AR positive

The nomogram based on HER2 status shows promising preliminary predictive performance in predicting pCR. Given the lack of external validation and single‑center design, this model remains exploratory and hypothesis‑generating.

The patient subsequently underwent therapeutic mastectomy. This case highlights the nonspecific imaging features of AC and emphasizes the key role of histopathology and immunohistochemical profiling in diagnosis and management.

Although enzalutamide (ENZA) has improved the overall survival of patients with metastatic prostate cancer, ENZA resistance (ENZA-resistant) inevitably develops, largely limiting its efficacy...In AR-sensitive LNCaP cells, changes in EARS2 expression were explored before and after stimulation with dihydrotestosterone (DHT) or bicalutamide...Mechanistically, EARS2 inhibited mitochondrial biogenesis and ROS generation in PCa cells by targeting STRN4. EARS2 targets STRN4 to modulate mitochondrial biogenesis and ROS homeostasis mediating ENZA-resistant.

We developed a first-in-class SARM-based AR tracer that displays high affinity and selectivity for AR in vitro and in vivo. This represents a suitable PET tracer to image AR status in rodent models and provides a strong rationale for clinical translation of [18F]F-SARM3 as a high-affinity AR agonist PET imaging agent.

Mechanistically, our data indicate that ELF1 transcriptionally regulates EGFR and that ERK1/2 interacts with ELF1, suggesting the existence of a positive ELF1/EGFR/ERK feedback loop that sustains resistance. This study elucidates a possible mechanism of resistance to AR inhibition driven by an ELF1/EGFR/ERK feedback loop in AR-Vs positive cells and provides a rationale for combining EGFR inhibitors with AR-targeted therapy as a potential treatment strategy for patients with advanced, enzalutamide-resistant prostate cancer.

Given the small sample size and the inclusion of immune checkpoint inhibitors in a subset of patients, all of whom achieved pCR, these observations should be considered strictly hypothesis-generating. Larger and more homogeneous cohorts will be required to validate these findings and to determine their potential clinical relevance.

These findings indicate that the conversion of ARPC to NEPC involves coordinated loss of AR, YAP1, and REST activity alongside sustained TEAD1 expression and altered RNA processing. Our data identify TEAD1 as a transcriptional regulator associated with the NEPC state and suggest a role for TEAD1-linked transcriptional and post-transcriptional mechanisms in prostate cancer lineage plasticity.

The patient remained recurrence-free 12 months after surgery. Careful assessment of characteristic cytomorphological features, particularly a dual population of basaloid epithelial cells with peripheral palisading and specialized follicular stromal cells, is vital for the accurate preoperative cytological characterization of trichoblastoma, even at atypical anatomical sites.

Further, KLK2 and STEAP1 expression states were associated with distinct transcriptional programs and immune microenvironmental features. Implications: These findings establish KLK2 and STEAP1 as key prostate adenocarcinoma-lineage antigens and provide critical insights to inform the rational design and clinical development of cell-surface antigen-directed therapies in prostate cancer.

HER2-low and HER2-zero TNBC are biologically distinct subgroups. HER2-low tumors are enriched in luminal AR-like characteristics, whereas HER2-zero tumors exhibit basal-like, highly proliferative, and immunogenic features. Although the treatment outcomes did not differ significantly, these findings suggest that HER2-low and HER2-zero TNBC may require different therapeutic approaches. Prospective studies are warranted to validate these findings and further explore tailored treatment strategies.

Increasing interest in AR biology has led to the evaluation of several anti-androgen therapies in AR-positive TNBC, including agents such as enzalutamide, enobosarm, orteronel, bicalutamide, and seviteronel. Although clinical activity has generally been modest, these studies highlight the potential relevance of AR-targeted strategies in selected patient subgroups. This review summarizes current knowledge on androgen and AR signaling in TNBC, integrating molecular mechanisms, preclinical evidence, and clinical studies, and discusses emerging therapeutic strategies aimed at improving patient treatment outcomes.

These findings identify the YAP1-NPM1 axis as a key regulatory node that integrates oncogenic transcriptional programs and confers therapeutic vulnerabilities. Targeting this axis may enhance the efficacy of androgen receptor-directed therapies and provide new strategies for treating advanced prostate cancer.