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EGFR Antibodies
AND EGFR ELISA kits, EGFR Proteins
Many biological assays use antibodies to detect EGFR, such as Western Blot (WB), ELISA, Flow Cytometry, Immunocytochemistry (IHC). These antibodies can be polyclonal or monoclonal, and react with EGFR in Human, Mouse, Rat, and many other animal samples. Boster Bio use mainly mouse and rabbit to develop EGFR antibodies...
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EGFR Biomarker Info
A comprehensive clinical reference covering EGFR biomarker testing, ALK inhibitor therapy, MET amplification, KRAS mutation analysis, pre-validated protocols, and pemetrexed efficacy in non-small-cell lung cancer.
Topics Covered
Understanding EGFR Biomarker Info in Lung Cancer Management
Why molecular biomarkers are redefining non-small-cell lung cancer care
The landscape of non-small-cell lung cancer (NSCLC) treatment has been transformed over the past two decades by the identification and clinical application of actionable molecular biomarkers. Chief among these is the epidermal growth factor receptor (EGFR), whose activating mutations predict sensitivity to targeted tyrosine kinase inhibitors (TKIs). Alongside EGFR, markers including ALK rearrangements, MET amplifications, and KRAS mutations collectively guide treatment stratification, enabling clinicians to select or exclude specific therapeutic agents with a precision that was impossible under purely histological classification.
This article consolidates current egfr biomarker knowledge across six clinical domains: integrating EGFR mutation testing into routine NSCLC workup, leveraging ALK inhibitor crizotinib for advanced disease, addressing acquired resistance through MET amplification detection, applying KRAS analysis for therapy exclusion, implementing pre-validated testing protocols to shorten turnaround times, and reviewing the clinical evidence base for pemetrexed in lung cancer trials.
EGFR Mutation Testing in NSCLC
Integrating EGFR biomarker analysis as a standard diagnostic step in non-small-cell lung cancer treatment planning.
Rationale for EGFR Testing
Identifying patients most likely to benefit from EGFR-targeted therapy
EGFR mutations are detected in approximately 10-15% of Western NSCLC patients and up to 50% of Asian patients with adenocarcinoma histology. The most common activating mutations are exon 19 deletions and the L858R point mutation in exon 21, together accounting for roughly 85-90% of all sensitizing EGFR alterations. Patients harbouring these mutations derive substantial clinical benefit from first-, second-, and third-generation EGFR TKIs, including erlotinib, afatinib, and osimertinib.
Current guidelines from major oncology bodies recommend reflex EGFR mutation testing at diagnosis for all patients with advanced, non-squamous NSCLC, and selectively for mixed or unknown histology. Testing should be performed on tumour tissue whenever possible, with plasma-based liquid biopsy serving as a complementary option when tissue is insufficient or unavailable. Real-time PCR platforms, next-generation sequencing (NGS) panels, and allele-specific PCR are the principal methodologies deployed in certified molecular pathology laboratories.
Common EGFR Sensitizing Mutation Types
| Mutation | Exon | Frequency | TKI Sensitivity |
|---|---|---|---|
| Exon 19 Deletion | 19 | ~45% | High (1st, 2nd, 3rd gen) |
| L858R Point Mutation | 21 | ~40% | High (1st, 2nd, 3rd gen) |
| G719X | 18 | ~3% | Moderate (afatinib) |
| Exon 20 Insertion | 20 | ~5-10% | Low (standard TKIs) |
| T790M (acquired) | 20 | ~50% post-progression | High (osimertinib) |
The detection of T790M in plasma following progression on first- or second-generation TKI therapy has become a pivotal indication for switching to osimertinib. Liquid biopsy in this context shortens the time from clinical progression to therapeutic decision, avoiding invasive re-biopsy procedures and preserving patient quality of life during a critical transition.
