While looking at CDK4 which is implicated in tumor

While looking at CDK4 which is implicated in tumor growth I ran across this -

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Similarly, CCR5 knockdown resulted in a significant decrease in the CCL5-induced protein expression of CDK2, CDK4, cyclin D1, cyclin E, pRB, and PCNA, while increasing the p27( kip1) level
https://www.karger.com/article/FullText/490024

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All that are downregulated are implicated in tumor cell division except pRB. pRB can actually inhibit tumor growth. Oh no that's not good!

But when tumors go completely out of control it's often because of pRB disregulation or complete absence due to genetics. But they've found even in the absence of pRB that upregulated p27 can do a fine job of stopping or slowing tumor growth.

https://www.cell.com/cancer-cell/pdf/S1535-61...0428-5.pdf

I was looking at CDK4 because someone needed a touch of reality over on stocktwits. Here's my post from there -

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@AskSlapper13

How is that $GTHX thing doing? 30% Severe adverse reactions and a 5% fatality rate in their drug Cosela. That certainly doesn't sound good. You would think a CDK4/6 inhibitor would be safer than that.

I've heard of CCR5 blockade doing the same thing. Leronlimab which has no drug related SAEs (safer and more effective than maraviroc) has that covered. Don't worry to much about the chemotherapy-induced myelosuppression indication. Leronlimab has so many indications we'll probably never specifically trial that. The downside is we are doing trials in cancer combined with chemotherapy so we'll fix that myleosuppression just as a side-effect. We also have some patients on monotherapy and may supplant chemotherapy in some case. In one of the patients on monotherapy with TNBC, brain lung and liver metastasis given 3 months to live she's still alive over 2 years later.
https://pubmed.ncbi.nlm.nih.gov/31954769/

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