CD66e
- Known as:
- CD66e
- Catalog number:
- 1B-479-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD66e
Related genes to: CD66e
- Gene:
- CEACAM5 NIH gene
- Name:
- carcinoembryonic antigen related cell adhesion molecule 5
- Previous symbol:
- CEA
- Synonyms:
- CD66e
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: CD66e
Related articles to: CD66e
- Lung cancer is currently the most frequently diagnosed malignancy worldwide, accounting for approximately 12.4% of all cancers and, despite major advances in molecularly targeted therapies and immunotherapy, represents the leading cause of cancer-related mortality. In recent years, antibody-drug conjugates (ADCs) have emerged as a novel therapeutic strategy, combining the specificity of monoclonal antibodies with the potent cytotoxic activity of highly active payloads to selectively target tumor cells while limiting systemic toxicity. This narrative review summarizes the current role of ADCs in lung cancer, with particular focus on their structural components, mechanisms of action, and the biological features that determine treatment efficacy. We discuss the rationale for targeting established and emerging antigens in non-small cell and small cell lung cancer, including HER2, TROP2, c-MET, HER3, CEACAM5, DLL3, and other promising targets currently under clinical investigation. The principal mechanisms of primary and acquired resistance are also reviewed, including antigen modulation, altered intracellular trafficking, lysosomal dysfunction, drug efflux, tumor microenvironment-mediated immune suppression, and intratumor heterogeneity. In addition, we provide an overview of the safety profile of ADCs, highlighting the most clinically relevant adverse events and their underlying biological mechanisms. We also examine the evolving landscape of predictive biomarkers beyond antigen expression, including genomic, transcriptomic, proteomic, and liquid biopsy-based approaches, together with emerging spatial and single-cell technologies that may improve patient selection. Finally, we discuss future directions in the field, including novel payloads, next-generation linker technologies, bispecific ADCs, combination strategies, and personalized ADC development. Overall, ADCs are rapidly reshaping the therapeutic landscape of lung cancer. Continued optimization of drug design, biomarker-driven patient selection, and a deeper understanding of resistance mechanisms will be essential to fully realize their clinical potential. - Source: PubMed
Publication date: 2026/08/26
Paliogiannis PanagiotisFara GiorgiaZinellu AngeloFois Alessandro GiuseppePalmieri Giuseppe - This opinion paper examines a recently reported 14-biomarker plasma panel designed to predict lung cancer development and identify patients who might benefit from preventive canakinumab treatment. While stratifying patients using this panel and clinical risk factors improves the number needed to treat (NNT) from 1,000 down to 50, the strategy still faces major hurdles due to the high economic cost and systemic side effects of canakinumab, which limits clinical benefit to a tiny fraction of the treated group. A closer biochemical examination reveals that the panel's 14 markers-such as CEACAM5 (CEA) and WFDC2 (HE4)-are already well-documented in classic tumor marker literature and are notoriously non-specific, frequently becoming elevated across various malignancies. Furthermore, notable established markers like CYFRA 21-1 and CA125 are missing from the panel. Ultimately, because these markers lack organ specificity, they are not utilized for early detection. The logical next step for this field will be the development of a single multiplex assay to quantify all 14 proteins simultaneously. - Source: PubMed
Publication date: 2026/09/18
Diamandis Eleftherios P - Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) has emerged as a promising therapeutic target for antibody-drug conjugates (ADCs) in nonsquamous non-small cell lung cancer (NSCLC). However, the landscape of CEACAM5 protein expression and its association with clinicopathological features in nonsquamous NSCLC remain poorly characterized. This study represents the first comprehensive investigation to profile CEACAM5 protein expression in this specific population using a clinical-grade immunohistochemistry (IHC) assay. - Source: PubMed
Publication date: 2026/07/14
