6. The genetic and phenotypic changes observed with Zfp36-loss in Pten GEMMs result in increased resistance to hormonal therapies. These phenotypic changes and treatment resistance are, in part, reversed by therapeutically inhibiting NF-kB.

5. Zfp36 loss induces tumor cell changes associated with phenotypic plasticity, including altered AR and synaptophysin expression. Prostate epithelial cells appear to also take on immune cell features, including increased CD45 expression, in a rarely reported leukocyte mimicking manner.

4. GSEA analysis of GEMM tumors indicated enrichment of inflammatory-associated signatures with Zfp36 loss - validated by IF/IHC. Zfp36-null tumors are also enriched for chemotaxis, proliferation and migration signatures. In vitro analysis validated increased metastatic potential with Zfp36 loss.

3. Loss of Zfp36 accelerates prostate tumor progression in the Pten mouse model. Mice develop PIN with loss of Zfp36 alone, not do not progress to adenocarcinoma.

2. ZFP36 expression is naturally upregulated in prostate tumors following Enza treatment, but not in patients with the lowest ZFP36 levels. In NCI clinical data, residual tumor burden post-Enza, negatively correlates with pre-treatment ZFP36 expression.

2. ZFP36 expression is upregulated in prostate tumors following Enza treatment, but not in patients with the lowest ZFP36 levels. In NCI clinical data, residual tumor burden post-Enza, negatively correlates with pre-treatment ZFP36 expression.

1. Loss of ZFP36 (tristetraprolin) in prostate cancer patients selects for aggressive disease. When prostate tumors have an additional loss of PTEN, the co-loss results in poorer patient outcomes.

Check out the tldr research snapshots from our latest paper in the comments below ⬇️ The study outlines a novel mechanism of #prostatecancer plasticity 🧬🧫

It's definitely worth the full read, though 😄 www.jci.org/articles/vie...

6. The genetic and phenotypic changes observed with Zfp36-loss in Pten GEMMs result in increased resistance to hormonal therapies. These phenotypic changes and treatment resistance are, in part, reversed by therapeutically inhibiting NF-kB.

5. Zfp36 loss induces tumor cell changes associated with phenotypic plasticity, including altered AR and synaptophysin expression. Prostate epithelial cells appear to also take on immune cell features, including increased CD45 expression, in a rarely reported leukocyte mimicking manner.

4. GSEA analysis of GEMM tumors indicated enrichment of inflammatory-associated signatures with Zfp36 loss - validated by IF/IHC. Zfp36-null tumors are also enriched for chemotaxis, proliferation and migration signatures. In vitro analysis validated increased metastatic potential with Zfp36 loss.

3. Loss of Zfp36 accelerates prostate tumor progression in the Pten mouse model. Mice develop PIN with loss of Zfp36 alone, not do not progress to adenocarcinoma

2. ZFP36 expression is naturally upregulated in prostate tumors following Enza treatment, but not in patients with the lowest ZFP36 levels. In NCI clinical data, residual tumor burden post-Enza, negatively correlates with pre-treatment ZFP36 expression.

1. Loss of ZFP36 (tristetraprolin) in prostate cancer patients selects for aggressive disease. When prostate tumors have an additional loss of PTEN, the co-loss results in poorer patient outcomes.

Our paper is out in @jclinical-invest.bsky.social 🎉 A great piece of collaborative science with Leigh Ellis and Chris Sweeney, looking at the role of tristetraprolin in #prostatecancer phenotypic plasticity (plus journal cover art by yours truly!) www.jci.org/articles/vie...