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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

PubMedCancer treatment and research communications2026-06-13

Real-world testing practices, treatment patterns, and outcomes of tyrosine kinase inhibitors (TKIs) in epidermal growth factor receptor-mutated advanced/metastatic non-small cell lung cancer: An international study.

Samol Jens J, Demedts Ingel I, Erman Mustafa M, Kozlov Vadim V et al.

To describe epidermal growth factor receptor (EGFR) mutation (EGFRm) testing practices and treatment patterns in EGFRm-positive patients with advanced/metastatic non-small cell lung cancer (NSCLC) and evaluate clinical outcomes. Data were drawn from a cross-sectional, retrospective chart review of adult patients with advanced/metastatic NSCLC in Argentina, Belgium, Brazil, India, the Netherlands, Russia, Singapore, Switzerland, and Türkiye between June-September 2021. Eligible patients had an initial advanced/metastatic stage NSCLC diagnosis, and positive first EGFRm test between April 2017-March 2018. Data were reported from NSCLC diagnosis to end of follow-up (June-2020) or death. Index was the receipt date of EGFRm result. Analyses were descriptive. Overall, 208 physicians reported data on 947 patients. Mean (standard deviation) age at diagnosis was 60.3 (10.9) years and 79.4% had an ECOG 0-1. EGFRm was identified by single-gene (64.0%) and multi-gene (36.0%) panel testing. Median (interquartile range) turnaround time was 14 (10-22) days. Prior to and following index, 26.9% and 68.6% of patients, respectively, were administered EGFR-tyrosine kinase inhibitors (EGFR-TKI) as first-line (1 L) treatment. Disease progression occurred in 60.4% and 70.1% pre-index and post-index, respectively. Among those receiving 1 L EGFR-TKI, partial response was reported in 56.5% of patients pre-index and in 65.0% post-index. The median overall survival on post-index 1 L EGFR-TKI was not reached. EGFRm status was mostly determined by single-gene testing, and around one-quarter of patients were prescribed pre-index 1 L EGFR-TKI. Further research into outcomes for EGFRm-positive patients not receiving 1 L EGFR-TKI, and pre-index vs post-index treatment would be valuable.

PMID 42284848
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PubMedBreast cancer (Tokyo, Japan)2026-06-13

Annual report of national clinical database-breast cancer registry in 2023: systemic therapy for small breast cancer.

Sasada Shinsuke S, Kumamaru Hiraku H, Kinukawa Naoko N, Iwamoto Takayuki T et al.

This annual report of the National Clinical Database-Breast Cancer Registry (NCD-BCR) by the Japanese Breast Cancer Society presents nationwide breast cancer statistics for patients registered in Japan in 2023. Among 107,372 patients with breast cancer at 1317 institutions, 99.3% were females with a median age of 62 years. The distribution of the clinical stages was as follows: stage 0 (15.5%); stage I (42.1%); stage II (31.1%); stage III (7.0%); and stage IV (2.1%). Estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2) positivity was observed in 78.9%, 70.0%, and 13.3% of patients, respectively. Among 102,717 patients without distant metastases, 41.2% underwent breast-conserving surgery, 76.5% underwent sentinel lymph node biopsy, and 6.0% underwent breast reconstruction. The distribution of radiotherapy was as follows: 75.2% received whole-breast irradiation, 15.7% chest-wall irradiation, and 20.7% regional irradiation. Among the 13,061 patients with pT1abN0M0 breast cancer, comprising 10,819 hormone receptor [HR]-positive/HER2-negative, 1479 HER2-positive and 763 HR-negative/HER2-negative individuals, 92.4% of HR-positive/HER2-negative patients received endocrine therapy, 46.9% of HER2-positive patients received chemotherapy and/or anti-HER2 therapy, and 31.2% of HR-negative/HER2-negative patients received chemotherapy. This annual report provides a nationwide overview of contemporary systemic therapy patterns in small breast cancer and highlights size‑dependent and subtype‑specific use of systemic therapy in Japan, reflecting a risk‑adapted treatment strategy.

PMID 42286387
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PubMedCell death & disease2026-06-13

Inflammation reprograms fibro-adipogenic progenitors to sustain immunopathogenic niches in myositis.

Nelke Christopher C, Sanchez-Dal Cin Julian J, Dallevet Charles-Antoine CA, Park Jin-Soo JS et al.

