Same with the paragraphs I had in itSorry -easier to read. BTW, the 57% is on the paragraph right after Fig 2 charts.
In the past, we've asked the question about getting a quantitative measure of just how many cells in a tumor express Sort1. I think I found a small answer that pushes our understanding along a bit for ER+ and ER- breast cancer tumors. I know just enough to be dangerous, so take that as a warning.
I was reading the Univ Gothenburg paper that shows how Sort1 is associated with cancer stem cell proliferation and metastases in breast cancer and that if you "turn off" Sort1, the spread of the tumor slows. In it, they did a study for just Sort1 positive tumor cells and ran a gene expression study on 60 samples. It was for one specific breast cancer line called MCF7.
For 60 sample MCF7 breast cancer tumor cells, they found that 57% of the cells expressed Sort1. Given ER Breast cancer is one that is considered Sort1 "overexpressed" in 90% or so of the cases, maybe we can roughly conclude that the High-Expression group shown with the staining process in various THTX journal charts means around 60% or higher of the tumor cells express Sort1. I seem to recall they've said they think it will be very effective for those in the "very high" and "high" categories, so maybe that would mean where your tumor has cells where 50%+ show express Sort1. Both THTX and I are just guessing and at some point they will roughly find that number for each different cancer type as I'm sure it won't be the same for each. But maybe that's a good starting estimate. It could work with lower numbers too for all I know.
It's known that Sort1 is a prerequisite for cancer stem cell propagation. As a reminder, The UnivGothem guys overall conclusion was this:
"The fact that we could show that progranulin mediates sortilin activation resulting in CSC propagation suggests that sortilin is a key molecule that genuinely affects tumour progression and metastatic properties. Further studies are needed in order to define the exact role for sortilin in this context, but our results clearly support an important role for sortilin in CSC propagation."
This impact on cancer stem cells, VM and the like via engaging sortilin somehow just may be the unique MOA that propels this platform for us. The paper is here:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6245804/