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epidermal growth factor receptor (EGFR pharmDx / EGFR pharmDx Kit)

✓ Approved

Dako · EGFR · 辅助诊断

什么是 epidermal growth factor receptor？

epidermal growth factor receptor 是一种辅助诊断，由Dako研发。该药已获批，用于治疗相关适应症，给药途径：Others。

药物档案

商品名EGFR pharmDx, EGFR pharmDx Kit
公司Dako
药物类别辅助诊断
分子靶点EGFR
给药途径Others
状态Approved
来源： ClinicalTrials.gov, Dako

作用机制

分子靶点

epidermal growth factor receptor 作用于 1 个分子靶点：

EGFRepidermal growth factor receptor (ERBB1, NNCIS)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

epidermal growth factor receptor 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancer✓ Approved

相关研究文献

PubMedJACC. CardioOncology2026-09-10

Real-World Cardiotoxicity of Biosimilar versus Reference Trastuzumab in Early HER2-Positive Breast Cancer.

Jackson Inimfon I, Zhang Ning N, Sullivan Marija M, Zhao Hui H et al.

Trastuzumab has greatly improved outcomes in patients with human epidermal growth factor receptor 2-positive breast cancer. To reduce costs and increase access, biosimilar products were approved after trials demonstrated short-term safety similar to that of reference trastuzumab. However, real-world data on cardiac safety are limited. We evaluated the adoption of biosimilar trastuzumab and compared heart failure (HF) risk between users of reference and biosimilar trastuzumab. Patients aged ≥18 years with breast cancer who received trastuzumab from 2018 to 2024 were identified in the IQVIA PharMetrics Plus Closed Health Plan Claims database. Patients who underwent surgery within the first year after cancer diagnosis were selected as a proxy for early-stage disease. Healthcare Common Procedure Coding System Level II codes were used to identify reference and biosimilar trastuzumab use, and International Classification of Diseases codes were used to identify HF diagnoses. Patients with an HF diagnosis before breast cancer surgery were excluded. Multivariable cause-specific Cox proportional hazards regression was used to examine the association of reference vs biosimilar trastuzumab use with HF risk. Among 5,135 patients identified, 43.9% received reference trastuzumab. Use of biosimilar trastuzumab increased from 0% in 2018 to 71.3% in 2024 (P < 0.001). The overall rate of HF was 5.9% (5.5% among reference trastuzumab users vs 6.3% among biosimilar trastuzumab users; P = 0.26). In multivariable analysis, there was no statistically significant difference in HF risk between patients treated with biosimilar trastuzumab and those treated with reference trastuzumab (adjusted HR [aHR]: 1.16; 95% CI: 0.92-1.46). Patients with a Charlson Comorbidity Index score ≥2 had a higher risk of HF than those with a score of 0 (aHR: 1.52; 95% CI: 1.11-2.08). Compared with patients aged 18 to 54 years, those aged 65 to 74 years (aHR: 1.61; 95% CI: 1.19-2.19) and ≥75 years (aHR: 1.95; 95% CI: 1.29-2.96) had a higher risk of HF. As biosimilar trastuzumab use continues to increase, our findings provide reassurance regarding its cardiac safety in the management of early-stage human epidermal growth factor receptor 2 breast cancer. Additional studies with longer follow-up are needed to confirm these findings and evaluate long-term cardiac outcomes.

PMID 42720642
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PubMedCancer communications (London, England)2026-09-10

The PROM1+SMAD5+ Tumor-Initiating Subpopulation Shapes Premetastatic Niches through Spatial Multi-Omics Landscapes in HER2-Positive Breast Cancer.

Yin Huijing H, Wang Wei W, Ge Jing J, Fan Guangjian G et al.

