BCAS1
- Known as:
- BCAS1
- Catalog number:
- 002452A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BCAS1
Related genes to: BCAS1
- Gene:
- BCAS1 NIH gene
- Name:
- breast carcinoma amplified sequence 1
- Previous symbol:
- -
- Synonyms:
- NABC1, AIBC1
- Chromosome:
- 20q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-12
- Date modifiied:
- 2014-11-19
Related products to: BCAS1
Related articles to: BCAS1
- Intrahepatic cholangiocarcinoma (iCCA) is histologically classified into the small duct type (SDT) and large duct type (LDT), although their morphological differential diagnosis can be difficult. We aimed to identify new immunohistochemical markers to classify SDT and LDT with high sensitivity and specificity. We compared the gene expression profiles of SDT and LDT using cases obtained from our institution (n = 8) and The Cancer Genome Atlas database (n = 28). We selected the candidate molecules that were up-regulated in LDT, were minimally or not expressed in SDT, and had specific and available antibodies suitable for immunohistochemistry. We finally selected ST6 N-acetylgalactosaminide alpha-2,6-sialyltransferase 1 (ST6GalNAc1), Breast carcinoma amplified sequence-1 (BCAS-1), and Olfactomedin 4 (OLFM4), which were expressed in 100%, 100%, and 98.3% of 58 LDT cases, respectively. ST6GalNAc1 was expressed in 3.8% of 52 SDT cases, whereas BCAS-1 and OLFM4 were expressed in 48.1% and 34.6% of SDT cases, respectively. ST6GalNAc1 was also expressed in intraductal papillary neoplasm of the bile duct (100%, n = 17) and only the adenocarcinoma component corresponding to LDT among the combined hepatocellular-cholangiocarcinoma cases (100%), but not in hepatocellular carcinoma (n = 26). In small biopsy specimens, ST6GalNAc1 was expressed in 100% of LDT (n = 18) and 12.5% of SDT (n = 16) samples. ST6GalNAc1 expression was associated with significantly shorter overall survival (P = 0.012) and remained significant after adjustment for tumor subtype (hazard ratio 2.595; 95% confidence interval, 1.433-4.699; P = 0.002). ST6GalNAc1 is useful for iCCA subtype identification with high sensitivity and specificity, showing promise to become a more powerful tool when combined with other markers. - Source: PubMed
Publication date: 2026/08/14
Umino RyosukeIshimoto-Namiki UtakoNaito ChieMizui TakahiroMiyata AkinoriNara SatoshiEsaki MinoruHiraoka Nobuyoshi - Trogocytosis, the contact-dependent exchange of membrane fragments between cells, is emerging as a critical regulator of tumor biology, yet its specific role in bladder cancer (BLCA) remains largely unexplored. In this study, we systematically characterized the trogocytosis-associated transcriptional landscape in BLCA and developed a robust prognostic framework, the Tro-score, based on five key genes (CLSTN2, CD109, KANK4, CTSE, and BCAS1). Validated across multiple independent cohorts, a high Tro-score was significantly associated with poor overall survival and a distinct immunosuppressive microenvironment characterized by the enrichment of Tregs, M2 macrophages, and myeloid-derived suppressor cells. Notably, the Tro-score served as a potent predictor of immunotherapy outcomes, with high-score patients exhibiting increased T-cell dysfunction and reduced clinical responsiveness to immune checkpoint inhibitors. Mechanistically, we pinpointed CD109 as a core molecular correlate of this immunosuppressive landscape through integrative analysis. To biologically validate these computational findings, we conducted extensive in vitro and in vivo experiments. Strikingly, in murine models receiving anti-PD-1 therapy and co-culture systems, we demonstrated that CD109 overexpression not only promotes tumor proliferation and invasion but also is associated with inhibited immune cell chemotaxis and CD8 T-cell cytotoxicity. These findings raise the hypothesis that tumor cells may exploit trogocytosis-related pathways to create a bidirectional interaction network that favors immune evasion-a concept that warrants direct experimental validation in future studies. - Source: PubMed
Publication date: 2026/08/11
Liu JinhuiHu MinghuiChen JinboZu XiongbingXiao JiatongPeng JianqiaoNie ZhenyuTong Shiyu - Myelination, driven by differentiation of oligodendrocyte precursor cells, is critical for metabolic and structural support and efficient axonal signal transmission in neurons. Loss of myelin is a hallmark of multiple sclerosis and other devastating demyelinating disorders. As demyelination persists, neurons become increasingly vulnerable, leading to neurodegeneration and chronic disability. Restoring myelin through endogenous repair mechanisms offers a promising therapeutic approach to mitigate progressive neuronal loss. One key regulator of myelination is the G protein-coupled receptor 17, GPR17, whose chronic upregulation in oligodendrocyte precursor cells is commonly seen with myelin injury. In line with single-nucleus transcriptomic data showing predominant expression of GPR17 in committed oligodendrocyte precursor cells, our postmortem immunohistochemical analyses of MS patient tissue revealed a significant upregulation of GPR17+/BCAS1+ oligodendrocyte precursor cells adjacent to and in demyelinated lesions. Importantly, remyelinated lesions lacked GPR17 immunoreactivity, consistent with a model in which sustained GPR17 expression is associated with demyelination and impaired oligodendrocyte precursor cell differentiation. To test the impact of