras regulates numerous signaling pathways related to cell survival and proliferation, mutations in this gene are powerful drivers of tumorigenesis and confer prodigious survival advantages to developing tumors. These malignant cells dramatically alter their local tissue environment and in the process recruit a powerful ally: inflammation. Inflammation in the context of the tumor microenvironment can be described as either antitumor or protumor (i.e., aiding or restricting tumor progression, respectively). Many current treatments, like immune checkpoint blockade, seek to augment antitumor inflammation by alleviating inhibitory signaling in cytotoxic T cells; however, a burgeoning area of research is now focusing on ways to modulate and mitigate protumor inflammation. Here, we summarize the interplay of tumor-promoting inflammation and K-ras mutant lung cancer pathogenesis by exploring the cytokines, signaling pathways, and immune cells that mediate this process.
AB - Kirsten rat sarcoma viral oncogene (K-ras) is a well-documented, frequently mutated gene in lung cancer. Since K-ras regulates numerous signaling pathways related to cell survival and proliferation, mutations in this gene are powerful drivers of tumorigenesis and confer prodigious survival advantages to developing tumors. These malignant cells dramatically alter their local tissue environment and in the process recruit a powerful ally: inflammation. Inflammation in the context of the tumor microenvironment can be described as either antitumor or protumor (i.e., aiding or restricting tumor progression, respectively). Many current treatments, like immune checkpoint blockade, seek to augment antitumor inflammation by alleviating inhibitory signaling in cytotoxic T cells; however, a burgeoning area of research is now focusing on ways to modulate and mitigate protumor inflammation. Here, we summarize the interplay of tumor-promoting inflammation and K-ras mutant lung cancer pathogenesis by exploring the cytokines, signaling pathways, and immune cells that mediate this process.
KW - K-ras
KW - cytokine
KW - inflammation
KW - lung cancer
KW - tumor microenvironment
UR - http://www.scopus.com/inward/record.url?scp=85079034421&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85079034421&partnerID=8YFLogxK
U2 - 10.3389/fonc.2019.01556
DO - 10.3389/fonc.2019.01556
M3 - Review article
C2 - 32039025
AN - SCOPUS:85079034421
SN - 2234-943X
VL - 9
JO - Frontiers in Oncology
JF - Frontiers in Oncology
M1 - 1556
ER -