CDC20B antibody
- Known as:
- CDC20B (anti-)
- Catalog number:
- orb100634
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CDC20B antibody
Related genes to: CDC20B antibody
- Gene:
- CDC20B NIH gene
- Name:
- cell division cycle 20B
- Previous symbol:
- -
- Synonyms:
- FLJ37927
- Chromosome:
- 5q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-07
- Date modifiied:
- 2019-04-05
Related products to: CDC20B antibody
Related articles to: CDC20B antibody
- Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) presenting with disseminated cutaneous involvement represents an aggressive disease subset with poor response to conventional chemotherapy and dismal prognosis. The tissue-specific molecular mechanisms driving cutaneous aggression remain poorly characterized at single-cell resolution. Here we report a 67-year-old male PTCL-NOS patient with hypertension and coronary artery disease history, presenting with generalized cutaneous nodules and rapid progression despite multi-line chemotherapy. Single-cell RNA sequencing (scRNA-seq) performed on paired skin lesions and peripheral blood at diagnosis revealed striking microenvironmental dichotomy: skin-resident malignant T cells exhibited hyperproliferative phenotypes (high CDC20B, HIST1H3B, MKI67+), activation of NF-κB and IL-17 signaling, and extensive crosstalk with endothelial cells; conversely, blood-derived lymphoma cells displayed immune evasion signatures and metabolic stress markers. Copy number variation analysis confirmed clonal expansion across both compartments with distinct tissue-specific transcriptional programs. Despite CHOP, CHOEP, DA-EPOCH, and AC-CHOP (azacitidine plus chidamide) regimens, the patient experienced primary refractory disease and died 6 months from diagnosis following COVID-19 superinfection. To our knowledge, this is the first case reporting single-cell transcriptomic comparison of skin versus blood compartments in PTCL-NOS, revealing how cutaneous microenvironment sculpts aggressive malignant phenotypes and providing potential targets for compartment-specific therapy. - Source: PubMed
Publication date: 2026/05/26
Zhang ShuchengLi ZhuqingLin YangSun XiaoyueQiao MengSi Xiaoqing - Gastric cancer (GC) and breast cancer (BC) are among the most common malignancies worldwide, with significant mortality rates despite advances in diagnosis and treatment. Genetic variants in the hypoxia-inducible factor (HIF) pathway, which plays an important role in tumor microenvironment adaptation, have emerged as potential contributors to cancer susceptibility and prognosis. Our study investigates the role of HIF pathway genetic variants in GC and BC among the Mizo population, an indigenous group living at high altitudes in north-eastern India. In addition, the EGLN1 c.12C > G (rs186996510) "Tibetan allele" was evaluated within this population-specific genetic framework. Whole-exome sequencing data from 74 cancer patients (59 GC, 15 BC) and 27 healthy controls were analyzed. Variants underwent quality filtering, in silico functional annotation, and association analyses including odds ratio (OR) and hazard ratio (HR) estimation. The EGLN1 Tibetan allele was prevalent in 29.62% of healthy Mizo controls and demonstrated a reduced association trend with GC (OR = 0.671) and BC (OR = 0.364). Common variants in CA9 (rs2071676), CDC20B (rs444527) and CDH11 (rs35195) showed associations for both cancers, with CA9 rs2071676 showing an association with poorer survival (HR = 4.097, p = 0.0139). Rare variants such as CA9 (rs77984049) and ABCB1 (rs2032582) also showed high ORs, particularly in GC. Overall, these findings provide exploratory, population-specific insight into HIF pathway genetic variation within a high-altitude indigenous population and contribute to the understanding of population-based cancer associations. Further investigation in larger cohorts with comprehensive clinical modeling and functional validation is warranted. - Source: PubMed
Publication date: 2026/04/24
