The deletion of Interleukin-17 receptor (IL-17R), a receptor gene that regulates inflammation, may help predict the aggressiveness of colorectal cancers (CRCs), according to a new study by a Nova Scotia research team partly funded by the TFRI.
Published in the International Journal of Cancer (February 2019), the finding may lead to the creation of tests that monitor IL-17R deletion as a prognostic tool for these patients.
“We found that IL-17R deletion was present in nearly half of all CRC patients with advanced cancer, and that these patients had worse overall survival rates than their peers,” said Dr. Jun Wang, an immunologist at Dalhousie University in Nova Scotia and the paper’s senior corresponding author.
According to Dr. Wang, IL-17R deletion leads to more aggressive cancers because it promotes atypical inflammation, altered cellular proliferation and cellular metabolism, all of which impacts overall survival rates, tumour grade and the expression of molecular markers associated with tumour invasion, growth and metastasis.
This discovery creates the possibility for developing prognostic tests that monitor IL-17R deletion, and may contribute to the establishment of IL-17R as a potential target for new therapies.
“We are currently conducting additional research to further characterize the impact of IL-17R-deletion on anti-tumour and pro-tumour immune responses,” said Dr. Wang. “It is anticipated that this information can be used to tailor immunotherapies and/or other novel therapies for CRC tumours with IL-17R deletion.”
First author Dr. Chi Yan, a TFRI trainee at Dalhousie University in Nova Scotia, and the study team performed a deep data analysis on several publicly available human datasets. He says their work reinforces the idea that “with the right question and proper design for data analysis, big data can really propel cancer research”.
Study
IL-17R deletion predicts high-grade colorectal cancer and poor clinical outcomes
Authors
Chi Yan, Weei-Yuan Huang, Jeanette Boudreau, Animamalar Mayavannan, Zhenyu Cheng and Jun Wang
Funding
This work was partly supported by the TFRI’s Cancer Research Training Program in Atlantic Canada.