Key Testing Indications
- All advanced non-squamous NSCLC at diagnosis
- Mixed or unknown histology with adequate sample
- Re-biopsy or liquid biopsy at disease progression
- Patients considered for adjuvant osimertinib after resection
- Early-stage tumours when adjuvant TKI eligibility is under review
Preferred Specimen Types
- Formalin-fixed paraffin-embedded (FFPE) tissue
- Fresh frozen tissue
- Cytology cell blocks
- Plasma circulating tumour DNA (ctDNA)
ALK Inhibitor Crizotinib for Advanced NSCLC
How the first ALK inhibitor transformed outcomes for a molecularly defined NSCLC subpopulation.
ALK Rearrangements and the Role of Crizotinib
Matching the right biomarker to the right agent
Anaplastic lymphoma kinase (ALK) gene rearrangements, most commonly the EML4-ALK fusion, occur in approximately 3-5% of NSCLC cases. These rearrangements define a distinct molecular subtype enriched in younger patients, never or light smokers, and adenocarcinoma histology. The identification of ALK rearrangement as a driver alteration led directly to the development of crizotinib, a first-in-class oral ALK/MET/ROS1 inhibitor approved for ALK-positive advanced NSCLC based on landmark phase III clinical evidence.
The PROFILE 1014 trial demonstrated that crizotinib significantly improved progression-free survival (PFS) compared to platinum-based chemotherapy in previously untreated ALK-positive advanced NSCLC (10.9 months vs. 7.0 months, HR 0.45). Overall response rate with crizotinib reached 74% versus 45% in the chemotherapy arm. These results established crizotinib as the standard first-line therapy for ALK-rearranged NSCLC and validated ALK as a central EGFR biomarker-class target alongside EGFR itself.
Fluorescence in situ hybridisation (FISH) remains the FDA-approved companion diagnostic for ALK-positive NSCLC, though immunohistochemistry (IHC) with D5F3 clone and NGS panels are increasingly accepted in clinical practice for their speed, throughput, and capacity to simultaneously screen multiple biomarkers. Co-testing for EGFR biomarker status and ALK in a multiplex panel is now recommended to streamline the diagnostic pathway for newly diagnosed advanced NSCLC patients.
FISH Testing
FDA-approved companion diagnostic for ALK-positive NSCLC. Detects chromosomal rearrangements with high specificity using fluorescent probes targeting ALK break-apart regions.
IHC (D5F3 Clone)
Rapid, cost-effective alternative for ALK detection on FFPE tissue. High sensitivity when performed with validated automated platforms such as the Ventana OptiView amplification system.
NGS Panel
Simultaneous detection of ALK, EGFR, ROS1, MET, KRAS, and other actionable alterations in a single assay. Preferred when tissue is limited and comprehensive biomarker profiling is required.
Drug Resistance and MET Amplification Detection
Overcoming acquired resistance in EGFR-mutant NSCLC through MET pathway characterisation.
MET Amplification as a Resistance Mechanism
The bypass signalling pathway that undermines EGFR-targeted therapy
Acquired resistance to EGFR TKI therapy is an inevitable clinical challenge. While T790M gatekeeper mutation accounts for approximately 50-60% of resistance to first- and second-generation TKIs, MET proto-oncogene amplification emerges as a resistance mechanism in 5-20% of cases, including as a co-occurring resistance event alongside T790M and as the predominant mechanism of resistance to osimertinib. MET amplification activates the PI3K/AKT and RAS/MAPK downstream signalling cascades independently of EGFR, effectively bypassing TKI blockade.
Identifying MET amplification at progression is therefore clinically actionable. Combinations of EGFR TKIs with MET inhibitors such as savolitinib, capmatinib, and tepotinib are under active clinical investigation and have shown promising activity in MET-amplified, EGFR-mutant post-progression cohorts. The SAVANNAH and GEOMETRY mono-1 trials exemplify this therapeutic strategy, with response rates in the 30-65% range depending on the degree of MET amplification (gene copy number or FISH-based MET-to-CEP7 ratio).
