AR positive

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.

P2, N=88, Active, not recruiting, Fudan University | Recruiting --> Active, not recruiting

AC is characterized by distinct metabolic reprogramming, with preferential upregulation of peroxisomal β-oxidation rather than mitochondrial pathways. These metabolic features are accompanied by a high prevalence of activating PIK3CA mutations, suggesting a link between genomic alterations and metabolic phenotype. These findings provide new insights into the pathobiology of AC and may assist in its histopathological differentiation from other breast cancer subtypes.

Moreover, pharmacological GRPR inhibitor represses FAM135A expression via MED15 activation. Together, we unveil FAM135A as an oncodriver and biomarker of PCa perineural invasion, and provide a novel strategy for PCa innervation therapeutics.

Furthermore, we explored a novel combination therapy involving the histone methyltransferase inhibitor MI-503 and enzalutamide in AR-positive and AR splice variant-positive cell lines. Our results confirmed the synergistic therapeutic effects of this combination, which can continue to inhibit the AR signaling pathway during the CRPC stage, thereby delaying disease progression. Taken together, our findings elucidate a critical KMT2D/G3BP1/SPOP/AR regulatory axis in prostate cancer progression and propose that targeted inhibition of histone methylation in combination with anti-androgen therapy represents a promising strategy for the management of advanced prostate cancer.

P2, N=51, Recruiting, Vandana Abramson | Not yet recruiting --> Recruiting

Our study revealed that BAP18, which acts as a novel AR corepressor, is involved in AR-positive TNBC progression, suggesting that BAP18 could be a potential therapeutic target for AR-positive TNBC patients.