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
- Neoadjuvant chemotherapy combined with human epidermal growth factor receptor 2 (HER2)-directed therapy is associated with high rates of pathologic complete response in patients with HER2-positive breast cancer. Response in the primary tumour is often assumed to reflect systemic treatment efficacy. However, metastatic disease in axillary lymph nodes may respond differently.We report a case of HER2-positive breast cancer demonstrating marked histological treatment response in the breast but persistent viable metastatic carcinoma in multiple axillary lymph nodes without histological evidence of treatment effect. This discordant response highlights the potential for biological heterogeneity between primary and metastatic disease and underscores the importance of independent pathological evaluation of nodal disease after neoadjuvant treatment.Recognition of discordant response between the primary tumour and nodal metastases is important for accurate staging, prognostic assessment and multidisciplinary treatment planning. - Source: PubMed
Publication date: 2026/09/21
Nikolaus Yanina - Male breast cancer (MBC) accounts for less than 1% of all breast cancer cases, yet its incidence is increasing worldwide. Research on MBC remains limited, particularly in Arab populations, where molecular and genetic characteristics are poorly characterized. Improved understanding of MBC biology is essential to support region-specific, biology-driven management strategies. - Source: PubMed
Publication date: 2026/09/21
Abunasser ShadenAl-Taweel RaghadElnatsheh ShahrazadBaraka AreejAl-Ismail MunaAldosari Waad RashidAlquran Baraah AAbdallah Atiyeh MAl-Haidose Amal - Neuroendocrine carcinoma (NEC) of the uterine cervix is a rare, highly aggressive malignancy with a poor prognosis. Expanding upon our previous work, which identified frequent mutations in HER2, KRAS, and PIK3CA in this disease, we sought to refine the genomic landscape by characterizing alterations in TP53 and PTEN, and their relationships with these oncogenic drivers. - Source: PubMed
Shen Huang-PinLee Ming-YungLee Yi-JuChen An-ChiChen Chi-KuanChao Wan-RuHan Chih-Ping - To analyze the clinicopathological and molecular characteristics of non-small cell lung cancer (NSCLC) with human epidermal growth factor receptor 2 (HER-2) variations (including mutations and amplifications) and their correlation with prognosis. Clinicopathological data of NSCLC patients with HER-2 variations who underwent targeted next-generation sequencing (NGS) at Ningbo Clinical Pathology Diagnostic Center from September 2022 to June 2024 were collected. The clinicopathological and molecular features were retrospectively analyzed, and a literature review was conducted. Among 2 795 NSCLC patients, HER-2 variations were identified in 148 cases (5.3%, 148/2 795). Of these, 128 cases had HER-2 mutations [86.5%, 128/148, including 63 exon 20 (Exon20) mutations], 16 cases had HER-2 amplifications (10.8%, 16/148), and 4 cases had concurrent HER-2 mutation and amplification (2.7%, 4/148). Compared with the HER-2 mutation group, patients with HER-2 amplification were more likely to have larger tumor size, lymph node metastasis, distant metastasis and higher TNM stage (all ＜0.05). Among HER-2 mutations, Exon 20 mutations were more common in females and associated with lower risks of larger tumor size, lymph node metastasis and distant metastasis (all ＜0.05). Cox regression analysis indicated that HER-2 amplification, larger tumor size, lymph node metastasis, distant metastasis and higher TNM stage were associated with poor prognosis (＜0.05). Molecular analysis revealed that Exon20 mutations rarely co-occurred with other gene variations, whereas non-Exon20 mutations were frequently accompanied by other genetic alternations, most commonly epidermal growth factor receptor (EGFR) mutations (55.4%, 36/65). In addition, 16 cases of HER-2 p.A270S mutation were identified, of which 11 were at advanced TNM stage (68.8%, 11/16), and 5 patient died. Different types of HER-2 variations (mutations/amplifications) exhibit distinct clinicopathological and molecular characteristics. Patients with HER-2 amplification have a poor prognosis, and the HER-2 p.A270S mutation may be associated with malignant phenotypes of NSCLC. It is necessary to integrate the characteristics of HER-2 variations to provide references for individualized treatment.. - Source: PubMed
Wang Y JXu J YZhang H ZZhao M - Gastrointestinal (GI) cancers remain a leading cause of cancer mortality, with durable benefit from current therapies limited to a subset of patients. Precision oncology is expanding options by targeting recurrent, actionable alterations, most notably in cholangiocarcinoma (CCA), in genes such as FGFR2, IDH1, KRAS, BRAF and ERBB2. Here, we review the evolving therapeutic landscape, emphasizing clinical efficacy, and indications for various treatment modalities. Key therapies include FGFR inhibitors (first and next-generation; both covalent and FGFR2-selective agents), IDH1 inhibitors, KRAS and BRAF inhibitors combined with EGFR blockade and/or chemotherapy, and HER2-targeted monoclonal antibodies, tyrosine kinase inhibitors (TKIs), and antibody-drug conjugates (ADCs). Central mechanisms of both primary and secondary resistance are detailed, with a focus on on-target mutations and convergent off-target MAPK signaling pathways. Finally, we discuss drug-tolerant persister cells, residual tumor cell states that survive therapy without canonical genetic resistance alterations and may contribute to relapse and secondary resistance. - Source: PubMed
Publication date: 2026/09/20
Aceituno LaiaValenzi ElenaSegatto OresteSaborowski AnnaVogel Arndt