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Prostate Cancer Treatment and Research / Prostate Cancer Diagnosis and Treatment · Journal article
Scientific Reports · September 7, 2026
Raises a question worth testing. It does not answer one.
This descriptive comparative study uses immunohistochemistry and Western blotting to document spatial and intensity differences in phosphorylated CREB (pS133CREB) and VASP between non-human primate and human prostate tissue. The authors propose that these patterns reflect different regulatory mechanisms—endocrine in primates versus paracrine/cell-autonomous in humans at invasion sites—but provide no functional evidence, clinical correlation, or mechanistic proof.
Descriptive cross-species comparative tissue analysis. Healthy prostate glands from non-human primates and prostatectomy specimens from men; specific eligibility criteria, clinical status, and cancer stage not stated.. Intervention: Examination of phosphorylated CREB and VASP by Western blotting and immunohistochemistry; no intervention applied.. Compared with: Cross-species comparison between non-human primate and human prostate tissue..
Homogenous pS133CREB staining in primate epithelial cells; large variations in signal intensity between individual acini in human prostatectomy samples Strongest pS133CREB signal at perineural invasion sites in human tissue Substantial heterogeneity in pS133CREB between individual cells at stroma invasion sites in men
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
These observations may inform future mechanistic studies of PKA signaling in human prostate cancer, but do not establish clinical relevance, diagnostic utility, or therapeutic targets without functional validation and correlation with clinical outcomes.
Descriptive comparative immunohistochemistry study raising mechanistic questions about CREB phosphorylation regulation in primate versus human prostate tissue, without clinical outcome data or functional validation.
As stated by the source record.
These observations may inform future mechanistic studies of PKA signaling in human prostate cancer, but do not establish clinical relevance, diagnostic utility, or therapeutic targets without functional validation and correlation with clinical outcomes.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
The cAMP-dependent protein kinase (PKA) signaling is associated with inhibition of apoptosis and therapy-resistance in preclinical models of prostate cancer; however, the information on activation of PKA pathway in men’s prostates is limited. We examined phosphorylation of PKA substrates cAMP response element-binding protein (S133CREB) and vasodilator-stimulated phosphoprotein (S157VASP) in healthy prostates of non-human primates and in prostatectomy samples from men by Western blotting and their spatial distribution across the prostate glands by immunohistochemistry. In monkeys’ prostates homogenous staining of pS133CREB in epithelial cells and of pS157VASP in stroma was observed throughout the caudal lobes. In contrast, large variations in pS133CREB signal intensity between individual acini were observed in men prostatectomies. A strongest pS133CREB signal was observed at the sites of perineural invasion. At the stroma invasion sites, a substantial heterogeneity between individual cells was evident. No overlap between phosphorylated forms of CREB, protein kinase Akt, or extracellular signal-regulated kinase staining was detected in primate or human prostates. The observed patterns of S133CREB phosphorylation suggest that CREB phosphorylation in healthy prostates of non-human primates is controlled by endocrine signals, whereas paracrine or cell-autonomous mechanisms prevail in men’s prostatectomies at the perineural and stroma invasion sites.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.