MET Amplification Detection Methods
| Method | Platform | Clinical Utility |
|---|---|---|
| FISH (MET/CEP7 ratio) | Tissue | Gold standard; stratifies high vs. low amplification |
| NGS (copy number variation) | Tissue / ctDNA | Comprehensive; concurrent biomarker profiling |
| IHC (MET protein expression) | FFPE tissue | Rapid screen; correlates imperfectly with amplification |
| RT-PCR (MET exon 14 skipping) | RNA-based | Detects splice-site mutations causing MET activation |
For optimal clinical decision-making, MET testing at progression should be incorporated into a comprehensive re-biopsy or liquid biopsy panel that simultaneously evaluates T790M status, MET amplification, EGFR amplification, and other emergent resistance alterations. This multi-biomarker approach at progression mirrors the expanded egfr biomarker profiling performed at initial diagnosis and ensures that therapeutic options are not overlooked.
Resistance Mechanisms at EGFR TKI Failure
- T790M mutation - ~50-60% of 1st/2nd gen TKI resistance
- MET amplification - 5-20% across TKI generations
- HER2 amplification - 8-13% post-osimertinib
- C797S EGFR mutation - ~10-15% post-osimertinib
- RET fusions - Emerging mechanism
- Small-cell transformation - 3-14% histological switch
Clinical Action Points
- Mandatory re-biopsy or ctDNA at progression
- MET FISH or NGS copy number analysis
- Consider clinical trial enrolment for MET inhibitor combination
- Multidisciplinary tumour board review for resistance workup
KRAS Mutation Analysis for Therapy Exclusion
Using KRAS status as a negative predictive biomarker to guide and exclude specific treatment strategies.
The Clinical Significance of KRAS Mutations
From therapy exclusion to emerging targeted options
KRAS mutations are the most common oncogenic driver in NSCLC, detected in approximately 25-30% of all lung adenocarcinomas, with KRAS G12C representing the most frequent single variant (approximately 13% of NSCLC overall). Historically, KRAS mutations have served primarily as a predictive biomarker for exclusion from anti-EGFR therapies in colorectal cancer and as a general negative prognostic indicator in lung cancer. In NSCLC, KRAS mutations and EGFR mutations are mutually exclusive at the clonal level in the vast majority of cases, making concurrent positivity a signal for scrutiny of the testing result rather than biological co-occurrence.
The mutual exclusivity of KRAS and EGFR mutations is clinically important because a patient harbouring a KRAS mutation is unlikely to benefit from EGFR TKI therapy. In clinical practice, KRAS mutation testing therefore serves as a rapid preliminary exclusion step: a positive KRAS result effectively removes EGFR-targeted therapy from the treatment algorithm, directs the clinician toward standard chemotherapy regimens or immunotherapy, and reserves EGFR testing resources for KRAS-negative cases when comprehensive NGS is not performed upfront.
The emergence of covalent KRAS G12C inhibitors, most notably sotorasib (AMG 510) and adagrasib (MRTX849), has fundamentally repositioned KRAS from an undruggable target to an actionable oncogene in its own right. The CodeBreaK 100 phase II trial demonstrated an objective response rate of 37.1% and a disease control rate of 80.8% with sotorasib in previously treated KRAS G12C-mutant NSCLC. KRAS G12C status is now a positive predictive biomarker in its own right, warranting reflex testing as part of a comprehensive lung cancer molecular panel. The broader KRAS mutation landscape (G12D, G12V, G13C) remains without approved targeted therapy, preserving the exclusion-focused role of non-G12C KRAS mutations for the time being.
KRAS Variants and Therapeutic Implications
| KRAS Variant | Frequency in NSCLC | Targeted Agent Available |
|---|---|---|
| G12C | ~13% | Sotorasib, Adagrasib |
| G12D | ~4% | None approved (trials ongoing) |
| G12V | ~5% | None approved |
| G13C | ~1% | None approved |
| Other KRAS | ~6% | None approved |
KRAS vs. EGFR: Clinical Decision Logic
- KRAS mutant:
- Exclude EGFR TKI therapy
- If G12C: sotorasib or adagrasib (post 1L)
- Consider pembrolizumab if PD-L1 high
- Platinum-based doublet as backbone
- KRAS wild-type:
- Proceed with EGFR mutation testing
- Test ALK, ROS1, MET, RET, NTRK
- Assess PD-L1 expression by IHC
- Select targeted therapy if driver found
Pre-Validated Protocols to Reduce Turnaround Time
Implementing standardised, pre-validated workflows to accelerate EGFR biomarker reporting and inform timely clinical decisions.
