Anti-Mouse CD66a (CEACAM1) PE 100 ug
- Known as:
- Antibody toMouse CD66a (CEACAM1) PE 100 ug
- Catalog number:
- 12-0661-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD66a (CEACAM1) 100
Related genes to: Anti-Mouse CD66a (CEACAM1) PE 100 ug
- Gene:
- CEACAM1 NIH gene
- Name:
- carcinoembryonic antigen related cell adhesion molecule 1
- Previous symbol:
- BGP
- Synonyms:
- BGP1, CD66a
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-01-14
Related products to: Anti-Mouse CD66a (CEACAM1) PE 100 ug
Related articles to: Anti-Mouse CD66a (CEACAM1) PE 100 ug
- HER2 expression is described along a biological continuum from null to positive and serves as a critical biomarker for therapeutic guidance in breast cancer (BC). While HER2-low and ultra-low categories have emerged as actionable targets for antibody-drug conjugates (ADCs) in female BC, their molecular and immune characteristics remain largely unexplored in male breast cancer. - Source: PubMed
Publication date: 2026/08/12
Trapani DarioDeshmukh Sachin KumarWu SharonXiu JoanneJayachandran PriyaGandhi ShipraLin Nancy UCurigliano GiuseppeSpanheimer Philip MAbravanel Daniel LRadovich MilanLustberg MaryamGraff Stephanie LSledge George WTolaney Sara MLeone José P - Despite advancements in immune checkpoint blockade (ICB) therapy, breast cancer shows limited response to anti-PD1/PD-L1 treatments, emphasizing the need for alternative ICB targets. Here, we reveal that endocrine therapeutics, specifically tamoxifen, create an immunosuppressive yet primed tumor microenvironment conducive to anti-TIM3 immunotherapy. Tamoxifen induces mitochondrial DNA damage and disrupts the RACK7/KDM5C histone demethylase complex, resulting in STING accumulation and activation of the type I interferon (IFN-I) pathway, thereby fostering an immunogenic tumor microenvironment. However, tamoxifen also elevates CEACAM1 expression via a RACK7/KDM5C axis, driving T-cell exhaustion and limiting tumor elimination. This dual effect of tamoxifen - promoting STING-mediated immunogenicity while upregulating CEACAM1 expression - shapes the tumor-immune microenvironment in both ER-positive and ER-negative tumors. Notably, combining anti-TIM3 immunotherapy with tamoxifen mitigates its immunosuppressive effects, potentially enhancing ICB efficacy. Our findings highlight the therapeutic potential of integrating anti-TIM3 immunotherapy with endocrine therapy to improve outcomes for breast cancer patients. - Source: PubMed
Publication date: 2026/08/17
Aberin Marvin Angelo ESingh SaurabhChatterjee SoumyaSui Guang-ZhiWang Yi-FuLu Ya-TingLee Yu-LingLin Kun-YuanKhag JoyLiu Ta-YuChang Shao-HanCheung Wai-MuiHong Hsiao-ChinHsu Ren-JunShen Chen-YangLi Chia-WeiYang Weng-LangChang Yao-MingChen Shih-YuGuha ChandanWang Shu-Ping - T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy characterized by aberrant epigenetic regulation. Although SET domain-containing 5 (SETD5) is structurally classified as a member of the histone methyltransferase family, it lacks canonical methyltransferase activity and functions primarily through nonenzymatic mechanisms. While recognized as a modulator in normal hematopoiesis, the role of SETD5 in T-ALL remains undefined. Here, we show that SETD5 contributes to efficient T-ALL initiation and progression in the models examined. Using ICN1-driven murine T-ALL models (Vav-Cre;Setd5 and Mx1-Cre;Setd5), we show that genetic ablation of Setd5 impairs efficient leukemia initiation. In transplantation assays, Setd5 depletion reduces leukemia burden, prolongs survival, and impairs leukemic infiltration into the spleen, liver, and thymus. Mechanistically, transcriptomic profiling of Setd5-deficient CD3 T-ALL cells reveals selective repression of transcriptional programs governing cell migration, motility, and cytoskeletal organization. Key regulators of actin cytoskeleton remodeling and extracellular matrix interaction-including Plxnb2, Mmp14, Ceacam1, and Clstn1-are among the most downregulated genes, as validated by RT-qPCR. Furthermore, SETD5 knockdown in the human T-ALL cell lines Jurkat and MOLT-4 results in a marked reduction in proliferation and migration. Our findings demonstrate that SETD5 contributes to T-ALL progression by regulating transcriptional programs that contribute to leukemic cell migration and infiltration, suggesting that SETD5-associated transcriptional programs warrant further investigation as potential vulnerabilities in T-ALL. - Source: PubMed
Publication date: 2026/08/13
Hao MingyueBian YujieLi MengkeLiu TongLi HaoyuanCao MutianHe YifeiCong LizhenLing YuanyiGu ShilongLi WantingZhang MingyueYuan WeipingChu Yajing - The heterogeneity in associations between circulating fatty acids (FA) and mortality remained underexplored. Proteomics can profile the human physiological status. This study aimed to estimate interactions between FA and proteins in relation to mortality. We randomly divided 30,190 UK Biobank participants into train and test datasets. Multivariable Cox regression was utilized to assess the associations between FA and all-cause mortality and to explore proteome-wide interactions of FA in relation to mortality. Subgroup analyses were conducted to examine heterogeneity across varied protein levels. We also explored interactions between proteins and FA in relation to cause-specific mortality. We documented 3,345 deaths during 13.9 years of follow-up. MUFA-pct, Non-LA Omega-6 pct, Omega-6/Omega-3 ratio and SFA-pct were positively associated with all-cause mortality, while PUFA-pct, DHA-pct, LA-pct, and Omega-3-pct were negatively associated. We identified several robust interactions of proteins with MUFA-pct (n = 3), Omega-3-pct (n = 4), and Omega-6/Omega-3 ratio (n = 2). In subgroup analyses, individuals with high-level TNFRSF1B, MMP10, and CRHBP had higher all-cause mortality risks associated with MUFA-pct, while protective associations between Omega-3-pct and all-cause mortality were stronger among individuals with high-level TSPAN8, PLAU, ITGA5, and CEACAM1. Moreover, participants with high-level TSPAN8 and PLAU had higher risks of all-cause mortality with Omega-6/Omega-3 ratio. For cause-specific mortality, interaction and subgroup results were largely consistent with those of all-cause mortality. Our findings can provide new insights into heterogeneity in FA-mortality associations and highlight potential protein targets for personalized interventions across individuals with different physiological status. - Source: PubMed
Publication date: 2026/08/10
Qiao ZiyanWang XinruTao ChengzheLiao SijingLu JiaweiYuan YitingXu QiaoqiaoFan YunWang XuLu Chuncheng - Patients with gastric cancer (GC) and peritoneal metastasis (PM) have poor prognoses due to drug resistance and metastatic relapse. The mechanism underlying PM recurrence remains unclear. - Source: PubMed
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