ErbB2 _ HER2 Antibody (Antigen Affinity Purified)
- Known as:
- ErbB2 _ HER2 Antibody (Antigen Affinity Purified)
- Catalog number:
- 10004-RP04
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- ErbB2 _ HER2 Antibody (Antigen Affinity Purified)
Related genes to: ErbB2 _ HER2 Antibody (Antigen Affinity Purified)
- 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: ErbB2 _ HER2 Antibody (Antigen Affinity Purified)
Related articles to: ErbB2 _ HER2 Antibody (Antigen Affinity Purified)
- ErbB2 overexpression occurs in 15-20% of invasive breast cancer (BC) and inactivation of Cyclin D1-CDK4/6 axis reduce mammary stem/progenitor cells in ErbB2-driven tumorigenesis. Here, we explored the preventive role of short-term palbociclib intervention in MMTV-ErbB2 mice. Palbociclib significantly inhibited the proliferation and stemness of ErbB2-overexpressed BC cells in vitro and in vivo. Furthermore, short-term palbociclib exposure during the early premalignant risk window significantly delayed mammary tumor development and reduced tumor multiplicity, accompanied by the suppression of epithelial proliferation and ductal/alveolar morphogenesis in premalignant tissues, as well as prolonged tumor-free survival compared with controls. Importantly, palbociclib reduced the luminal epithelial (CD24 /CD49f ), mammary reconstitution unit-enriched (CD24 /CD49f ) subpopulations, and luminal progenitor/TIC-enriched (CD61 /CD49f ) subpopulations. These changes were accompanied by diminished mammary epithelial cell stemness functions, including colony-forming, mammosphere-forming, and 3D growth activities of mammary epithelial cells. Mechanistically, palbociclib-treated tissues showed inhibition of the Cyclin D1-CDK4/6-RB-E2F axis and coordinated attenuation of ER-, ErbB2- and Wnt/β-catenin-associated signaling. Together, we demonstrate that short-term CDK4/6 inhibition during a premalignant risk window produces a sustained delay in ErbB2-driven mammary tumorigenesis, associated with remodeling of the mammary epithelial hierarchy and suppression of proliferative and stem/progenitor-associated activity, suggesting CDK4/6 inhibition as a strategy for ErbB2-positive BC prevention. - Source: PubMed
Publication date: 2026/09/17
Liu YongxuanParris Amanda BMa ZhikunWei LiminQi YijunYang Xiaohe - ZNF217 is a potent oncogene that drives ovarian cancer progression and therapeutic resistance. We show that ZNF217 overexpression markedly increases ERBB2 levels in ovarian cancer cells, suggesting its potential as a biomarker to identify ovarian tumors that will respond to ERBB2-targeted therapeutics. Unexpectedly, ZNF217-high ovarian cancer cells exhibit resistance to multiple ERBB2 inhibitors, revealing a disconnect between receptor abundance and drug sensitivity. Mechanistically, ZNF217 drives chemoresistance by elevating the expression of several key receptor tyrosine kinases, most notably AXL, that activates MAPK signaling. Further, ZNF217 also upregulates ERK1/2 levels in ovarian cancer cells. This induces rewiring of downstream signaling, promoting an ERK-dominant state that sustains survival despite ERBB2 inhibition. Therapeutic targeting of the AXL-ERK axis reduced cell viability and metastatic potential in vitro, while suppressing tumor burden and prolonging survival in xenograft models. Thus, by elevating the expression of several key signaling receptors and their downstream effectors in ovarian cancer cells, ZNF217 establishes signaling plasticity that defines a novel mechanism of chemoresistance. These findings identify ZNF217 as a key determinant of signaling state and drug response and provides rationale to evaluate targeting AXL and ERK signaling in ZNF217-high ovarian tumors. - Source: PubMed
Publication date: 2026/09/14
Pandya Megha JHoffman JessicaPadmanabhan Achuth - Progesterone is essential for establishing uterine receptivity and sustaining early pregnancy. However, how the uterus acquires the competence to respond to progesterone at the appropriate time remains poorly understood. Here we show that ERBB2 governs the timing of progesterone responsiveness required for uterine receptivity. In endometrial samples from women with recurrent spontaneous abortion (RSA), ERBB2 is downregulated specifically in the stromal compartment, accompanied by a parallel reduction in stromal progesterone receptor (PGR). Uterine deletion of in mice blunts the rise of stromal PGR at the onset of the receptive window, deferring implantation and impairing decidualization despite normal circulating progesterone and estrogen. Epithelial deletion has no such effect, placing the requirement in the stroma. High-dose progesterone fails to rescue the phenotype; advancing progesterone priming by 24 hours restores stromal PGR, HAND2, , and on-time implantation. Collectively, the present study provides evidence that ERBB2 directs the temporal window of stromal progesterone priming by setting the threshold for PGR induction, thereby synchronizing the maternal-fetal interface and safeguarding pregnancy. - Source: PubMed
Publication date: 2026/09/16