Clinical Efficacy of Pemetrexed in Lung Cancer Trials
Reviewing the evidence base for pemetrexed as a chemotherapy partner in NSCLC, particularly in the context of biomarker-informed patient selection.
Pemetrexed: Mechanism and Histology-Based Selection
Why pemetrexed efficacy is inherently linked to biomarker expression
Pemetrexed is a multitargeted antifolate that inhibits thymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT), disrupting folate metabolism and purine/pyrimidine synthesis. Its clinical efficacy in lung cancer is strongly associated with histological subtype, which serves as a surrogate biomarker for TS expression. Squamous cell carcinoma expresses significantly higher levels of TS compared to adenocarcinoma, conferring relative resistance to pemetrexed, while adenocarcinomas and large-cell carcinomas are more sensitive. This observation underpins current clinical practice guidelines that restrict pemetrexed use to non-squamous NSCLC.
The pivotal JMDB phase III trial (Scagliotti et al., 2008) established pemetrexed plus cisplatin as equivalent in overall survival to gemcitabine plus cisplatin across all NSCLC histologies, with a significant survival advantage for pemetrexed in non-squamous histology (OS: 12.6 vs. 10.9 months) and an inferior outcome in squamous histology (OS: 9.4 vs. 10.8 months). Subsequent studies extended pemetrexed into maintenance and combination settings, reinforcing its central role in non-squamous NSCLC management.
In the era of targeted therapy and immunotherapy, pemetrexed remains clinically relevant both as a chemotherapy backbone in combination with pembrolizumab (KEYNOTE-189 regimen) and as a component of chemotherapy-targeted therapy combinations under clinical investigation. For EGFR-mutant NSCLC patients who progress on TKI therapy and have exhausted targeted options, platinum-pemetrexed chemotherapy provides a well-tolerated and effective subsequent treatment choice, particularly in the context of EGFR biomarker-informed patient management where the therapeutic trajectory has been defined from the outset.
Key Pemetrexed Clinical Trials
- JMDB (2008): Pemetrexed + cisplatin vs. gemcitabine + cisplatin; non-squamous OS advantage established
- PARAMOUNT (2012): Pemetrexed maintenance after pemetrexed-cisplatin induction; improved PFS and OS in non-squamous NSCLC
- KEYNOTE-189 (2018): Pembrolizumab + pemetrexed + platinum vs. chemotherapy alone; significant PFS and OS benefit regardless of PD-L1 expression
- JMEN (2009): Pemetrexed maintenance vs. placebo post-platinum induction; PFS benefit established
Biomarker Correlation
- Low TS expression predicts pemetrexed sensitivity
- Non-squamous histology serves as clinical surrogate
- EGFR-mutant NSCLC patients benefit as post-TKI chemotherapy option
Frequently Asked Questions
Common clinical and scientific questions about EGFR biomarker testing and related molecular markers in NSCLC.
Q1. What is an EGFR biomarker and why does it matter in NSCLC?
An EGFR biomarker refers to a detectable molecular alteration in the epidermal growth factor receptor gene (EGFR) that carries predictive or prognostic significance in cancer management. In NSCLC, activating mutations in EGFR exons 18-21 predict sensitivity to EGFR tyrosine kinase inhibitors (TKIs), making EGFR biomarker testing a critical component of the diagnostic workup for all newly diagnosed advanced non-squamous NSCLC patients. Identifying EGFR-positive patients enables precision oncology: the right patient receives the right drug at the right time, avoiding the toxicity and limited efficacy of non-selected chemotherapy as a first-line option.
Q2. Can EGFR and KRAS mutations occur simultaneously in the same tumour?
True co-occurrence of activating EGFR and KRAS mutations in the same tumour cell clone is biologically rare and has been estimated at less than 1% of cases in well-conducted molecular series. The two oncoproteins operate in the same downstream signalling cascade (RAS-MAPK pathway), and selection pressure during oncogenesis typically favours one driver over the other. When apparent co-occurrence is reported, it usually reflects either tumour heterogeneity (different mutations in different clonal populations within the specimen), a subclonal resistance mechanism arising during treatment, or laboratory error. Concurrent EGFR and KRAS positivity should therefore prompt expert review of the testing result before clinical decisions are made.
