STEAP1 (STEAP Family Member 1)

These findings suggest that systemic inflammation induced by T-cell activation following BSTP0204A treatment may have resulted in increased STEAP1 expression, inducing additional inflammation and tissue damage. This work demonstrated the need to understand not only baseline target expression for T-cell engaging therapies, but also expression under conditions such as inflammation, injury, or disease.

P1, N=50, Active, not recruiting, Amgen | Recruiting --> Active, not recruiting | Trial completion date: Jun 2029 --> Dec 2028 | Trial primary completion date: Apr 2027 --> Oct 2026

P=N/A, N=30, Active, not recruiting, Universita di Verona

We expanded the phenotype to include cytopenia and neonatal HLH. Our report on two affected male siblings highlights the expanded phenotype, clarifies the phenotypic spectrum of STEAP3, and broadens its genetic inheritance, ultimately providing a clinical and molecular workup for neonatal patients with unexplained HLH.

Nonetheless, challenges remain around long-term hematologic and renal safety, radionuclide supply, protocol standardization, and global accessibility. Ongoing and future multicenter trials, collaborative consortia, and innovations in theranostics will be critical to defining optimal patient selection, sequencing with existing therapies, and embedding RLT as a key pillar in the management of advanced PCa.

However, further evaluation of MT and STEAP gene responses to CdCl2, HgCl2, PbCl2, and ZnCl2 (0, 5, 10, 15 μM for 24 h) revealed that the expressions of the MT and STEAP genes were each regulated differently in a metal-specific manner, suggesting distinct cytotoxic mechanisms in response to each heavy metal. This study represents the first systematic investigation of MT and STEAP gene responses to heavy metals providing a new perspective for further research in metal toxicity assessment.

IDC-P possesses a distinct molecular and immunological profile. Understanding these molecular underpinnings is crucial for the development of personalized treatment strategies for histologically distinct prostate cancer subsets.

B7H3, STEAP1, and PSMA might be the predominant targets in both PL and BML. Our findings reveal the dynamic and heterogeneous nature of TAA expression in PCa and may provide insights for integrating ADC-based targeted therapies into the existing treatment landscape for PCa.

These data establish STEAP1 as a clinically relevant and highly expressed target in EwS and demonstrate that IL-18 armoring significantly improves CAR T cell efficacy by enhancing potency evident through antitumor activity at reduced cell dose. STEAP1 CAR T cells are currently under evaluation in a first-in-human phase 1/2 dose-escalation clinical trial for metastatic castration-resistant prostate cancer ( NCT06236139 ) and these studies support future clinical translation of STEAP1 CAR T cell therapy for relapsed/refractory EwS.

Our findings uncover a mechanistic basis for EGFR inhibitor resistance of CDK4 and CDK6 amplified EGFR-mutant LUAD. They also provide a rationale for the biomarker-driven clinical development of combination EGFR and CDK4/6-targeted therapies for the treatment of a subset of EGFR-mutant LUAD patients.

BsAbs are a promising therapeutic strategy for mCRPC, with potential to improve outcomes in this poorly treatable disease. Addressing challenges (toxicity, tumor microenvironment, response durability) via research and trials is key to unlocking their full potential. Future research should focus on optimizing constructs, exploring novel targets, and developing combination therapies to advance BsAbs in prostate cancer.