Li BoZhang ChenDewar AmandaLiu XiaoliDeng WenboQi HongboDey Sudhansu KSun Xiaofei - To investigate the association between ultrasound response assessment during neoadjuvant therapy and pathological outcomes in patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer. This retrospective study included 609 patients with HER2-positive breast cancer who received neoadjuvant therapy at the Breast Center of Peking University Cancer Hospital between June 1, 2018, and December 31, 2024. Ultrasound response was assessed at cycles 2, 4, 6, and 8 according to the World Health Organization (WHO) response criteria and Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 and categorized as clinical complete response (cCR), clinical partial response (cPR), clinical stable disease (cSD), or clinical progressive disease (cPD). Patients with cCR or cPR were classified into the response group, whereas those with cSD or cPD were classified into the poor-response group. Pathological complete response (pCR) and Miller-Payne (MP) grade were determined from surgical pathology. The test was used to analyze the associations of ultrasound response with pCR and MP grade. Receiver operating characteristic (ROC) curves and areas under the curves (AUC) were used to assess the performance of ultrasound response in predicting pCR. The overall pCR rate was 67.5% (411/609), with rates of 68.7% (338/492) among patients receiving sequential anti-HER2 neoadjuvant therapy and 62.4% (73/117) among those receiving upfront anti-HER2 neoadjuvant therapy. Except for the WHO assessment at cycle 2, pCR rates differed significantly between the response and poor-response groups at all assessment time points according to both criteria (all <0.05). The proportions of patients with MP grades 4-5 also differed significantly between the two groups at all assessment time points (all <0.05). When ultrasound response according to each criterion was combined with clinicopathological factors, all AUC were<0.8, indicating poor predictive performance for pCR. In the upfront anti-HER2 therapy group, pCR rates differed significantly between the response and poor-response groups at cycles 2-6 (all <0.05); in the sequential anti-HER2 therapy group, significant differences were observed at cycles 4-8 (all <0.05). The pCR rate did not differ significantly between patients with SD accompanied by tumor enlargement and those with SD accompanied by tumor shrinkage (all >0.05). During neoadjuvant therapy for HER2-positive breast cancer, a treatment response identified by ultrasound at cycle 2 in patients receiving upfront anti-HER2 therapy or at cycle 4 in those receiving sequential anti-HER2 therapy may be associated with pCR; however, ultrasound assessment has limited predictive value for pCR. - Source: PubMed
Zhang YLi G CHe Y JWang X YZhang NMa J LWang X GCao WFan Z Q - ObjectiveThis study aims to conduct a comprehensive, multidimensional evaluation of how clinical and pathological factors influence invasive disease-free survival (IDFS) and cancer-specific survival (CSS) in patients with human epidermal growth factor receptor 2 (/HER2) positive breast cancer receiving adjuvant trastuzumab therapy. Additionally, a stratified assessment will be conducted based on the hormone receptor (HR) status; thereby providing a practical basis for clinical treatment.MethodA total of 643 patients with HER2-positive breast cancer who received adjuvant trastuzumab therapy were retrospectively included. The patients' clinical and pathological information, as well as IDFS and CSS data, were systematically collected and evaluated. Survival analysis was conducted via the Kaplan-Meier method. Univariate and multivariate Cox proportional hazards regression models were used to assess the effects of menstrual status, tumor size, vascular invasion, lymph node involvement, histological grade, histological type, HR status, MKI67 expression, tumor-infiltrating lymphocytes (TILs), HER2 expression, and anthracycline-based chemotherapy on IDFS and CSS. Additionally, clinicopathological characteristics of patients with HER2-positive breast cancer who received trastuzumab treatment were analyzed.ResultAmong all patients, HER2(3+), absence of lymph node metastasis, and anthracycline-based chemotherapy were independently associated with prolonged CSS. Notably, anthracycline use was an independent predictor of longer CSS in HR-negative patients. In the HR-positive subgroup, patients with HER2(3+) status demonstrated a significant CSS benefit compared to those with HER2(2+)/FISH(+) status.ConclusionHER2 expression status affects CSS in patients with HER2-positive breast cancer receiving adjuvant trastuzumab therapy. HR-negative patients may derive clinical benefit from anthracyclines, providing evidence to support anthracycline-based regimens combined with trastuzumab as the adjuvant treatment for HR-negative, HER2-positive breast cancer. - Source: PubMed
Publication date: 2026/09/23
Guan LeiWang LuLiu ChenyingWang XiaoziLi JiazhenYang YihangYang LiuLiu JiameiZhao YafangLi WeidongQian XiaolongGuo Xiaojing