Q3. How does MET amplification differ from MET exon 14 skipping as a biomarker?
MET amplification and MET exon 14 skipping are two distinct molecular mechanisms of MET pathway activation. MET amplification refers to an increase in gene copy number, leading to overexpression of MET protein and constitutive downstream signalling. It occurs as both a primary oncogenic driver (rare in treatment-naive NSCLC, approximately 2-4%) and as an acquired resistance mechanism following EGFR TKI exposure. MET exon 14 skipping mutations, by contrast, are splice-site alterations that prevent normal CBL-mediated ubiquitination and degradation of MET protein, prolonging its signalling activity. Exon 14 skipping mutations define a distinct NSCLC subgroup (approximately 3-4% of cases) enriched in older patients and pleomorphic carcinomas. Both are actionable with MET inhibitors, but detection requires different assay strategies: FISH or NGS copy number analysis for amplification; RNA-based NGS or RT-PCR for exon 14 skipping.
Q4. What is the recommended turnaround time for EGFR biomarker testing?
Professional society guidelines, including those from ESMO and CAP/IASLC/AMP, recommend that EGFR biomarker results be available within 10 working days of specimen receipt for tissue-based testing, with an aspirational target of 5 working days where infrastructure supports it. Rapid single-gene assays such as cobas EGFR Mutation Test v2 can return results within 24-48 hours when required for urgent clinical decision-making. Liquid biopsy platforms using digital droplet PCR or NGS typically report ctDNA-based EGFR results within 5-7 working days. Institutions implementing pre-validated protocols with defined specimen triage priorities, batching strategies, and bioinformatic pipelines consistently achieve shorter turnaround times compared to ad hoc testing workflows.
Q5. Is pemetrexed effective in EGFR-mutant NSCLC patients?
Pemetrexed-based chemotherapy is a recognised and effective therapeutic option for EGFR-mutant NSCLC patients who have progressed on EGFR TKI therapy and have exhausted targeted treatment options. Since EGFR-mutant tumours are predominantly adenocarcinomas, they belong to the non-squamous histological category where pemetrexed demonstrates its greatest efficacy. Retrospective and prospective data from studies such as the NEJ009 trial (erlotinib plus bevacizumab, then chemotherapy) support the use of platinum-pemetrexed as post-TKI chemotherapy, with response rates of 20-30% and median PFS of 4-6 months in the post-TKI setting. The EGFR biomarker status of a patient, therefore, not only guides first-line treatment selection but also informs subsequent chemotherapy planning.
Q6. Should ALK testing be performed even if EGFR is positive?
In standard clinical practice, concurrent EGFR mutations and ALK rearrangements are considered mutually exclusive at the clonal level, occurring together in fewer than 1% of cases. Consequently, many guidelines allow for sequential testing (EGFR first; if negative, then ALK), although comprehensive upfront NGS panel testing that simultaneously evaluates all actionable biomarkers including EGFR, ALK, ROS1, KRAS, MET, and others is increasingly favoured for efficiency, tissue conservation, and completeness. Upfront panel testing eliminates the risk of missing a concurrent or secondary actionable alteration, is cost-effective when tissue NGS is implemented at scale, and avoids diagnostic delays that might otherwise arise from sequential reflex testing algorithms.
Advance Your EGFR Biomarker Research
Explore validated antibodies, ELISA kits, and molecular reagents for EGFR, ALK, MET, and KRAS research. Contact our scientific support team for guidance on assay selection and protocol optimisation.
References
Key clinical and scientific publications underpinning this article
- Scagliotti GV, et al. Phase III study comparing cisplatin plus gemcitabine with cisplatin plus pemetrexed in chemotherapy-naive patients with advanced-stage non-small-cell lung cancer. J Clin Oncol. 2008;26(21):3543-51.
- Solomon BJ, et al. First-line crizotinib versus chemotherapy in ALK-positive lung cancer. N Engl J Med. 2014;371(23):2167-77.