Xue Qian-QianJin YanShen Xu-XiaZheng QiangFu YaoXia Qing-XinLi Yuan - The carcinoembryonic antigen cell adhesion molecule 5 (CEACAM5) is highly overexpressed in carcinomas of different origins. Affibody molecules are non-immunoglobulin-based affinity proteins capable of in vivo recognition of cancer-associated targets. Affibody C9 was previously generated to bind selectively to CEACAM5. In an earlier in vivo study, C9 was engineered as a dimer, and the effects on the biodistribution from the addition of an N- or C-terminal-fused albumin-binding domain (ABD) were investigated using Tc labeling. The variant ABD-C9-C9 with N-terminal ABD placement (20,296 Da; affinities of 2.5 and 1.9 nM to CEACAM5 and albumin, respectively) was found to provide the most favorable biodistribution for the delivery of cytotoxic payloads. In this study, we tested the hypothesis that ABD-C9-C9 labeled with a cytotoxic radionuclide would be suitable for targeted radiopharmaceutical therapy (RPT). ABD-C9-C9, labeled with the β-emitting radionuclide Lu via DOTA or DOTAGA chelators, was evaluated. CEACAM5-positive (BxPC3, LS174T) and CEACAM5-negative (HT-29) cell lines were used to assess binding specificity, kinetics, and internalization in vitro. The biodistribution of [Lu]Lu-ABD-C9-C9-DOTA and [Lu]Lu-ABD-C9-C9-DOTAGA was compared in BALB/c mice with BxPC3 xenografts. The biodistribution of [Lu]Lu-ABD-C9-C9-DOTA was measured for dosimetry calculation. Modeling was performed to maximize tumor control probability. The effect of a single injection of 12 MBq of [Lu]Lu-ABD-C9-C9-DOTA on the growth of BxPC3 xenografts was evaluated. In vitro, both [Lu]Lu-ABD-C9-C9-DOTA and [Lu]Lu-ABD-C9-C9-DOTAGA constructs demonstrated saturable, CEACAM5-dependent binding, with a minor difference in internalization rate (∼40% internalization after 24 h). In vivo, [Lu]Lu-ABD-C9-C9-DOTA showed significantly lower kidney uptake than the DOTAGA-conjugated variant. [Lu]Lu-ABD-C9-C9-DOTA demonstrated a significantly reduced renal uptake (14-fold, 4 h postinjection) and an increased uptake in BxPC3 xenografts (3.6-fold) compared with a [Lu]Lu-C9-C9-DOTA reference construct without ABD This experimental RPT study demonstrated a significant increase in the survival of tumor-bearing mice and mild, transient toxicity. ABD-C9-C9-DOTA is a promising candidate for the development of targeted RPT of CEACAM5-expressing tumors. - Source: PubMed
Publication date: 2026/09/10
Li RuonanPapalanis EleftheriosOroujeni MaryamBezverkhniaia EkaterinaKonijnenberg MarkOrlova AnnaNygren Per-ÅkeGräslund TorbjörnTolmachev Vladimir - Pancreatic adenocarcinoma (PAAD) remains one of the most lethal cancers, largely due to the lack of reliable diagnostic biomarkers. Through integrative transcriptomic and proteomic analyses, we evaluated a four-gene signature comprising CLDN18, CEACAM5, FUT3, and FUT6, capable of distinguishing tumor from normal pancreatic tissue with high accuracy (AUC > 0.80). Among these genes, CLDN18 emerged as a structurally distinct and underappreciated biomarker, showing strong transcriptional association with CEACAM5 and the glycosyltransferases FUT3/FUT6, which are involved in the biosynthesis of CA19.9, the current clinical standard for PAAD diagnosis. Functional enrichment analyses indicated that CLDN18 is involved in pathways related to epithelial polarity, tight junction organization, and extracellular vesicle (EVs)-mediated transport. Machine learning models demonstrated robust classification performance, with CLDN18 consistently ranking among the top predictive features. In vitro validation confirmed the overexpression of CLDN18 in pancreatic cancer cells compared with non-tumoral pancreatic epithelial cells and its selective enrichment in tumor-derived EVs. Furthermore, by immunohistochemical evaluation of primary pancreatic adenocarcinomas, we demonstrated that CLDN18 was indeed overexpressed in tumor samples compared to corresponding normal tissues. Overall, these findings underscore the value of integrating junctional, glycosylation-related, and antigenic markers into multi-marker classifiers to improve diagnostic accuracy. Given its consistent overexpression, prognostic relevance, and compatibility with emerging immunotherapeutic strategies, CLDN18 represents a promising addition to current biomarker panels and a potential target for molecular imaging and drug development in PAAD. - Source: PubMed
Publication date: 2026/09/03
Santoro JessieAgnello LisaColacino AndreaLeone IlariaVerísimo-García JoelViscusi EleonoraLaudati StefanoIannaci GiuseppeD'Antonio AntonioGonzález-Fernández ÁfricaDe Falco ValentinaMaietta Immacolata