From YMB: Have not seen part 2, but felt part 1 was very clear and informative.
1/2
This will take two posts. If Yahoo doesn’t accept the second one, that will appear later.
Interesting sections from September 2, 2020 cc.
-- D Adams from Creativ MicroTech, which CYDY “has used to analyze all of our ongoing cancer trials”
-- Nader on blood markers vs. clinical results
-- SK on promise and difficulties in cancer treatment
15:50 DA
So yeah, my name is Daniel Adams and I am the Director of Clinical Research and Development at Creativ MicroTech, as Nader said.
My company studies and specializes all aspects of blood-based biopsies, and for the past ten years we have focused specifically on the communication axis of tumor cells and their pro-tumorigenic immune cells and their ability to migrate through the bloodstream during invasion. Specifically, we study how these cells and immune macrophages work in coordination to allow tumor invasion, tumor spread. So I’m hoping to discuss a little bit about the background because it is a novel field, and also the context of the CCR5 work.
Many years ago, we actually discovered during our large-scale proteomic metadata analysis, encompassing a few hundred different cancer patient sub-types, that CCR5 was actually one of the most commonly-expressed protein biomark receptors in both circulating tumor cells and the pro-tumorigenic macrophages invading through the bloodstream to metastatic sites.
Now, CCR5 has always been well-known as a migratory cell receptor that has for well over 20 years of published work described it as the receptor responsible for cell motility from one part of the tissue into invading space. It has numerous ligand activators: MIP1, RANTES (also known as CCL5), MCP2, and eotaxin, as well as many others.
But in general the activation of CCR5 is usually in the context of RANTES, which allows pro-tumorigenic cells, both macrophages and tumor cells (as I said earlier), to migrate and invade. And that’s really where our interests kind of lie. Interestingly that what we discovered, and again this was very many years coming, is that CCR5 expression has historically been very difficult to quantify, specifically as cells tend to down-regulate when they’re in their stagnant state within primary tumors per se and when they’re growing. But when they’re invading, they upregulate CCR5 as their motility marker. And this is where our work really found a clear parallel with CytoDyn’s, and when we started working with them.
Now, while CCR5 can often be low in primary and metasite biopsies, when in circulation we’ve actually seen extremely high expression of CCR5 in both circulating tumor cells and in circulating pro-tumorigenic macrophages. To that end, we partnered with CytoDyn as to evaluate these invasive migratory tumor cells during and after treatment with leronlimab.
Now, based on our previous pre-clinical models, before we started working with patients specifically with leronlimab, we expect that most of the migratory cells and pro-tumorigenic macrophages should see a precipitous drop in both number and expression of CCR5 when leronlimab should be added.
Now, our models to date have largely been -- and again we’re talking about hundreds if not thousands of cancer patients across a broad range of cancer sub-types -- now, with most of our studies have been without the context of leronlimab. But one thing we have constantly seen is that our models have found that patients with diminished CCR5 expression is always associated with fewer migratory tumor cells and better clinical outcomes. And that our models clearly have shown that a prediction that treatment with leronlimab will further diminish any existent migratory tumor cells and result in less patient progression...
NP
Thank you, Dan. I appreciate that explanation. So I want to make sure everybody is very clear that lab data, whatever marker that we use for HIV, cancer, for anything, will not give the company approval, and FDA will not consider that as approval. What we need is clinical outcome.
1/2
This will take two posts. If Yahoo doesn’t accept the second one, that will appear later.
Interesting sections from September 2, 2020 cc.
-- D Adams from Creativ MicroTech, which CYDY “has used to analyze all of our ongoing cancer trials”
-- Nader on blood markers vs. clinical results
-- SK on promise and difficulties in cancer treatment
15:50 DA
So yeah, my name is Daniel Adams and I am the Director of Clinical Research and Development at Creativ MicroTech, as Nader said.
My company studies and specializes all aspects of blood-based biopsies, and for the past ten years we have focused specifically on the communication axis of tumor cells and their pro-tumorigenic immune cells and their ability to migrate through the bloodstream during invasion. Specifically, we study how these cells and immune macrophages work in coordination to allow tumor invasion, tumor spread. So I’m hoping to discuss a little bit about the background because it is a novel field, and also the context of the CCR5 work.
Many years ago, we actually discovered during our large-scale proteomic metadata analysis, encompassing a few hundred different cancer patient sub-types, that CCR5 was actually one of the most commonly-expressed protein biomark receptors in both circulating tumor cells and the pro-tumorigenic macrophages invading through the bloodstream to metastatic sites.
Now, CCR5 has always been well-known as a migratory cell receptor that has for well over 20 years of published work described it as the receptor responsible for cell motility from one part of the tissue into invading space. It has numerous ligand activators: MIP1, RANTES (also known as CCL5), MCP2, and eotaxin, as well as many others.
But in general the activation of CCR5 is usually in the context of RANTES, which allows pro-tumorigenic cells, both macrophages and tumor cells (as I said earlier), to migrate and invade. And that’s really where our interests kind of lie. Interestingly that what we discovered, and again this was very many years coming, is that CCR5 expression has historically been very difficult to quantify, specifically as cells tend to down-regulate when they’re in their stagnant state within primary tumors per se and when they’re growing. But when they’re invading, they upregulate CCR5 as their motility marker. And this is where our work really found a clear parallel with CytoDyn’s, and when we started working with them.
Now, while CCR5 can often be low in primary and metasite biopsies, when in circulation we’ve actually seen extremely high expression of CCR5 in both circulating tumor cells and in circulating pro-tumorigenic macrophages. To that end, we partnered with CytoDyn as to evaluate these invasive migratory tumor cells during and after treatment with leronlimab.
Now, based on our previous pre-clinical models, before we started working with patients specifically with leronlimab, we expect that most of the migratory cells and pro-tumorigenic macrophages should see a precipitous drop in both number and expression of CCR5 when leronlimab should be added.
Now, our models to date have largely been -- and again we’re talking about hundreds if not thousands of cancer patients across a broad range of cancer sub-types -- now, with most of our studies have been without the context of leronlimab. But one thing we have constantly seen is that our models have found that patients with diminished CCR5 expression is always associated with fewer migratory tumor cells and better clinical outcomes. And that our models clearly have shown that a prediction that treatment with leronlimab will further diminish any existent migratory tumor cells and result in less patient progression...
NP
Thank you, Dan. I appreciate that explanation. So I want to make sure everybody is very clear that lab data, whatever marker that we use for HIV, cancer, for anything, will not give the company approval, and FDA will not consider that as approval. What we need is clinical outcome.
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