- Oxnard GR, et al. Association between plasma genotyping and outcomes of treatment with osimertinib (AZD9291) in advanced non-small-cell lung cancer. J Clin Oncol. 2016;34(28):3375-82.
- Cappuzzo F, et al. Erlotinib as maintenance treatment in advanced non-small-cell lung cancer: a multicentre, randomised, placebo-controlled phase 3 study (SATURN). Lancet Oncol. 2010;11(6):521-9.
- Soria JC, et al. Osimertinib in untreated EGFR-mutated advanced non-small-cell lung cancer. N Engl J Med. 2018;378(2):113-25.
- Skoulidis F, et al. Sotorasib for lung cancers with KRAS p.G12C mutation. N Engl J Med. 2021;384(25):2371-81.
- Gandhi L, et al. Pembrolizumab plus chemotherapy in metastatic non-small-cell lung cancer (KEYNOTE-189). N Engl J Med. 2018;378(22):2078-92.
- Wolf J, et al. Capmatinib in MET exon 14-mutated or MET-amplified non-small-cell lung cancer (GEOMETRY mono-1). N Engl J Med. 2020;383(10):944-57.
All EGFR Products
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EGFR Overview
Facts about Epidermal growth factor receptor.
Epidermal growth factor receptor (EGFR)
Receptor tyrosine kinase binding ligands of the EGF family and activating several signaling cascades to convert extracellular cues into appropriate cellular responses (PubMed:2790960, PubMed:10805725, PubMed:27153536). Ligand binding activates receptor homo- and/or heterodimerization and autophosphorylation on crucial cytoplasmic residues.
The phosphorylated receptor recruits adapter proteins like GRB2 which in turn activates complex downstream signaling cascades. Activates at least 4 major downstream signaling cascades including the RAS- RAF-MEK-ERK, PI3 kinase-AKT, PLCgamma-PKC and STATs modules (PubMed:27153536).
Gene Information
| Human | |
|---|---|
| Gene Name: | EGFR |
| Uniprot: | P00533 |
| Entrez: | 1956 |
Family
| Belongs to: |
|---|
| protein kinase superfamily |
Alternative Names
avian erythroblastic leukemia viral (v-erb-b) oncogene homolog; cell growth inhibiting protein 40; cell proliferation-inducing protein 61; EC 2.7.10; EC 2.7.10.1; EGF R; EGFR; epidermal growth factor receptor (avian erythroblastic leukemia viral (v-erb-b)oncogene homolog); epidermal growth factor receptor; ErbB; ErbB1; ERBB1PIG61; HER1; HER-1; mENA; Proto-oncogene c-ErbB-1; Receptor tyrosine-protein kinase erbB-1
Molecular Weight
Mass (kDA):
134.277 kDA
Genomic Context
| Human | |
|---|---|
| Location: | 7p11.2 |
| Sequence: | 7; NC_000007.14 (55019017..55211628) |
Tissue Specificity
Ubiquitously expressed. Isoform 2 is also expressed in ovarian cancers.
Subcellular Localizations
Cell membrane; Single-pass type I membrane protein. Endoplasmic reticulum membrane; Single-pass type I membrane protein. Golgi apparatus membrane; Single-pass type I membrane protein. Nucleus membrane; Single-pass type I membrane protein. Endosome. Endosome membrane. Nucleus. In response to EGF, translocated from the cell membrane to the nucleus via Golgi and ER (PubMed:20674546). Endocytosed upon activation by ligand (PubMed:2790960, PubMed:17182860, PubMed:27153536). Colocalized with GPER1 in the nucleus of estrogen agonist-induced cancer-associated fibroblasts (CAF) (PubMed:20551055).; [Iso
Diseases
- Malignant Neoplasms
- Neoplasms
- Carcinoma
- Malignant Neoplasm Of Lung
- Lung Neoplasms
- Non-small Cell Lung Carcinoma
- Adenocarcinoma
- Malignant Neoplasm Of Breast
- Neoplasm Metastasis
- Malignant Squamous Cell Neoplasm
- Mammary Neoplasms
- Malignant Paraganglionic Neoplasm
Pathways
- Cell Proliferation
- Cell Growth
- Cell Cycle
- Angiogenesis
- Pathogenesis
- Localization
- Cell Death
- Cell Migration
- Endocytosis
- Secretion
- Drug Resistance
- Cell Adhesion
- Transport
PTMs
- Phosphorylation
- Cleavage
- Ubiquitination
- Methylation
- Dephosphorylation
- Glycosylation
- Acetylation
- Biotinylation
- Reduction
- Oxidation
For details, visit:
bosterbio.com/bosterbio-gene-info-cards/EGFR
bosterbio.com/bosterbio-gene-info-cards/EGFR
References
PMID: 6328312 by Ullrich A., et al. Human epidermal growth factor receptor cDNA sequence and aberrant expression of the amplified gene in A431 epidermoid carcinoma cells.
