This is worth following - SRC-3 gene potential omni-cure for cancer

[Derf4223]

genengnews.com/topics/cance...

biorxiv.org/content/10.1101...

Currently in phase 1 trials, lots of ground to cover before human approval.

Steroid Receptor Coactivator 3.

[Blackholes]

Yes I’ve been following this for a while now. Let’s hope that this ACT with these Tregs translates to humans.

I truly believe that immunotherapy approaches will ultimately change cancer into a chronically manageable disease if not completely curable.

[Scout4answers in reply to Blackholes]

I truly believe that immunotherapy approaches will ultimately change cancer into a chronically manageable disease if not completely curable.

Yes!

[Spyder54]

SRC-3. T-regs. The O’Malley Labs.

Go-Go-Go. Getting closer. Hoping the Phase 1 Trial plays out with acceleration into Phase 2 & 3. Thanks Derf. Keeping me optimistic.

Mike

[austinsurvivor]

Is there a link to the phase I trials? very promising

[KocoPr]

The research has known this since at least 2005 but I can’t understand why this science moves slower than a snail. It’s been what 18 years.

Here is an article on it from 2006

pubmed.ncbi.nlm.nih.gov/171...

Abstract

Steroid receptor coactivator (SRC)-3, also called amplified in breast cancer 1, is a member of the p160 nuclear receptor coactivator family involved in transcriptional regulation of target genes. SRC-3 is frequently amplified and/or overexpressed in hormone-sensitive and hormone-insensitive tumors. We reported previously that SRC-3 stimulated prostate cell growth in a hormone-independent manner through activation of AKT signaling pathway. However, the underlying mechanism remains undefined. Here, we exploited the mifepristone-induced SRC-3 LNCaP prostate cancer cell line generated in our laboratory to identify SRC-3-regulated genes by oligonucleotide microarray analysis. We found that SRC-3 up-regulates the expression of multiple genes in the insulin-like growth factor (IGF)/AKT signaling pathway that are involved in cell proliferation and survival. In contrast, knockdown of SRC-3 in PC3 (androgen receptor negative) prostate cancer cells and MCF-7 breast cancer cells reduces their expression. Similarly, in prostate glands of SRC-3 null mice, expressions of these components in the IGF/AKT signal pathway are also reduced. Chromatin immunoprecipitation assay revealed that SRC-3 was directly recruited to the promoters of these genes, indicating that they are direct targets of SRC-3. Interestingly, we showed that recruitment of SRC-3 to two target promoters, IRS-2 and IGF-I, requires transcription factor activator protein-1 (AP-1). Taken together, our results clearly show that SRC-3 and AP-1 can coordinately regulate the transcription of multiple components in the IGF/AKT pathway to ensure ligand-independent cell proliferation and survival of cancer cells.

Here is a 2019 article on TREG

Past, Present, and Future of Regulatory T Cell Therapy in Transplantation and Autoimmunity

frontiersin.org/articles/10...

here is a 2023 article

Opportunities for Treg cell therapy for the treatment of human disease

ncbi.nlm.nih.gov/pmc/articl...