Human ErbB2 _ CD340 Protein Vector: HEK293
- Known as:
- Human ErbB2 _ CD340 Protein Vector: HEK293
- Catalog number:
- 10064-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human ErbB2 _ CD340 Protein Vector: HEK293
Related genes to: Human ErbB2 _ CD340 Protein Vector: HEK293
- Gene:
- ERBB2 NIH gene
- Name:
- erb-b2 receptor tyrosine kinase 2
- Previous symbol:
- NGL
- Synonyms:
- NEU, HER-2, CD340, HER2
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: Human ErbB2 _ CD340 Protein Vector: HEK293
Related articles to: Human ErbB2 _ CD340 Protein Vector: HEK293
- Pancreatic ductal adenocarcinoma carries a poor prognosis, with the worst outcomes observed in UICC stage IV disease characterized by hepatic-and less frequently pulmonary-metastases. Considerable genetic heterogeneity, including mutations in , , and , enables the development of individualized therapeutic strategies. We report here a patient with - and -wild-type but mutant and disease who achieved apparent remission of hepatic metastases. - Source: PubMed
Publication date: 2026/09/03
Kolb HubertHartwig WernerBeyna TorstenAuf der Horst DanielaKempf KerstinMartin StephanStruse-Soll KerstinDommach Markus - There is an ongoing need for first-line (1L) chemotherapies for metastatic HER2-negative breast cancer. This study evaluated the efficacy and safety profile of the dose-expansion part 6 of Study 114 in patients receiving E7389-LF as a 1L chemotherapy for metastatic/advanced HER2-negative breast cancer. - Source: PubMed
Publication date: 2026/09/17
Ishiguro HiroshiMiyoshi YasuoYasojima HiroyukiWatanabe JunichiroTakano ToshimiShimomura AkihikoTokunaga ErikoMukohara ToruNaoi YasutoMatsuoka DaikoOkumura ShioriOtake YoheiSuzuki TakuyaTakase TakaoSemba TaroZhao ZimingYonemori Kan - A novel entity of ERBB2/ERBB3-mutated S100/SOX10-positive uterine sarcoma has recently been proposed. However, the detailed clinicopathologic spectrum and molecular features of this emerging entity remain to be further elucidated. Here, we describe 6 cases of ERBB2-altered uterine sarcoma. The patients ranged from 41 to 65 years old (median, 48 years). Most tumors (5/6; 83.3%) were centered in the cervical stroma. An infiltrative, interdigitating border was a consistent finding, with neoplastic cells intimately admixed with entrapped pre-existing smooth muscle fascicles. The tumor exhibits alternating hypercellular and hypocellular areas. Most cases (5/6; 83.3%) showed a predominantly spindled architecture arranged in a fascicular, herringbone, or storiform pattern. The tumor cells typically showed mild-to-moderate cytologic atypia, scant cytoplasm, and a brisk mitotic count (median: 28.5/10 HPFs). Intriguingly, the remaining case (1/6; 16.7%) harbored a concurrent TP53 nonsense mutation and exhibited a predominantly epithelioid architecture with marked cytological atypia. Notably, another distinctive finding was the presence of neoplastic multinucleated giant cells exhibiting a characteristic floret-like nuclear arrangement in all cases. The background stroma exhibited focal myxoid change, hyalinization, and variable inflammatory infiltrates. All cases exhibited strong and diffuse positivity for S100 and SOX10. Next-generation sequencing revealed a highly recurrent molecular signature characterized by universal oncogenic ERBB2 missense mutations (including the canonical V777L variant as well as other activating mutations) and CDKN2A copy number loss, frequently accompanied by inactivating ATRX mutations (66.7%), CDKN2B (66.7%), MTAP (50.0%) copy number loss, ERBB3 mutations (50.0%), and concurrent ERBB2 amplification (33.3%). Of the 6 patients, 1 (harboring a TP53 nonsense mutation) had bone metastasis at diagnosis and was lost to follow-up, 2 progressed at 3.5 and 5 months (one death at 10 months), and 3 remained alive with no evidence of disease at 10-12 months. Our results support this emerging entity as a distinct, aggressive gynecologic mesenchymal neoplasm harboring actionable ERBB2 alterations. - Source: PubMed
Publication date: 2026/09/17
Lyu ZhuoyaoHan WenqiLi HuiLiang XiaolongSu XinWu Huanwen - Gastric cancer (GC) is currently the fifth most common cancer globally, often driven by dysregulation of tumor suppressor pathways. While individual studies on genetic variations of proteins are common, a comprehensive systems-level analysis of proteins regulating GC pathways showing both expression dysregulation and high mutation frequency remains unexplored. Therefore, our study aimed to identify critical genes and their pathogenic variations disrupting the tumor-suppressive capacity of the GC pathway. We employed a deep learning-based graph neural network model to identify genes exhibiting both dysregulated expression and high mutation propensity in GC. Key tumor suppressor proteins (TP53, CDH1, and APC), their genetic variants, and molecular components were subjected to in-depth computational analyses, including evolutionary conservation profiling, biophysical energetics assessment, and unsupervised machine learning for conformational change detection. Variants were validated from the cBioPortal database and patient survival data. Our deep learning model demonstrated exceptional performance (MSE: 0.00482 ± 0.00023 to 0.07108 ± 0.00437; R²: 0.85098 ± 0.01903 to 0.85899 ± 0.01987; AUC-ROC: 0.93095 ± 0.01758 to 0.93309 ± 0.00725) and identified 1,886 genes exhibiting both differential expression and mutation propensity. Graph neural network analysis revealed TP53 as the most prominent hub gene (47.6% mutation frequency), followed by ERBB2 (8.8%), CDH1 (8.2%), and APC (6.8%). Variants validation from cBioPortal confirmed the association of GC with 36 missense SNPs that critically affect post-translational modification (methylation and phosphorylation) sites and 60 nonsense SNPs. Furthermore, TP53, CDH1, and APC were significantly upregulated in GC tissues and associated with altered patient survival (p < 0.05). The transcription factor EZH2 and miRNA miR-129-5p were identified as key regulatory elements affecting all three tumor suppressors. Additionally, mutations trigger dysregulation of multiple common oncogenes, including CCNE1/2 and FGFR2. This systems-level analysis provides a molecular framework demonstrating how pathogenic variants fundamentally compromise tumor suppressor proteins in GC pathways, leading to the identification of potential biomarkers and precise therapeutic decisions for GC intervention. - Source: PubMed
Publication date: 2026/09/17
Mim Faria FerdouseSumiya Taslima AkterKhanam RoksanaAkter JannatiArzu FarhanaHaque SamiaMiah Md RomanIslam K M TanjidaMahmud Shahin - Human epidermal growth factor receptor (HER) 3, encoded by the gene, transduces signals most effectively when dimerized with HER2. Although HER3 protein expression has been considered a poor prognostic factor in ovarian cancer, limited data exist on changes in HER3 protein expression and messenger RNA (mRNA) expression during recurrence. This study evaluated HER3/ERBB3 expression before and after recurrence and its association with prognosis using paired samples. We also evaluated HER2/ERBB2 expression. - Source: PubMed
Publication date: 2026/09/11
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