Asset Details
Do you wish to reserve the book?
Carbonic anhydrase 9 (CA9) expression in non-small-cell lung cancer: correlation with regulatory FOXP3+T-cell tumour stroma infiltration
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Carbonic anhydrase 9 (CA9) expression in non-small-cell lung cancer: correlation with regulatory FOXP3+T-cell tumour stroma infiltration
Do you wish to request the book?
Carbonic anhydrase 9 (CA9) expression in non-small-cell lung cancer: correlation with regulatory FOXP3+T-cell tumour stroma infiltration
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Carbonic anhydrase 9 (CA9) expression in non-small-cell lung cancer: correlation with regulatory FOXP3+T-cell tumour stroma infiltration
2020
Overview
Background
Low pH suppresses the proliferation and cytotoxic activity of CD8+ cytotoxic and natural killer lymphocytes. The hypoxia-regulated transmembrane protein, carbonic anhydrase CA9, converts carbon dioxide produced by the Krebs cycle to bicarbonate and protons that acidify the extracellular milieu. We examined whether CA9 is also involved in intratumoural immunosuppression pathways.
Methods
A series of 98 tissue samples of primary non-small-cell lung carcinomas (NSCLC) from patients treated with surgery were analysed for the expression of CA9 and programmed-death ligand PD-L1 by cancer cells, and of FOXP3 by tumour-infiltrating lymphocytes (TILs).
Results
There was no direct association of CA9 with PD-L1 expression or the density of TILs in the tumour stroma, but CA9 was directly related to the extent of FOXP3+ TIL density (
p
= 0.008). Double-stratification survival analysis showed that patients with high CA9 expression and low TIL score had significantly poorer survival compared with all other groups (
p
< 0.04). In a multivariate analysis stage (
p
< 0.0001, HR 1.95, 95% CI: 1.3–2.7), TIL score (
p
= 0.05, HR 0.55, 95% CI: 0.2–1.0) was an independent prognostic variable of death events. CA9 expression by cancer cells is associated significantly with FOXP3+ regulatory T-cell abundance in the tumour stroma of NSCLC.
Conclusion
The study provides a basis for testing CA9 as a marker of resistance to immune-checkpoint inhibitors and as a therapeutic target to enhance the efficacy of immunotherapy.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Adult
/ Aged
/ Antigens, Neoplasm - analysis
/ Antigens, Neoplasm - physiology
/ Biomedical and Life Sciences
/ Cancer
/ Carbonic Anhydrase IX - analysis
/ Carbonic Anhydrase IX - physiology
/ Carcinoma, Non-Small-Cell Lung - enzymology
/ Carcinoma, Non-Small-Cell Lung - immunology
/ Carcinoma, Non-Small-Cell Lung - mortality
/ Carcinoma, Non-Small-Cell Lung - pathology
/ Female
/ Forkhead Transcription Factors - analysis
/ Humans
/ Hypoxia
/ Immune checkpoint inhibitors
/ Lymphocytes, Tumor-Infiltrating - immunology
/ Male
/ Non-small cell lung carcinoma
/ Oncology
/ Protons
/ Stroma
/ Surgery
/ T-Lymphocytes, Regulatory - immunology
/ Tumors
