TROP2 _ TACSTD2 Antibody
- Known as:
- TROP2 _ TACSTD2 Antibody
- Catalog number:
- 10428-MM01
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TROP2 _ TACSTD2 Antibody
Related genes to: TROP2 _ TACSTD2 Antibody
- Gene:
- TACSTD2 NIH gene
- Name:
- tumor associated calcium signal transducer 2
- Previous symbol:
- M1S1
- Synonyms:
- TROP2, GA733-1, EGP-1
- Chromosome:
- 1p32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-11-20
- Date modifiied:
- 2019-03-01
Related products to: TROP2 _ TACSTD2 Antibody
Related articles to: TROP2 _ TACSTD2 Antibody
- High-grade serous carcinoma (HGSC) is a remarkably heterogeneous tumor. The purpose of this study was to directly compare the reproducibility of transcriptomic profiles and biologically relevant molecular features across two spatial transcriptomics platforms-GeoMx Digital Spatial Profiler (GeoMx) and Visium Spatial Gene Expression (Visium) using AI-defined tumor regions associated with clinical outcome. - Source: PubMed
Publication date: 2026/05/15
Youssef OmarSelander LarsZheng ShuyuCsellar LillaHänninen SatuTang JingCarpén OlliLaury Anna Ray - Targeted therapy for advanced colorectal cancer (CRC) remains a significant unmet clinical need. Here, we investigate the mechanism of the anti-TROP2 antibody-drug conjugate IMMU132, delivering SN-38 to induce TOP1-mediated DNA damage and cytotoxicity. We further discover that it concurrently suppresses the PERK-eIF2α-ATF4 axis of the unfolded protein response, a key adaptive survival pathway activated by therapy-induced endoplasmic reticulum (ER) stress. This dual action of direct killing and stress adaptation disruption may dismantle a key resistance mechanism. Furthermore, combining IMMU132 with the PERK inhibitor GSK2606414 yields potent synergy across various CRC preclinical models. Mechanistically, this synergy stems from the enhanced suppression of ER stress and the oncogenic Wnt/β-catenin pathway. Thus, our findings reveal that co-targeting the DNA damage response, the PERK pathway, and the Wnt/β-catenin pathway is a promising strategy to overcome resistance to TROP2-directed antibody-drug conjugates (ADCs) in advanced CRC, providing a rational framework for combination therapies. - Source: PubMed
Publication date: 2026/04/23
Liu JieLi MeiHuang JianmingXia YujieJiang GuanfengZhang Hong'anYang JiaxinJiang MingfengLiu YalanLuo YilunWang LiefengZhang Shuyong - Antibody-drug conjugates (ADCs) and bispecific antibodies (BiAbs) are emerging treatments for small cell lung cancer (SCLC). However, optimal patient selection remains unclear. Delta-like ligand 3 (DLL3) is a promising therapeutic target, but its clinical utility is not fully established, and data on other targetable proteins such as trophoblast cell-surface antigen 2 (TROP2) and B7-H3 remain limited. To our knowledge, no prior study has assessed multiple therapeutic targets within the same patient before and after treatment. This study examined changes in DLL3 and other targets in de novo and transformed SCLC. - Source: PubMed
Publication date: 2026/04/17
Murata SaoriKashima JumpeiHorinouchi HidehitoKishikawa SatsukiMasuda KenShinno YukiOkuma YusukeYoshida TatsuyaGoto YasushiYamamoto NoboruWatanabe Shun-IchiMatsumoto YujiOkuma KaeYatabe Yasushi - Acquired resistance limits the therapeutic efficacy of KRAS-MAPK inhibitors in pancreatic ductal adenocarcinoma (PDAC). As transcriptional plasticity and epithelial-to-mesenchymal transition (EMT) have been implicated in resistance, we sought to study the molecular mechanisms driving these changes to uncover actionable vulnerabilities. Sustained KRAS-MAPK inhibition induced interferon and NF-κB signaling and promoted cell state change mimicking an EMT state associated with drug resistance. Network analysis identified the interferon-inducible E3 ubiquitin ligase TRIM22 as a central regulator of this response. Mechanistically, TRIM22 promoted proteasomal degradation of IκBα, resulting in sustained NF-κB and EMT program activation that coincided with a basal-like transcriptional cell state. TRIM22 expression was driven by IRF1 and IRF9 following relief of ERK-mediated transcriptional repression during pathway inhibition. EMT induction was accompanied by marked upregulation of TROP2 (TACSTD2), an NF-κB target gene enriched in basal-like PDAC cell states. Combining TROP2-directed antibody-drug conjugate sacituzumab govitecan with KRAS or ERK inhibitors significantly suppressed PDAC tumor growth in xenograft models. Overall, prolonged KRAS-MAPK inhibition activates an interferon-TRIM22-NF-κB axis that drives EMT and therapeutic resistance in PDAC, while revealing TROP2 as a clinically actionable vulnerability to overcome acquired resistance. - Source: PubMed
Publication date: 2026/04/20
Bulle AshenafiChen YaliLi HuapingChen Timothy Hung-PoKhawar Iftikhar AliLi LinWang YuLiu PengSomani Vikas KumarKurupi RichardGeng YutongPereye Ofejiro BlessingBansod SapanaLe Son BRuzinova Marianna BTran David DLim Kian-Huat - Concordance of NECTIN-4 gene and protein expression and clinic-pathologic associations in matched bladder cancer (BC) triplets, defined as histological specimens from transurethral resection of the bladder (TUR-B), radical cystectomy (RC), and lymphadenectomy (LA) from the same patient, remains unknown. With Enfortumab Vedotin (EV) potentially moving into earlier treatment settings, understanding expression of NECTIN-4 and other targets in archival tissue samples is important. This study characterized protein expression of NECTIN-4 and gene expression of NECTIN4, TACSTD2, ERBB2, PD-L1 and PD1 in matched BC triplet specimens and correlated findings with survival endpoints. - Source: PubMed
Publication date: 2026/04/14
Uysal DanielReible BrunoWildner LukasSteidler AnnetteStöth ManuelWessels FrederikNientiedt MalinWorst Thomas StefanErben PhilippEgen LuisaNitschke KatjaBrochhausen ChristophMichel Maurice StephanNuhn PhilippKowalewski Karl-Friedrich