Background: Human epidermal growth factor receptor 2 (HER2)-positive breast cancer exhibits high metastatic potential, linked not only to intrinsic cancer cell traits but also to critical crosstalk with the tumor microenvironment. However, the coevolutionary mechanisms between cancer cells and multiple stromal subpopulations in driving distant metastasis remain poorly understood. Therefore, this study aimed to explore the microenvironmental regulatory mechanisms of breast tumor-initiating cells and their roles in HER2-positive breast cancer metastasis. Methods: Integrated multi-omics analyses (spatial transcriptomics, metabolomics, spatial in situ analysis, and proteomics) were used to identify novel cell subpopulations and their interactions. High-throughput sequencing of exosomal microRNAs (miRNAs) and single-nucleus RNA from the same tissue was performed to explore the molecular mechanisms underlying cell crosstalk. In vitro experiments were conducted to verify the interaction between stromal cells and prominin 1 (PROM1)+ SMAD family member 5 (SMAD5)+ cells. In vivo murine breast cancer models were established to confirm the role of stromal subpopulations in pulmonary metastasis, and parabiosis assays were carried out to compare key cell subpopulations between tumor-bearing mice and normal mice. Clinical samples were analyzed to correlate key cell subpopulations with clinicopathological features and prognosis. Results: A breast tumor-initiating subpopulation, PROM1+ SMAD5+ cells, and its interactions with stromal cells, specifically adiponectin (ADIPOQ)+ notch receptor 4 (NOTCH4)+ adipocytes and decorin (DCN)+ transmembrane 4 L six family member 1 (TM4SF1)+ fibroblasts, were identified by integrated multi-omics analyses. Mechanistically, these 2 stromal subpopulations delivered functional miRNAs and mediated coatomer protein complex subunit alpha (COPA)-dependent epidermal growth factor receptor (EGFR) activation in PROM1+SMAD5+ cells, thereby triggering the EGFR-SMAD5-cytochrome P450 family 3 subfamily A member 4 (CYP3A4) axis to induce partial epithelial-mesenchymal transition (pEMT) and metastasis. Additionally, stroma-secreted exosomal miR-671-3p down-regulated Claudin1 in PROM1+SMAD5+ cells, promoting their evolution into PROM1+SMAD5+Claudin1- subpopulations with enhanced stemness and metastatic potential. In vivo experiments confirmed that the 2 stromal subpopulations markedly promoted pulmonary metastasis, and the 3 identified subpopulations preferentially accumulated in the primary tumors, lymph nodes, and pulmonary metastatic lesions of tumor-bearing mice. Clinically, these 3 subpopulations form a "trinity niche", whose aggregation associated with HER2 positivity, high malignancy, and lymph node/pulmonary metastasis, and predicted poor prognosis. Conclusion: This study clarified the microenvironmental regulation of breast tumor-initiating cells and provided new insights into precision therapy.

PMID 42718887
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PubMedJournal of ginseng research2026-09-10

Ginsenosides Rh2 and Rg3 in first-line combination therapy: Prospects for rapid clinical translation in drug-resistant triple-negative breast cancer.

Yoon Sungpil S, Cho Jae Youl JY

Triple-negative breast cancer (TNBC), defined by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2), remains one of the most aggressive breast cancer subtypes, characterized by high metastatic potential, poor prognosis, and limited therapeutic options. Despite extensive clinical efforts, durable improvements in survival have been limited due to the intrinsic heterogeneity of TNBC and the rapid emergence of multidrug resistance (MDR), primarily mediated by P-glycoprotein (P-gp) overexpression. P-gp-enriched cancer stem cells frequently survive initial chemotherapy, repopulate tumors, and drive relapse. Therefore, effective first-line strategies capable of eliminating heterogeneous, drug-resistant populations are urgently needed. Ginsenosides derived from Panax ginseng have gained increasing attention as natural compounds with potent anticancer activity and excellent safety profiles. Among them, the panaxadiol-type ginsenosides Rg3 and Rh2 exhibit strong translational potential and are being actively explored as candidate adjuvant or first-line agents. Their multifaceted activities-anticancer efficacy in TNBC, inhibition of P-gp, MDR sensitization, cytoprotection of normal cells, compatibility with nanoparticle delivery systems, and availability of preclinical and clinical data-underscore their promise in overcoming resistance in TNBC. This review summarizes the evidence supporting Rg3 and Rh2 as multi-targeted agents capable of enhancing therapeutic efficacy and accelerating clinical application in drug-resistant TNBC.

PMID 42719336
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PubMedFrontiers in oncology2026-09-10

Case Report: Synergistic potential of RANKL and ACLY inhibition in a breast cancer patient with acquired resistance to CDK4/6 inhibitors.

Samusieva Anastasiia A, Gorodetska Ielizaveta I, Socha Oleg O, Lytovchenko Yuliia Y et al.

