Ask about this productRelated genes to: STEAP1 antibody
- Gene:
- STEAP1 NIH gene
- Name:
- STEAP family member 1
- Previous symbol:
- STEAP
- Synonyms:
- PRSS24
- Chromosome:
- 7q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-10
- Date modifiied:
- 2016-10-05
Related products to: STEAP1 antibody
Related articles to: STEAP1 antibody
- Patients with prostate cancer who develop androgen pathway modulation resistant (APMR) disease face lethal outcomes despite advances in androgen receptor-pathway inhibitors, chemotherapy, and PSMA-directed radioligands. Antibody-drug conjugates (ADCs) have demonstrated transformative efficacy in multiple malignancies, yet ADCs evaluated in patients with metastatic APMR have largely focused on direct tumor cytotoxicity without assessing immune mechanisms that may underpin durable therapeutic responses. Whether immune activation contributes to ADC efficacy in prostate cancer remains unexplored. - Source: PubMed
Publication date: 2026/04/24
Wang John ShuhanSodhi Sirajbir STsao Li-ChungLin Guang HanMoon NicoleZhang QiangLiu BushangqingPenaranda JulietTrotter Timothy NSomarelli Jason AArmstrong Andrew JLyerly H KimWang GuangdiHartman Zachary C - The present study aimed to investigate the expression and biological behaviour of the six-transmembrane epithelial antigen of the prostate 1 (STEAP1) in oral squamous cell carcinoma (OSCC), and to further analyse its underlying mechanisms. - Source: PubMed
Jin KuangyuLiu ShitongJin HuiZhang DongLu RunzeWang Wei - Lu-PSMA-617 represents a transformative treatment for metastatic castration-resistant prostate cancer (mCRPC), yet biomarkers of benefit beyond prostate-specific membrane antigen positron emission tomography (PSMA-PET) imaging remain lacking. Here, we present findings from a prospective study of 100 mCRPC patients receiving Lu-PSMA-617, using shotgun proteomics to profile plasma-derived extracellular vesicle (EV) proteins alongside PSMA-positive circulating tumor cell (CTC) enumeration. We identify 5,137 EV-derived proteins, including the cell-surface targets PSMA, B7-H3, Trop-2, and STEAP1, with high levels of these proteins associating with worse overall survival (OS). All four EV proteins positively correlate with molecular tumor volume on PSMA-PET imaging, serum PSA, and serum alkaline phosphatase. CTC subpopulations, including PSMA+/EpCAM+ and PSMA-/EpCAM+ cells, associate with worse progression-free survival (PFS) and OS. Pathway analysis reveals that p53 upregulation associates with poor PFS and OS, while an activated E2F pathway unexpectedly portends better PFS and OS. These findings support the integration of liquid biopsy proteomics into biomarker-driven mCRPC trials to improve patient stratification. - Source: PubMed
Publication date: 2026/04/20
Arafa Ali TBoytim EllaLudwig Megan LKollitz LilyYang TianzhongStorey Kathleen MBloom StuartJha GautamOkazaki IanRyan Charles JZorko Nicholas ASteinberger DanielCayci ZuzanZhao YingchunVillalta Peter WDehm Scott MHwang Justin HDrake Justin MAntonarakis Emmanuel S - T-cell-engaging bispecific antibodies (TCEs) have transformed haematological malignancy treatment (blinatumomab > 40% complete remission), yet solid tumour efficacy remains limited (<15% response rates) due to antigen heterogeneity, immunosuppressive microenvironments, and T-cell dysfunction. Systematic molecular engineering, biomarker-driven patient selection, and rational tumour microenvironment modulation are now collectively transforming TCEs from experimental agents into an adaptable platform therapy for solid tumours. - Source: PubMed
Publication date: 2026/03/27
Zeyaullah MdAlShahrani Abdullah MKhan Mohammad SuhailAhmad Md FaruqueAltijani Abdelrhman A GMohamed Awad Osman AbdallaHummad HythamMohieldin AliAhmad S Rehan - T-cell engagers (TCEs) are a diverse class of bispecific and multispecific molecules that co-bind CD3 on T cells and tumor-associated antigens to form an immune synapse and induce targeted T-cell-mediated cytotoxicity. While TCEs have demonstrated remarkable efficacy in hematologic malignancies, translation into solid tumors has been more challenging. Recent advances seen with tebentafusp in metastatic uveal melanoma and tarlatamab in small-cell lung cancer have validated the approach and driven a rapidly expanding pipeline targeting other tumor associated antigens such as STEAP1, MUC16, and PRAME among others. Unique challenges in solid tumors include antigen heterogeneity and density thresholds, on-target/off-tumor toxicities, and physical and immunologic barriers within the tumor microenvironment. To address these, next-generation engineering strategies, such as half-life extension, protease- or context-dependent masking, multispecificity, and "armed" constructs incorporating cytokine or co-stimulatory payloads, are being developed to enhance intratumoral activity while limiting systemic toxicities. Combination regimens with checkpoint blockade, chemotherapy, targeted therapies, and oncolytic platforms are also being actively investigated to overcome immune resistance and improve durability of response. Collectively, next-generation TCEs guided by rational target selection, context-dependent activation, and biomarker-driven patient stratification, are poised to broaden the reach of immunotherapy in solid tumors. In this review, we synthesize the recent advances that aim to expand the therapeutic window of TCEs for the treatment of solid tumors. - Source: PubMed
Garcia-Lorenzo EstherDorta MiriamDoger BernardPedregal ManuelMoreno Victor