Idiopathic inflammatory myopathies (IIMs) are autoimmune disorders defined by persistent muscle inflammation, fibrosis, and frequent resistance to current therapies. However, the mechanisms perpetuating disease activity despite immunosuppressive treatment remain elusive. Here, we describe a novel role for tissue-resident stromal cells, specifically fibro-adipogenic progenitors (FAPs), in sustaining skeletal muscle inflammation. Utilizing single-nucleus and spatial transcriptomics in 24 IIM patients and six non-diseased controls, we describe how FAPs adapt to their tissue context, favoring T-cell-centric programs in T-cell environments and myeloid programs in macrophage environments. At the spatial level, FAPs form inflammatory niches by co-localizing with muscle stem cells and activated macrophages, positioning them to participate in cell-to-cell communication with both immune and muscle cells. Trajectory and ligand-receptor analyses suggest a dual-input mechanism whereby infiltrating immune cells (via TGF-β) and myofibers (via epidermal growth factor (EGF)) converge on the AP-1 transcription factor to drive FAP differentiation toward a pro-inflammatory and pro-fibrotic phenotype. Mechanistically, exposure of primary human FAPs to TGF-β and EGF induces a primed state by altering the accessibility to AP-1 regulatory elements. Together, our findings reveal a previously unrecognized role of tissue-resident stromal cells in IIM, highlighting microenvironmental cross-talk centered on FAPs as a promising and actionable therapeutic target.

PMID 42285969
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PubMedBiochemical pharmacology2026-06-13

RRBP1 promotes osimertinib resistance by activating fatty acid oxidation-dependent metabolic and immune reprogramming in EGFR-Mutant lung adenocarcinoma.

Huang Yajie Y, Zhang Yaozhong Y

Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that improves clinical outcomes in patients with EGFR-mutant lung adenocarcinoma (LUAD); however, acquired resistance remains a major limitation. Increasing evidence suggests that metabolic reprogramming within the tumor microenvironment contributes to drug resistance, whereas the molecular mechanisms linking lipid metabolism and immune regulation remain incompletely defined. In this study, lipid metabolic remodeling in osimertinib resistance was investigated to identify resistance-associated molecular factors. By integrating single-cell RNA sequencing, bulk transcriptomic analysis, machine learning-based modeling, Mendelian randomization and whole-genome sequencing, ribosome-binding protein 1 (RRBP1) was identified as a core resistance-associated factor. Resistant tumors showed enrichment of lipid metabolism-active M2 macrophages. Mechanistic analyses showed that RRBP1 activated the sterol regulatory element-binding protein 1 (SREBP1)-carnitine palmitoyltransferase 1A (CPT1A)-fatty acid oxidation (FAO) pathway, leading to increased lipid metabolic activity in tumor cells. This metabolic shift promoted M2 macrophage polarization through lipid-dependent signaling and was associated with an immunosuppressive microenvironment and reduced osimertinib sensitivity. Pharmacological inhibition of FAO partially reversed macrophage polarization and restored drug responsiveness in resistant cells. These findings support a relationship among RRBP1, SREBP1-CPT1A-FAO-related lipid metabolic remodeling, M2 macrophage polarization and osimertinib resistance. RRBP1 and FAO-related metabolic activity may represent candidate factors for further investigation in osimertinib-resistant LUAD.

PMID 42285369
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PubMedJournal of medical Internet research2026-06-13

Application Value of Radiomics-Based Machine Learning for Preoperative Risk Stratification of Bladder Cancer: Systematic Review and Meta-Analysis.

He Zirong Z, Liu Yinghua Y, Jiang Qin Q, Hou Fang F et al.

