AR positive

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.

This case shows the diagnostic complexity of synchronous AR + malignancies with overlapping metastatic profiles and emphasizes the need for integrated clinical, radiological, and pathological assessment to ensure optimal patient management. It highlights the need to biopsy metastatic bone lesions in cases of SDC-especially in older men-to rule out osseous metastases from more frequent carcinomas such as PCa.

In AR-positive cells, CREB5 overexpression promoted cell colony growth with tumorigenic properties and increased tumor size in vivo. These findings implicate CREB5 as a driver of the transcriptional programs underlying AR-independent basal and SCL CRPC subtypes, and this activity is detectable in primary PC.

In this study, AR status showed no association with DFS, BCSS, or OS; and was not a prognostic factor in TNBC. Further studies exploring the role of AR in TNBC are warranted as AR expression could be a potential target with antiandrogen therapy.

P2, N=57, Completed, National Cancer Center Hospital East | Active, not recruiting --> Completed

In this review, we explore the unconventional tumor-suppressive function of YAP/TAZ and the mechanisms through which they inhibit tumor growth, with an emphasis on recent findings in hormone-regulated cancers and ccRCC. Finally, we discuss the therapeutic implications of these emerging findings for cancer treatment.

P1, N=2, Terminated, Brown University | N=32 --> 2 | Trial completion date: Jan 2032 --> Oct 2025 | Recruiting --> Terminated | Trial primary completion date: Jan 2027 --> Jul 2025; Principal Investigator left institution

P2, N=88, Active, not recruiting, Fudan University | Trial primary completion date: Dec 2025 --> Dec 2026

Mechanistically, VIC-1911 disabled HR-mediated repair of DSBs in otherwise HR-proficient PC cells, leading to a "BRCAness" phenotype and pronounced accumulation of DNA damage and mitotic catastrophe. In summary, our study uncovers what we believe a novel mechanism to functional "BRCAness" by inducing mitotic arrest and highlights VIC-1911 as a promising therapeutic agent for advanced PC, either as a single agent or in combination, sensitizing HR-proficient tumors to PARP inhibitors.

In summary, this study reveals the molecular mechanism by which AKR1C3 is involved in metabolic reprogramming to promote radioresistance in prostate cancer through PKM2/UBE2T. These findings indicate that targeting AKR1C3 has potential for overcoming radioresistance, providing novel insight into the clinical treatment of prostate cancer.

During a mean follow-up of 97.2 months, distant metastasis occurred in 4/62 patients (6.5%) and locally invasive disease in 4/62 (6.5%), with an overall survival rate of 95%. Overall, these findings highlight the biological heterogeneity of SPNs and indicate that, despite a shared molecular background, aggressive behavior is not defined by a single reproducible pathological or molecular feature.