Krishnasamy VigneshRalte LalengkimiLalhruaizela SamuelRalte Ruby ZothankimiVanlalpeka HarveyLalrinpuia BenjaminKumar Nachimuthu Senthil - The quality of hatching eggs and their hatchability are key factors affecting the production efficiency of breeding flocks. The quality of hatching eggs is commonly graded directly based on the eggshell quality. Our study monitored the eggshell quality and hatchability in Hy-Line Brown laying hens aged 23 to 73 weeks, to determine core eigenvectors that influence hatchability from multiple eggshell quality indicators. Hatching performance indicators, including fertile egg rate, hatchability of fertile eggs and hatchability of eggs set, were found to exhibit a trend of low level in early laying stage, and increased to a peak at 39 weeks of age during mid-laying stage, followed by a continuous decline in late laying stage. Similar trend also observed in eggshell quality indicators, such as eggshell strength, eggshell thickness, eggshell weight, eggshell rate and eggshell microstructure. Canonical correlation analysis revealed egg weight, equatorial eggshell thickness and pointed end eggshell thickness showed strong correlation with the main indicators affecting hatchability of fertile eggs (r = 0.987, P = 0.013). Further, shell gland RNA sequencing was applied to explore candidate genes or pathways that might affect eggshell thickness. Short time series expression miner (STEM) analysis identified several key genes (ATP2C2, CA9, CDC20B, WNT4, WNT7A and CACNB3) that were enriched in pathways related to calcium signaling, bicarbonate metabolism, vesicle transport and Wnt signaling, thereby highlighting their potential critical roles in eggshell thickness regulation. Our findings preliminarily delineate the relationship between easily measurable eggshell quality and hatchability, which provides a theoretical basis and candidate gene targets for improving hatching performance. - Source: PubMed
Publication date: 2026/01/18
Zhang ChenxiCao RanranWei SiqinWang ShuCai ZhaoShi JunlaiLei YanruWang KejunTian YadongSun GuirongKang XiangtaoLi Wenting - Aromatase inhibitors (AI) are drugs that are widely used in treating estrogen receptor (ER)-positive breast cancer patients. Drug resistance is a major obstacle to aromatase inhibition therapy. There are diverse reasons behind acquired AI resistance. This study aims at identifying the plausible cause of acquired AI resistance in patients administered with non-steroidal AIs (anastrozole and letrozole). We used genomic, transcriptomic, epigenetic, and mutation data of breast invasive carcinoma from The Cancer Genomic Atlas database. The data was then separated into sensitive and resistant sets based on patients' responsiveness to the non-steroidal AIs. A sensitive set of 150 patients and a resistant set of 172 patients were included for the study. These data were collectively analyzed to probe into the factors that might be responsible for AI resistance. We identified 17 differentially regulated genes (DEGs) among the two groups. Then, methylation, mutation, miRNA, copy number variation, and pathway analyses were performed for these DEGs. The top mutated genes (FGFR3, CDKN2A, RNF208, MAPK4, MAPK15, HSD3B1, CRYBB2, CDC20B, TP53TG5, and MAPK8IP3) were predicted. We also identified a key miRNA - hsa-mir-1264 regulating the expression of CDC20B. Pathway analysis revealed HSD3B1 to be involved in estrogen biosynthesis. This study reveals the involvement of key genes that might be associated with the development of AI resistance in ER-positive breast cancers and hence may act as a potential prognostic and diagnostic biomarker for these patients. - Source: PubMed
Publication date: 2023/06/30
Sadasivam KirithikaManoharan Jeevitha PriyaPalanisamy HemaVidyalakshmi Subramanian - Allergic inflammation affects the epithelial cell populations resulting in goblet cell hyperplasia and decreased ciliated cells. Recent advances in single-cell RNA sequencing (scRNAseq) have enabled the identification of new cell subtypes and genomic features of single cells. In this study, we aimed to investigate the effect of allergic inflammation in nasal epithelial cell transcriptomes at the single-cell level. - Source: PubMed
Publication date: 2023/03/18
Cho Hyung-JuChung Youn WookMoon SungminSeo Ju HeeKang MiranNam Jae SungLee Sang-NamKim Chang-HoonChoi Augustine M KYoon Joo-Heon