HER2 Antibody Clone: GR011 Concentrate
- Known as:
- HER2 Antibody Clone: GR011 Concentrate
- Catalog number:
- 61-0154-5
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- HER2 Antibody Clone: GR011 Concentrate
Ask about this productRelated genes to: HER2 Antibody Clone: GR011 Concentrate
- 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: HER2 Antibody Clone: GR011 Concentrate
Related articles to: HER2 Antibody Clone: GR011 Concentrate
- The hallmarks of cancer, first proposed in 2000, have since provided a unified framework for understanding the complexity of carcinogenesis. This conceptual model has profoundly influenced the treatment landscape of primary liver cancer, which includes hepatocellular carcinoma (HCC, ∼85%) and intrahepatic cholangiocarcinoma (iCCA, 10%)-malignancies with high mortality. Key hallmarks exhibited by HCC include sustaining proliferative signaling, inducing or accessing vasculature, and avoiding immune detection. Over the past two decades, outcomes for patients with advanced HCC have significantly improved with immunotherapies. iCCA is characterized by hallmarks such as sustaining proliferative signaling, deregulating cellular metabolism, and avoiding immune detection. Unlike HCC, roughly 45% of iCCA harbor alterations amenable to precision oncology approaches, including fibroblast growth factor receptor 2 (FGFR2) fusions, isocitrate dehydrogenase 1 (IDH1) mutations, ERBB2 alterations, and BRAF mutations. In this review, we explore how this framework has reshaped liver cancer care and discuss the resulting breakthroughs in management and emerging directions that may further improve therapeutic strategies. - Source: PubMed
Llovet Josep MPinyol RoserAffo SilviaYarchoan MarkGores Gregory JKelley Robin KateLowe Scott WSia DanielaVillanueva Augusto - This study aims to elucidate the molecular mechanisms underlying luteolin's therapeutic effects on polycystic ovary syndrome (PCOS) and endometriosis (EM), thereby providing a theoretical foundation for developing novel treatment strategies. An integrated approach combining network pharmacology, molecular docking, and molecular dynamics simulation was employed. Potential targets of luteolin intersecting with PCOS/EM pathogenesis were identified through database mining, followed by the construction of a protein-protein interaction network to screen hub genes. Mechanistic insights were further explored through bioinformatics validation, gene enrichment analysis, molecular docking verification, and molecular dynamics simulations. Luteolin exerted synergistic therapeutic effects through core targets such as ESR1, MMP9, and ERBB2, mediated by triple pathways involving "nuclear receptor modulation-proliferation inhibition-metabolic improvement." Molecular docking and dynamics simulations confirmed its high binding stability and low binding free energy with key targets (e.g., ESR1, MMP9, and ERBB2). Additionally, the identification of shared risk genes between PCOS and EM offers novel targets for cross-disease interventions. Luteolin demonstrates significant potential in treating PCOS and EM through multi-target and multi-pathway mechanisms, aligning with the complex pathological networks characteristic of reproductive endocrine disorders. These findings provide a scientific rationale for its clinical translation. - Source: PubMed
Chen RongTian LiXu YingboZhang JuanPan SiyingZhao GuodongRaveendran Aravind - HER2-positive cancers present challenges of drug resistance, toxicity, and immune tolerance. HER2-targeted peptide vaccines have failed clinically, while nucleoside-modified mRNA-lipid nanoparticle (mRNA-LNP) vaccines show promise for robust antitumor immunity. This study utilized heterologous immunity (rat HER2 extracellular domain, rHER2 ECD) to circumvent HER2 tolerance, developing a safe mRNA-LNP vaccine and exploring its synergy with anti-PD-1 therapy. - Source: PubMed
Publication date: 2026/04/01
Li KexinLi XiaoyaZhang CongDai SuliLi LeiWang JunZhang HongtaoZhao Lianmei - Cerebellar liponeurocytoma (cLNC) is a rare tumor. It affects adults with no sex predilection. It appears as a heterogeneously enhancing mass, most commonly unifocal. Histologically, it is a biphasic neurocytic tumor with lipomatous component, with minimal atypia, and low proliferative index, corresponding to central nervous system (CNS) World Health Organization (WHO) grade 2. missense mutation is reported in 20% of cases. Gross total resection, with or without radiotherapy, is considered an adequate treatment. Bifocality and features of anaplasia are rarely reported. We are reporting a 41-year-old lady with bilateral cerebellar contrast-enhancing masses who underwent gross total resection 3 months apart. Pathology revealed features consistent with cLNC. However, the tumor resected from the right cerebellar hemisphere demonstrated atypical morphological features, including microvascular proliferation and necrosis. Ki-67 proliferative marker was estimated at 10% in the most active areas. Next-generation sequencing (NGS) revealed 2 pathogenic mutations within exonic regions of , and genes, and a variant mutation of unknown significance (VUS) involving the gene. DNA methylation profiling confirmed the diagnosis of cLNC. The patient has been under observation without any further intervention for 70 months since diagnosis, with no evidence of disease recurrence. In addition to the rarity of cLNC, this is a unique case in terms of bifocality, anaplastic histology, and the described genetic abnormalities. - Source: PubMed
Publication date: 2026/04/17
Al-Hussaini MaysaAl Sharie SarahAzzam SaifErashdi MadihaMansour AsemObeidat Mouness - The development of endocrine resistance is frequent in hormone receptor-positive, HER2-negative advanced breast cancer (HR + /HER2-ABC), particularly after CDK4/6 inhibitor exposure. Next-generation oral selective estrogen receptor degraders (SERDs) have been developed to improve estrogen receptor blockade; however, randomized trials have yielded heterogeneous results with uncertain clinical benefit. - Source: PubMed
Publication date: 2026/04/17
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