Comment by biotechbio
20 hours ago
This is a pretty cool study with some interesting findings! Cancer immunotherapy has a long history but has become very prominent in recent years. (Fun fact: the senior author on this paper, Ed Engleman, co-founded of one of the first cancer cell therapy companies, Dendreon, in the early 90s). However, the success of immunotherapies has been limited by the immune-exclusionary nature of the tumor microenvironment (TME). Why some tumors are immune-hot and others are immune-cold is still a very open research question.
In this study, the authors demonstrate pretty convincingly that erythropoietin (EPO, a hormone that stimulates red blood cell production in the bone marrow) reduces the recruitment of tumor-cell-killing T cells to the TME. It does this by acting on tumor macrophages, another type of immune cell, and changes the state of these cells to facilitate accumulation of immunosuppressive cells.
They work out the mechanism largely through mouse models and associative analysis in human tissue samples, but I thought it was interesting that this finding aligns with the clinical observation that cancer patients who receive recombinant EPO for treatment of anemia frequently experience tumor progression.
After reading this, I am going back to check out EPO expression in old datasets that I worked with haha.
I actually don't mind if it's true, but your comment was the first time I got a tingle that this was AI generated but I still could tell it likely wasn't. Maybe used it to rewrite parts of your comment? Anyways i appreciate it and agree with you. I myself am gonna go check in the cancer cell line encyclopedia, which IME is the single cleanest large dataset curated in biology in decades.
For others who might be curious, this study is genuinely good (evidenced somewhat by it being published in Science, as a study that is not in humans but still showing actual cancer curing efficacy not just some pathway finding) is that they use difficult but necessary model systems that emulate real tumor environments - these are spontaneous tumors that show up in mice that have full immune systems. Literally 99.9% of cancer study papers don't use such systems and in my opin9on get fully invalidated for most interpretation.
Anyways I'm curious if the microenvironment will just evolve quickly to be EPO independent, as it typically seems to do something like that in real long term tumor environments you encounter in people compared to mouse models.