In this study, we retrospectively examined the relationship between ERG expression and PTEN loss in 119 surgically treated prostate cancer patients from Northeastern Brazil through immunohistochemical analysis.
The evolution from local PCa to castration-resistant PCa, an end-stage of disease, is often associated with changes in genes such as p53, androgen receptor, PTEN, and ETS gene fusion products.
Expression and significance of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and Claudin-3 in the blood of patients with prostate cancer [prostate cancer (PCa)] were investigated.
In summary, we identify ARID4B as a master regulator in the PTEN-PI3K pathway, thus providing a potential therapeutic target for prostate cancer carrying PTEN mutations.
A total of 6744 patients from 17 studies were included in this analysis Overall, The pooled results showed that PTEN loss predict pooled BRF (HR 1.79, 95% CI 1.49-2.16, P < 0.001) and RFS (HR 1.71, 95% CI 1.50-1.95, P < 0.001) in patients after radical prostatectomy or brachytherapy for prostate cancer.
For example, we find multiple known (e.g., miR-20a-PTEN-PTENP1) and novel (e.g., miR-375-SOX15-PPP4R1L) microRNA-gene-pseudogene associations in prostate cancer.
Knockdown of Phospholipase Cε (PLCε) Inhibits Cell Proliferation via Phosphatase and Tensin Homolog Deleted on Chromosome 10 (PTEN)/AKT Signaling Pathway in Human Prostate Cancer.
Dual-label species (ie, human vs mouse) specific centromere and telomere Fluorescence In Situ Hybridization (FISH) and immuno-histochemical (IHC) staining of tissue microarrays (TMAs) containing replicates of the PDX models were used for characterization of expression of a number of phenotypic markers important for prostate cancer including AR (assessed by IHC and FISH), Ki67, vimentin, RB1, P-Akt, chromogranin A (CgA), p53, ERG, PTEN, PSMA, and epithelial cytokeratins.
ABA treatment also inhibited testosterone synthesis and alleviated Pten loss-induced tumorigenesis <i>in vivo</i><i>Pten</i> deletion induced TME remodeling, but <i>Runx2</i> heterozygous deletion or ABA treatment reversed the effect of Pten loss by decreasing expression of the collagenase Mmp9.<b>Conclusions:</b> Abnormal RUNX2 activation plays a pivotal role in PTEN loss-induced IAS and TME remodeling, suggesting that the identified signaling cascade represents a viable target for effective treatment of PTEN-null prostate cancer, including CRPC.<i></i>.
Here we show that a patient-derived prostate-specific microbe, CP1, in combination with anti-PD-1 immunotherapy, increases survival and decreases tumor burden in orthotopic MYC- and PTEN-mutant prostate cancer models.
The use of new probe designs to recognize truncation artifacts is illustrated with a four-color PTEN FISH set optimized for prostate cancer tissue sections.
In addition, <i>in vitro</i> and in silico analysis reveals PTEN loss is associated with widespread increases in FGF ligands and receptors in prostate cancer.