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Posted On: 05/07/2025 5:47:45 PM
Post# of 154570
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I don't have good sources and not sure about hearing that Crisper and Leronlimab are involved with the above. Anyone have anything on this?
If leronlimab had been involved we would have heard about it from Cytodyn by now.
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The Phase I trial — meaning it is the first in humans and had the goal of showing the therapy is safe — examined 12 patients with gastrointestinal cancers, including colon and rectal cancer. Like Dimery, the other 11 participants had Stage 4 colorectal cancer and had failed other treatments. This experimental therapy provided a median survival rate of 129 days.
Ihttps://www.today.com/health/news/colon-cancer-crispr-cish-immunotherapy-rcna203485
CRC and mTNBC are different types of cancers so different outcomes with treatment. But it will be interesting to see our CRC results in light of this. If our mTNBC correlates to our colorectal cancer trial we could surpass this median overall survival.
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The study shows that this therapy safely “unleashes the immune system” without causing an overreaction, Lou explains. A highlight is Dimery’s outcome.
That's one of the main components of leronlimab activity. So I went looking for what genes Dr. Lou was editing with CRISPR. He was editing CISH to downregulate its expression. CISH acts as a tumor protectant so downgrading it would allow killer T-cells to attack the tumor. CISH is upregulated in response to upregulation of inflammatory cytokines as are most tumor protectants. The main upregulators for CISH are IL-2, IL-3 and GM-CSF. IL-2 and GM-CSF are on the regulator list as downregulated. IL-3 would almost certainly be downregulated by leronlimab since it is upregulated by inflammatory cytokines. A very high probability that leronlimab also downregulates CISH. But of course that would be only one of leronlimab's anti-tumor activities.
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