pharmacological GPR17 inhibition on remyelination, we evaluated the effects of a novel, selective GPR17 antagonist in cuprizone-induced murine demyelination models. This toxin-induced approach has been widely used to study mechanisms of de- and remyelination, in the absence of the full inflammatory complexity of demyelinating diseases such as multiple sclerosis. We show that oral treatment results in robust functional recovery consistent with remyelination, as evidenced by improved spatial memory and recovery of visual evoked potential latency delays. GPR17 antagonism also accelerated structural remyelination in the corpus callosum and optic nerve. Together, these findings support a role for pharmacological GPR17 antagonism in promoting remyelination and highlight this G protein-coupled receptor as a promising therapeutic target for demyelinating disorders. - Source: PubMed
Publication date: 2026/07/27
De Herdt DilleLefevere EvyBrouwers VéroniqueHartvig LineGeeraerts EmielHsiao Cheng-ChihChen J Q AlidaPinto RuiDuvey GuillaumeBurbidge StephenHarmeier AnjaKnuesel Irene - Cortical demyelination is a critical contributor to progressive disease in multiple sclerosis (MS). The barriers to cortical remyelination following demyelination are not fully understood, and there are no remyelinating treatments for MS. We previously took advantage of the spatial and temporal resolution of longitudinal in vivo imaging to study cortical oligodendrocyte regeneration following cuprizone-induced demyelination and found that oligodendrocyte regeneration was impaired. In this study, we investigated whether cortical reactive microglia disrupt oligodendrocyte regeneration. To do so, we used a combination of in situ RNA and immunofluorescence labeling to characterize cortical microglia reactive states following cuprizone-mediated demyelination. We then depleted cortical microglia by administering a Csf1r inhibitor during the recovery period from cuprizone and quantified oligodendrocyte recovery. We found that following cortical demyelination, deep cortical microglia change morphology, downregulate homeostatic markers (P2RY12, TMEM119), and upregulate a marker (CD68) associated with activated macrophages. These reactive changes persisted through early recovery post-cuprizone but resolved by late recovery. Depleting cortical microglia post-cuprizone restored the baseline density of deep cortical ASPA+ oligodendrocytes at early and late recovery. There were also more deep cortical BCAS1+ differentiating oligodendrocytes at early recovery when microglia were depleted, suggesting that transient deep cortical reactive microglia impair oligodendrocyte differentiation following demyelinating injury. Together, we found that cortical microglia adopt spatially restricted reactive functions after demyelination and deep cortical reactive microglia transiently reduce differentiating oligodendrocytes. A potential therapeutic strategy for progressive MS could involve targeting transiently reactive microglia at the right time and place in cortical lesions to promote oligodendrocyte regeneration. - Source: PubMed
Loo Hannah KatherineGallegos JosephMialki ChristinePerrin Gregory EMalloy ThomasOrthmann-Murphy Jennifer L - Keel bone fractures (KBF) in laying hens are a major welfare problem in the egg production industry. While housing design and nutrition are known contributing factors, the role of genetics in KBF susceptibility is not well understood. The objective of this study was to estimate the heritability of KBF susceptibility and identify associated genomic regions and candidate genes in commercial laying hens. We used KBF assessment scores derived from radiographs of 1,060 white-feathered two-way crossbred hens housed in a quasi-commercial aviary system. A log-transformation was applied to the KBF scores to normalize the data. All hens were genotyped with a 60 K SNP chip. We fit a linear mixed model with a genomic relationship matrix to estimate variance components and heritability, and conducted a genome-wide association study to identify SNPs associated with KBF. Our results showed that KBF was low to moderately heritable, with an estimated heritability of 0.08 on the original trait scale, and 0.22 on the log-transformed scale. We identified four significant or suggestive haplotype blocks on chromosomes 2 and 20 that together explained 13.2 % of the total additive genetic variance. These blocks contain several candidate genes (including BCAS1, CYP24A1, PFND4, TSHZ2, and GDF6) that have been linked to calcium and vitamin D homeostasis, skeletal development, and bone density in humans and mice. These findings support the possibility that susceptibility to KBF is determined not only by genes influencing bone strength directly, but also by genes affecting the vitamin D metabolic pathway that regulates calcium reabsorption. Finally, one of the genomic regions on chromosome 20 was in close proximity to QTL that have previously been associated with egg production levels and age at sexual maturity in chickens. Overall, our findings contribute to our understanding of the genetic architecture of KBF susceptibility, its possible relationship to early egg production, and the physiological pathways that influence skeletal health in laying hens. - Source: PubMed
Publication date: 2025/11/07
Duenk PascalBovenhuis HenkWillemsen PaulineMakanjuola Bayode OPetelle Matthew BGebhardt-Henrich Sabine GBaes Christine FToscano Michael J