Men with testicular cancers called testicular germ cell tumours – which are most common in younger men – could benefit from a new combination of treatments if their chemotherapy stops working.
In a new study, scientists at The Institute of Cancer Research, London, show that a targeted drug blocking the action of a cancer-driving protein can kill testicular cancer cells and, alongside chemotherapy, could reverse drug resistance.
Building on previous work at the ICR, the scientists analysed the activity of proteins called receptor tyrosine kinases, and identified activity of insulin growth factor receptor-1 (IGF1R) in testicular cancer cells.
Receptor tyrosine kinases play a critical role in important cellular processes such as cell growth and division, and are implicated in the development and progression of many types of cancer.
Increased sensitivity to platinum-based chemotherapies
In the study, published in the Journal of Pathology, the researchers discovered that IGF1R was highly active in some testicular cancer cells, compared with normal tissue.
Molecularly depleting IGF1R or silencing IGF1R activity using chemical inhibitors reduced tumour cell growth – particularly testicular germ cell tumour cells with the highest levels of IGF1R activity.
Importantly, blocking the protein’s activity in chemotherapy-resistant cells increased their sensitivity to platinum-based chemotherapy drugs – meaning that IGF1R inhibitors could prove to be a treatment for drug-resistant testicular germ cell tumours.
Some existing IGF1R inhibitors have been tested in clinical trials for other types of cancer.
This article has been republished from materials provided by Institute of Cancer Research . Note: material may have been edited for length and content. For further information, please contact the cited source.
Selfe, J., Goddard, N. C., Mcintyre, A., Taylor, K. R., Renshaw, J., Popov, S. D., . . . Shipley, J. M. (2018). IGF1R signalling in testicular germ cell tumour cells impacts on cell survival and acquired cisplatin resistance. The Journal of Pathology, 244(2), 242-253. doi:10.1002/path.5008