AR positive

Small-molecule tyrosine kinase inhibitors such as lenvatinib and axitinib may provide disease stabilization in adenoid cystic carcinoma, although tumor shrinkage is uncommon and toxicity limits their long-term use. For most patients without a targetable alteration, platinum-based combinations remain the pragmatic choice, though expectations for benefit should be tempered. Future strategies will likely hinge on optimizing biomarker-driven therapies, expanding access to antibody-drug conjugates, and pursuing collaborative trial designs to overcome the rarity and heterogeneity of these tumors.

Consequently, combination therapies targeting DHODH and glutamine metabolism were synergistic in impairing PCa cell proliferation. Altogether, these results highlight DHODH as a metabolic vulnerability of AR-positive and AR-negative PCa cells by regulating central carbon and nitrogen metabolism.

AR expression is associated with improved prognosis in ER-positive BC, but its role in TNBC and HER2-positive BC remains unclear due to heterogeneity and non-significant results. Standardized AR evaluation and prospective studies are needed to confirm its prognostic and predictive value for personalized BC treatment.

P1/2, N=37, Active, not recruiting, Kari Wisinski | Recruiting --> Active, not recruiting | Trial completion date: Sep 2025 --> Oct 2026 | Trial primary completion date: Sep 2025 --> Oct 2026

P2, N=20, Recruiting, Manish Patel | Trial completion date: Oct 2025 --> Aug 2026 | Trial primary completion date: Sep 2025 --> Apr 2026

This case underscores several diagnostic challenges: (1) histology from the primary lesion initially suggested a benign tumour, discordant with aggressive radiological features; (2) ancillary molecular testing with PLAG1 FISH was critical in linking the primary PA with metastatic carcinoma; and (3) HER2 overexpression and androgen receptor positivity highlighted potential therapeutic targets, though the rapid disease course precluded treatment. Correlation of imaging, histology, cytology, and molecular studies is crucial, particularly when biopsy findings appear discordant with clinical behaviour.

This may be the result of a functional interaction between ERβ and p53 or AR. The role of ERβ in TNBC will be elucidated in further complex studies considering multiple molecules.

These findings suggest that the circulating 3LS is not just a prognostic biomarker, but an actionable signature reflecting changes in PC biology. The plasma lipid milieu identified by the 3LS drives a pro-survival phenotype by modifying lipid metabolism and upregulating ceramide/S1P signalling. The study provides the biological rationale to target ceramide-S1P signalling in patients, who are 3LS-positive.

We report the case of a 38-year-old male with unresectable intra-abdominal DSRCT treated with the VAC-IE regimen (vincristine, doxorubicin, and cyclophosphamide, alternating with ifosfamide and etoposide) as first-line therapy...As second-line therapy, he received gemcitabine and docetaxel...Alternative regimens include temozolomide plus irinotecan or gemcitabine plus doxorubicin. In patients with androgen receptor positivity, hormonal blockade with leuprolide and bicalutamide may be a therapeutic option, particularly in frail patients...DSRCT is a challenging and aggressive malignancy requiring a multidisciplinary and individualized approach. The combination of systemic therapy and local control measures remains critical for improving patient outcomes.

The HOXB13/SMARCD2 interaction alters chromatin accessibility at HOXB13-binding sites, causing increased proliferation in AR-negative PCa. Overall, this work demonstrates a distinct mechanism of action for HOXB13 and highlights its critical role in AR-negative castration-resistant PCa.

No ABC showed AR positivity, while this was observed in rare cells (IRS 1-2) in 30.8%, 16.6%, and 37.5% of TSCs, EPTs, and ABHs, respectively. HoxB13 can be a useful and reliable marker for identification of TSPs, EPTs and ABCs.

Interestingly, RSGs and the AR have non-genomic interactions via membrane-localized AR (mAR) not affected by AR inhibitors. Drugs that target RSGs are needed along with AR inhibitors to prevent mPCa progression.