AR positive

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.

Together, these findings establish DALTACs as a broadly applicable strategy to rewire disease-defining protein complexes by altering their domain topology, expanding the conceptual and therapeutic landscape of induced proximity agents. The precision and lineage-selective action of DALTAC-1 highlight its strong translational potential for treating AR-driven prostate cancer.

This synergy is abolished by FDX1 loss or copper chelation, confirming dependence on AR-FDX1 axis activation. Together, these findings uncover FDX1 as a mechanistic effector of AR pathway inhibition and propose a well-tolerated combination strategy that exploits cuproptosis to improve therapeutic responses in prostate cancer.

AR was positive in 48.3% of patients and was significantly associated with HR and HER2 status, tumor biology, trastuzumab, and hormonal therapy. AR status was not significantly associated with DFS and OS.

HER2-low and HER2-zero TNBC represent biologically distinct subgroups. HER2-low tumors are enriched for luminal AR-like characteristics, while HER2-zero tumors exhibit basal-like, highly proliferative, and immunogenic features. Although 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.

This profile supported the diagnosis of primary vulvar apocrine adenocarcinoma, allowing for appropriate surgical management and successful excision of the lesion. This case highlights the diagnostic complexity of vulvar adenocarcinomas and underscores the importance of systematic clinicopathologic evaluation, particularly in patients with a history of malignancy.