Some researchers have explored the application of radiomics-based machine learning to detect preoperative muscle invasion, high-grade tumors, human epidermal growth factor receptor 2 expression, and other risk factors for bladder cancer. However, systematic evidence proving its effectiveness remains lacking. This study aimed to evaluate the performance of radiomics-based machine learning in preoperative risk stratification for patients with bladder cancer. These findings could contribute to advancing the development or updating of intelligent risk assessment tools for bladder cancer. The Embase, Cochrane Library, PubMed, and Web of Science databases were systematically retrieved for publicly available studies on the effectiveness of radiomics-based machine learning (ML) in the preoperative risk stratification of bladder cancer up to October 17, 2025. The risk of bias in the included studies was evaluated using the Prediction Model Risk of Bias Assessment Tool for Artificial Intelligence. The overall quality of the studies was quantified using the Radiomics Quality Scoring tool. The certainty of the evidence was graded using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) framework. Subgroup analyses were conducted according to the type of imaging source and modeling method. This meta-analysis ultimately incorporated 57 studies with a total of 11,933 participants. These studies primarily used radiomics-based ML to identify muscle invasion (n=34) and high-grade tumors (n=16). Additionally, the methodology was used to evaluate human epidermal growth factor receptor 2 positive expression (n=3), Ki-67 expression (n=2), and lymph node staging (n=2) preoperatively in bladder cancer. In the validation sets, the pooled area under the receiver operating characteristic curve (AUROC) for identifying muscle invasion was 0.893 (95% CI 0.840-0.948), 0.916 (95% CI 0.891-0.942), and 0.840 (95% CI 0.737-0.958) for computed tomography (CT)-, magnetic resonance imaging (MRI)-, and ultrasound-based radiomics, respectively. The AUROC was 0.874 (95% CI 0.852-0.896) and 0.921 (95% CI 0.867-0.979) for models integrating clinical features with CT- or MRI-based radiomics, respectively. The pooled AUROC for diagnosing high-grade tumors was 0.874 (95% CI 0.775-0.985), 0.846 (95% CI 0.663-1.000), and 0.750 (95% CI 0.636-0.884) for CT-, MRI-, and ultrasound-based radiomics, respectively. Furthermore, the AUROC was 0.919 (95% CI 0.774-1.000) for MRI-based radiomics combined with clinical features. This is the first systematic review to comprehensively evaluate the role of radiomics in preoperative risk stratification for bladder cancer. It provides evidence to inform the development and refinement of future ML-based tools for image analysis in this setting. However, this evidence faces significant challenges, including methodological shortcomings and a high risk of bias and low GRADE level, which preclude its readiness for clinical translation. Future studies should standardize the methodological workflows in radiomics, conduct multicenter research, and thoroughly evaluate and discuss the validity of external validation.

PMID 42285048
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PubMedSignal transduction and targeted therapy2026-06-13

Anlotinib combined with neoadjuvant chemotherapy for HR+/HER2- breast cancer (ACNTBC): a prospective, single-arm, single-center phase II clinical study with real-world validation.

Ding Jiajun J, Meng Huimin H, Wang Yidi Y, Zi Haoyi H et al.

Despite being an option for high-risk or inoperable cases, existing neoadjuvant therapies for hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) breast cancer yield suboptimal pathological responses, necessitating novel strategies. This prospective, phase II ACNTBC trial (NCT05558722) investigated the efficacy and safety of combining anlotinib with chemotherapy as a neoadjuvant treatment for HR+/HER2- breast cancer. Enrolled patients received 5 cycles of anlotinib (12 mg qd, d1‒14; q3w) plus 6 cycles of nab-paclitaxel (200 mg/m2, q3w), pirarubicin (50 mg/m2, q3w), and cyclophosphamide (500 mg/m2, q3w). The primary endpoint was the total pathological complete response (tpCR) rate, with the major secondary endpoints including residual cancer burden (RCB) 0/I rate, objective response rate (ORR), and safety. The study enrolled 31 patients, and the ORR was 93.5% (29/31, 95% CI, 78.6-99.2). In the per-protocol set of 28 patients completing treatment and surgery, the tpCR rate was 14.3% (4/28, 95% CI, 4.0-32.7), with RCB 0/I rate of 25.0% (7/28, 95% CI, 10.7-44.9). Grade 3/4 adverse events included hematologic toxicities, hypertension, proteinuria, and headache, all manageable. Post-hoc biomarker analysis showed that high baseline VEGFR2 expression and microvessel density (MVD) were significantly associated with superior efficacy, and the treatment significantly reduced Ki-67 index, VEGFR2 expression, and MVD. Supporting evidence from an exploratory inverse probability of treatment weighting (IPTW) analysis using a real-world cohort receiving chemotherapy alone indicated a potential benefit of the combination over chemotherapy alone. In conclusion, neoadjuvant anlotinib plus chemotherapy demonstrates promising efficacy and manageable safety in HR+/HER2- breast cancer with a high Ki-67 index.

PMID 42285923
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