HER2 (Phospho_Tyr1248) Antibody
- Known as:
- HER2 (Phospho_Tyr1248) Antibody
- Catalog number:
- E011079-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- HER2 (Phospho_Tyr1248) Antibody
Related genes to: HER2 (Phospho_Tyr1248) 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_Tyr1248) Antibody
Related articles to: HER2 (Phospho_Tyr1248) Antibody
- Cancer neuroscience highlights the critical role of neural signaling in tumors, yet a pan-cancer understanding of neuroregulatory dysregulation is lacking. We systematically characterized 130 neurotransmitter receptor (NTR) genes across 9,125 tumors from 33 cancer types. Our analysis revealed heterogeneous NTR mutations, with 17 cancer types showing elevated rates. Notably, amplification of the muscarinic receptor gene CHRM2 exhibited mutual exclusivity with the clinically actionable gene ERBB2, suggesting its potential as a therapeutic target. NTR expression was widely dysregulated and associated with altered DNA methylation, microRNA (miRNA) expression, and patient prognosis. Unsupervised clustering identified five recurrent neuroregulatory subtypes with distinct clinical and molecular features across cancers. Using low-grade glioma and liver cancer as examples, we validated that the S4 and S1 subtypes were consistently correlated with aggressive disease and poor outcomes in these two cancers, respectively. This study establishes a foundational framework for advancing cancer neuroscience and targeting neuroregulatory signaling in cancer therapy. - Source: PubMed
Publication date: 2026/05/05
Luo ShangyiQiao ShupeiLiu LiXiong ZhuangGuo LeiHao XinZhang XueZhang Yajing - Interdigitating dendritic cell sarcomas (IDCSs) are rare tumors that commonly arise in the hematopoietic system and rarely outside. The genetic drivers of IDCS carcinogenesis are unknown; therefore, therapeutic options are limited. We investigated somatic gene mutations and copy-number alterations (CNAs) in nine IDCSs arising in the lung by whole-exome sequencing (WES) paired with shallow whole-genome sequencing (sWGS). Using a panel of immunohistochemical markers, follicular dendritic sarcomas and Langerhans cell sarcomas were excluded, and inflammatory myofibroblastic tumors were excluded based on morphology. The Ki-67 score was used to stratify the tumors into low-grade (≤ 20%) and high-grade (> 20%) tumors. The main question addressed by the study was whether genetic aberrations can be identified in IDCSs and whether these are druggable. High-grade IDCSs showed a higher fraction of genome altered by CNA (48.42%) than low-grade IDCSs (18.15%) and tended to have greater tumor mutation burden (7.56 versus 0.88 mut/Mb; not significant). Heterogeneous gains on chromosome 17 were characteristic of almost all IDCS cases (eight of nine cases, 89%), independent of grade. CNA in cancer-actionable genes was independent of clinicopathological characteristics and included amplifications in EGFR, MYC, MDM4, ERBB2, CCNE1, and BRAF and losses in MTAP, CDKN2A, CDKN2B, MLH1, and VHL, as well as homozygous losses in SMAD2/4, ATM, and TP53. Somatic gene mutations in cancer-related genes were identified in seven of nine IDCSs. No common driver mutations were identified. The heterogeneous genetic landscape suggests a mixed etiology of IDCS carcinogenesis and genomic instability in high-grade tumors. Distinct druggable biomarkers have been identified in almost all tumors, providing novel therapeutic options. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/05/06
Ermakov Mikhail SFilipe Juliana FariaEidenhammer SylviaOtt GermanHalbwedl IrisKashofer KarlPopper Helmut - Human epidermal growth factor receptor 2 (HER2) is a membrane tyrosine kinase encoded by ERBB2, which is amplified in 15%-20% of breast cancers and serves as a critical prognostic and predictive biomarker for targeted therapy. Fluorescence in situ hybridization (FISH) is the reference standard for HER2 gene amplification assessment. The 2023 American Society of Clinical Oncology/College of American Pathologists (ASCO/CAP) guidelines recommend assessing at least 20 cells in FISH but do not specify an optimal count. It remains unclear whether counting additional cells improves interobserver agreement. In this study, we aimed to determine the optimal number of cells to evaluate to accurately assess ERBB2 amplification status. We analyzed 179 invasive breast cancer cases with archival formalin-fixed, paraffin-embedded tissue subjected to HER2 immunohistochemistry and FISH, as well as clinical and pathologic data. Three independent observers selected the specimen areas to assess and determined HER2 status by examining 20, 40, or 60 cells. Interobserver agreement on HER2 status (HER2 positive vs. HER2 negative) was consistently strong across all counting tiers (Fleiss' κ = 0.81-0.87), with no clinically meaningful improvement at higher cell counts. Stratified analysis revealed that unequivocal cases (Groups 1 + 5, approximately 84% of the cohort) maintained excellent concordance (coefficient of variation <5%) at all tiers, while equivocal cases (Groups 2-4) exhibited persistently higher variability regardless of cell count. These findings validate the 20-cell minimum for routine FISH-based HER2 assessment and demonstrate that enhanced concordance in borderline cases requires adjudicatory workflows beyond additional cell counting. - Source: PubMed
Publication date: 2026/04/30
Jangyubol KanthidaKittikongwat SomboonYimnoon JutamasPetcharat BongkodSinthuwiwat ThivaratanaLaohawetwanit ThiyaphatHerabutya Priyavudh - Ribociclib improves progression-free and overall survival (PFS and OS) in women with advanced HR+/HER2- breast cancer (BC), but real-world evidence in Uruguay is limited. - Source: PubMed
Publication date: 2026/05/06
Camejo-Martínez NataliaStrazzarino-Peluffo NoeliaAmarillo-Hernández C DahianaCastillo-Leska CeciliaKrygier-Waltier Gabriel - It is now recognized that mitochondria play a crucial role in tumorigenesis; however, it has become clear that tumor metabolism varies significantly between cancer types. The failure of recent clinical trials aimed at directly targeting tumor respiration through oxidative phosphorylation inhibitors underscores the critical need for further studies providing an in-depth evaluation of mitochondrial bioenergetics. Accordingly, we comprehensively assessed the bulk tumor and mitochondrial metabolic phenotype in murine HER2-driven mammary cancer tumors and benign mammary tissue. Transcriptomic and proteomic profiling revealed a broad downregulation of mitochondrial genes/proteins in tumors, including OXPHOS subunits comprising Complexes I-IV. Despite reductions in tumor mitochondrial proteins, mitochondrial respiration was several-fold higher compared to benign mammary tissue, which persisted regardless of normalization method (wet weight, total protein content, and when corrected for mitochondrial content). This upregulated respiratory capacity could not be explained by OXPHOS uncoupling, suggesting HER2 signaling regulates intrinsic mitochondrial bioenergetics. In further support, lapatinib, an EGFR/HER2 tyrosine kinase inhibitor, attenuated mitochondrial respiration in NF639 murine mammary tumor epithelial cells. Together, this data highlights that the typical correlation between mitochondrial content and respiratory capacity may not apply to all tumor types and implicates HER2-linked activation of mitochondrial respiration supporting tumorigenesis in this model. - Source: PubMed
Publication date: 2026/05/06
Frangos Sara MBrunetta Henver SWang DongdongJabile Maria Joy ThereseJeffries Leslie MMencfeld GraceMa David W LMuller William JKhursigara Cezar MFisher-Wellman Kelsey HPetrik JimSteinberg Gregory RHolloway Graham P