Cachexia affects up to 80% of cancer patients. It is estimated to cause one in four cancer deaths, primarily when their diaphragm muscle becomes some wasted and weak they can no longer breathe. Doctors try to fight cachexia by feeding the patient up, but this approach rarely works.
When Hoogenraad’s team implanted mice with cancer cells genetically engineered to lack the Fn14 protein, the tumours grew almost as aggressively as a regular tumour. Yet the mice remained bafflingly fit, strong and healthy.
This adult male cachexia patient has suffered extreme muscle and fat loss.
“We scratched our head and thought, ‘What the hell have we done?’” Hoogenraad says. Then they realised they had switched off the cachexia.
The team moved quickly, making antibodies that block Fn14. A mouse with a normal, Fn14-producing tumour will start to lose weight and sicken within eight days. But when mice with Fn14-expressing tumours were injected with the antibody, the weight loss never materialised.
I assume that if the lack of this doesn't change the tumor growth, then cancers could appear without it. One thing to try to learn is whether different cancers produce this protein. This article suggests to me a list of candidates: gastric, lung, prostate. Pancreatic is on the list of frequent cachexia, but I think it might be hard to distinguish the effects of the destruction from those of any additional mechanism in that case.