The development of acquired resistance to cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) represents a major clinical challenge in the management of hormone receptor-positive (HR+), human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer. Overcoming this resistance requires novel therapeutic strategies that target the underlying molecular escape pathways. We report the case of a patient initially diagnosed in 2011 with pT2N0M0, ER+/HER2- invasive ductal carcinoma. Following multimodality treatment, she experienced disease progression with bone metastases after five years, followed by lymph node metastases at the ten-year mark. Subsequent treatment with the CDK4/6i ribociclib in combination with fulvestrant resulted in disease progression approximately one year later, indicating acquired resistance. Due to progressive bone loss, denosumab was initiated for skeletal support, and bempedoic acid was later added for dyslipidemia. This case provides a clinical basis for exploring two innovative therapeutic concepts to overcome resistance. First, we discuss the complex role of receptor activator of nuclear factor kappa-B ligand (RANKL) inhibition. Given that leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4) functions as a decoy receptor for RANKL, we hypothesize that a patient's LGR4 expression status may dictate the efficacy and safety of denosumab, potentially serving as a predictive biomarker to personalize its use. Second, we propose that bempedoic acid, a supportive care medication, may exert a direct anti-neoplastic effect. Its dual mechanism, inhibiting ATP-citrate lyase (ACLY) to disrupt lipid synthesis and activating AMP-activated protein kinase (AMPK) to suppress mammalian target of rapamycin complex 1 (mTORC1) signaling, positions it as a potential agent to counteract the metabolic reprogramming associated with therapeutic resistance. This case report illustrates the sequential development of acquired therapeutic resistance in the long-term management of metastatic breast cancer. Although a single clinical observation cannot establish definitive efficacy, this scenario generates compelling hypotheses for future studies. It highlights the potential need to explore biomarker-driven approaches-such as evaluating LGR4 expression to guide RANKL inhibition-to personalize treatment. Additionally, it raises the possibility that repurposed supportive care medications, such as bempedoic acid, might offer hypothetical anti-neoplastic benefits, warranting broader clinical validation to overcome complex resistance mechanisms.

PMID 42718642
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PubMedNature physics2026-09-10

Decaying and expanding Erk gradients process memory of skeletal size during zebrafish fin regeneration.

Rich Ashley A, Lu Ziqi Z, De Simone Alessandro A, Garcia Lucas L et al.

Amputated salamander limbs or fish fins precisely regenerate to their pre-injury size, providing a paradigm for positional memory. Although this phenomenon has been appreciated for centuries, how position-dependent cues control tissue growth remains unresolved. Here we quantify extracellular signal-regulated kinase (Erk) activity in whole populations of osteoblasts during zebrafish fin regeneration. We show that Erk activity scales with the amount of amputated tissue, predicts the likelihood of osteoblast cycling, and predicts the size of regenerated skeletal structures. We find that osteoblast Erk activity depends on fibroblast growth factors receptor signalling and organizes into millimetre-long gradients spanning from the distal tip to the amputation site. Mathematical modelling suggests gradients are established by acute, distally restricted deposition of ligand, whose activity is long-lived and transported by tissue growth. This mechanism is supported by the observed scaling of expression of the essential epidermal ligand Fgf20a with extents of amputation. Our work provides evidence that localized, scaled expression of pro-regenerative ligands instructs long-range signalling and cycling to control size in regenerating appendages.

PMID 42719339
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PubMedFrontiers in microbiology2026-09-10

Endogenous Amphiregulin promotes muscle repair and function through expansion of fibro-adipogenic progenitors during chronic Toxoplasma gondii infection in mice.

Shihab Ronzon R, Alfaro-Chacon Andrea A, Humby Monica M, Buerger Caleb C et al.

Skeletal muscle regeneration relies on coordinated interactions between immune cells and resident stem cell populations. While most studies have focused on sterile injury, the impact of infections on muscle repair remains less understood. Toxoplasma gondii, a widespread parasite that establishes chronic infection in skeletal muscle and also the central nervous system, induces myositis, fibrosis, and loss of muscle function. In mice, a natural intermediate host, chronic infection sustains a robust Th1 response dominated by IFNγ-producing CD4+ and CD8+ T cells. Regulatory T cells (Tregs), which normally promote resolution of inflammation, instead adopt a pathogenic phenotype, increasing inflammation and impairing repair. Amphiregulin (Areg), a ligand of the epidermal growth factor receptor, has been implicated in tissue repair by enhancing Treg function, promoting macrophage polarization, and supporting mesenchymal differentiation. While exogenous Areg improves muscle function during chronic T. gondii infection, the role of endogenous Areg remains unknown. Here, we used Areg-deficient mice to investigate its contribution to muscle repair during chronic infection. We show that Areg deficiency impaired Areg deficiency impaired fibro-adipogenic progenitor (FAP) expansion, reduced IFNγ-producing CD8+ T cells, and diminished the frequency of Tbet+ Tregs. Additionally, following CTX injury, Areg-deficient mice, particularly females, exhibited impaired regeneration characterized by smaller, more heterogeneous myofibers, and increased damaged area. These findings reveal a critical role for endogenous Areg in timely FAP expansion, proper effector and regulatory T cell polarization, and efficient muscle regeneration in the setting of chronic T. gondii infection.

PMID 42718992
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