HER2 (Phospho_Tyr877) Antibody
- Known as:
- HER2 (Phospho_Tyr877) Antibody
- Catalog number:
- E011075-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- HER2 (Phospho_Tyr877) Antibody
Related genes to: HER2 (Phospho_Tyr877) Antibody
- 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 (Phospho_Tyr877) Antibody
Related articles to: HER2 (Phospho_Tyr877) Antibody
- The age cut-off for early-onset lung cancer (EOLC) varies across studies (40-50 years). Here, we define EOLC as diagnosis at ≤ 40 years, a threshold identifying a subgroup with distinct clinical characteristics. However, whether EOLC differs fundamentally from late-onset lung cancer (LOLC) at the molecular level and represents a distinct subtype requiring different management remains unclear. - Source: PubMed
Publication date: 2026/07/27
Wang JianhuaLu ZhongyuGe MinghuiZhang XingChen DongshengPeng Xiaohong - Biliary tract cancers (BTCs) are aggressive malignancies associated with a poor prognosis. Although molecular profiling is recommended to guide therapeutic decision-making, real-practice data on the prevalence and prognostic significance of genomic alterations in European BTC cohorts remain limited. This retrospective cohort study characterized the molecular landscape of BTCs in a Belgian real-practice setting and evaluated its prognostic relevance. Patients with BTC who underwent informative molecular testing as part of routine diagnostics at Antwerp University Hospital between 2016 and 2024 were included. Demographic, clinical, and molecular data were extracted from electronic health records. Survival outcomes were analyzed using Kaplan-Meier methods and Cox proportional hazards regression. Among 224 included patients, genomic alterations were identified in 59.4% of tumors, with clear subtype-specific patterns. IDH1 mutations (17.3%) and FGFR2 fusions (13.9%) were exclusively observed in intrahepatic cholangiocarcinoma, KRAS mutations were most prevalent in extrahepatic cholangiocarcinoma (42.9%), and ERBB2 amplification was enriched in gallbladder cancer (16.7%). Co-occurring alterations were present in 7.8% of cases. KRAS mutation was the most frequent alteration overall (20.4%) and remained significantly associated with worse overall survival in multivariate analysis adjusted for tumor subtype and tumor stage (HR = 1.54, 95% CI: 1.03-2.31, p = 0.04). Although 32.6% of tumors harbored a potentially actionable alteration, only 31.6% of eligible patients received matched targeted therapy. These findings underscore the clinical value of routine molecular profiling in BTC and highlight its importance for identifying therapeutic opportunities in clinical practice. - Source: PubMed
Publication date: 2026/08/21
Arnouts Jorinevan Kempen Léon CKoljenović SenadaOliveres HelenaVanclooster PieterjanPrenen HansDe Weerdt CaroChhajlani SiddharthRoeyen GeertSorber LaureDe Winne KoenDahnoun JonasVanhoutte GreetjeVandamme TimonZwaenepoel Karen - ErbB ligands activate distinct receptor dimers that regulate cell proliferation, but how they influence cell-cycle commitment remains unclear. Here, we show that EGF and HRG induce different modes of G1/S progression in ErbB2-amplified BT474 breast cancer cells. Unexpectedly, HRG, despite activating the more potent ErbB2-ErbB3 heterodimer, failed to accelerate G1/S progression; instead, EGF promoted earlier passage through the restriction point and faster S-phase entry. Mechanistically, EGF drove rapid and coordinated cell-cycle progression through ERK-FOS signaling, whereas HRG induced sustained MYC activity, elevated transcriptional heterogeneity, and caused extensive rewiring of cell-cycle regulatory networks. Together, these findings reveal that ligand-specific ErbB signaling controls not only the timing of cell-cycle entry but also the transcriptional architecture that governs proliferative fate decisions. - Source: PubMed
Publication date: 2026/08/21
Febri Ririn RahmalaNagasato-Ichikawa AyakaIida KeitaKimura ShuheiImamoto AkiraOkada Mariko - HER2 immunohistochemistry (IHC) 2 + breast cancer represents a clinically challenging subgroup requiring confirmatory fluorescence in situ hybridization (FISH) testing. This multicenter retrospective study included 284 patients with HER2 IHC 2 + breast cancer from a regional cohort to evaluate the FISH positivity rate and identify associated clinicopathological factors. Overall, 52 patients (18.3%) were FISH-positive. Compared with FISH-negative patients, the FISH-positive group showed significantly higher Ki-67 levels, lower PR expression, and a higher proportion of histological grade III tumors. Multivariable analysis identified histological grade III as the only clinicopathological characteristic independently associated with FISH positivity (OR = 2.43, 95% CI: 1.26-4.71, P = 0.008). The multivariable model demonstrated moderate discriminatory ability, with an area under the curve of 0.703 (95% CI: 0.628-0.777). Exploratory categorical analysis showed higher FISH positivity rates in patients with Ki-67 ≥ 30% and histological grade III tumors, with a stepwise increase in FISH positivity according to the number of these risk factors.These findings suggest that histological grade and Ki-67 may provide supportive information for characterizing the likelihood of HER2 gene amplification in HER2 IHC 2 + breast cancer. However, these routinely available clinicopathological features should not replace guideline-recommended confirmatory FISH testing. - Source: PubMed
Publication date: 2026/08/08
Yang WenDeng HanqingGuo WenyanLan QiuhongHuang GuojieZhang ShiyiDong ShiwenChen Wenxin - Colorectal cancer (CRC) is a malignancy with high global incidence and significant therapeutic challenges, where chemotherapy resistance is a key factor leading to treatment failure. Aberrant activation of the PI3K-Akt signaling pathway plays a central role in CRC progression and drug resistance. Fraxetin, a major active coumarin component of the traditional Chinese medicine Cortex Fraxini, possesses various biological activities, but its anti-CRC effects and underlying mechanisms remain unclear. This study aimed to systematically elucidate the mechanism of action of Fraxetin against CRC, particularly its regulation of the PI3K-Akt pathway and potential to reverse drug resistance, by integrating network pharmacology, computational simulation, and in vitro experiments. Network pharmacology screening identified 108 common targets of Fraxetin and CRC. Protein-protein interaction (PPI) analysis pinpointed 10 core targets, including TNF, AKT1, and EGFR. KEGG enrichment analysis suggested the PI3K-Akt pathway as one of the primary pathways involved. Molecular docking and dynamics simulations confirmed that Fraxetin could stably bind to core targets such as EGFR and ERBB2. In vitro experiments demonstrated that Fraxetin dose-dependently inhibited the proliferation of HCT116 and HT-29 cells, induced reactive oxygen species (ROS) generation, and significantly downregulated the phosphorylation levels of key PI3K-Akt pathway proteins, p-PI3K and p-Akt. Furthermore, Fraxetin combined with 5-fluorouracil (5-FU) or irinotecan exhibited synergistic antiproliferative effects and significantly restored the sensitivity of 5-FU-resistant cells to chemotherapeutic agents. This study systematically demonstrate that Fraxetin exerts multi-faceted effects against colorectal cancer, including anti-cancer activity, synergy with chemotherapy, and restoration of 5-FU sensitivity in 5-FU-resistant CRC cells in vitro, through multi-target inhibition of the PI3K-Akt signaling pathway. - Source: PubMed
Publication date: 2026/08/20
Guo MinfangZhu LiangdongGuo JianjinYang XunGuo TingZeng Qingling