PMID: 7654368 by Ilekis J.V., et al. Possible role of variant RNA transcripts in the regulation of epidermal growth factor receptor expression in human placenta.
22 Publications of Boster EGFR Antibodies & ELISA Kits
- PubMed ID: 10.1186/s12935-021-02277-0, RHBDF2 gene functions are correlated to facilitated renal clear cell carcinoma p...
- PubMed ID: 10.1159/000101926, Epidermal Growth Factor Receptor in Cultured Human Retinal Pigment Epithelial Ce...
- PubMed ID: 10.1111/cbdd.12383, Synthesis and Evaluation of Salicylanilide Derivatives as Potential Epidermal Gr...
- PubMed ID: 10.1080/10286020.2019.1702028, Synthesis, characterization and preliminary biological evaluation of chrysin ami...
- PubMed ID: 10.1016/j.jff.2019.103523, Cultured Cordyceps sinensis polysaccharides attenuate cyclophosphamide-induced i...
- PubMed ID: 10.1016/j.jdiacomp.2018.11.007, Epidermal growth factor receptor and podocin predict nephropathy progression in ...
- PubMed ID: 10.1016/j.ejphar.2011.06.013, Inhibition of angiogenesis involves in anticancer activity of riccardin D, a mac...
- PubMed ID: 10.1016/j.bmcl.2020.127557, Design, synthesis and biological evaluation of novel heptamethine cyanine dye-er...
- PubMed ID: 33537094, Chen X,Gao A,Zhang F,Yang Z,Wang S,Fang Y,Li J,Wang J,Shi W,Wang L, Zheng Y,Sun ...
- PubMed ID: -, Study of the correlation between the expression of nuclear factor kappa B and pr...
- PubMed ID: 30545560 , Epidermal growth factor receptor and podocin predict nephropathy progression in ...
- PubMed ID: 29072695, Glucocorticoid mediates prenatal caffeine exposure-induced endochondral ossifica...
- PubMed ID: 27609096, Anti-tumor activity of erlotinib in the BxPC-3 pancreatic cancer cell line
- PubMed ID: 22507221, YC-1 exerts inhibitory effects on MDA-MB-468 breast cancer cells by targeting EG...
- PubMed ID: 2744159, Anti-tumor activity of erlotinib in the BxPC-3 pancreatic cancer cell line
- PubMed ID: 20092659, Gu Y, Zhang S, Wu Q, Xu S, Cui Y, Yang Z, Zhao X, Sun B. J Exp Clin Cancer Res. ...
- PubMed ID: 19263229, Wang Sb, Cheng Yn, Cui Sx, Zhong Jl, Ward Sg, Sun Lr, Chen Mh, Kokudo N, Tang W,...
- PubMed ID: 21349701, Yue P, Gao Zh, Xue X, Cui Sx, Zhao Cr, Yuan Y, Yin Z, Inagaki Y, Kokudo N, Tang ...
- PubMed ID: 21208277, Qin Li L, Huang Hl, Ping Jl, Xu W, Li J, Dai Lc. Apmis. 2011 Feb;119(2):103-10. ...
- PubMed ID: 24567178, Zhang H, Mao Y, Zhang F, Ye C, Tong H, Su Y, Zhu J. Mol Cell Biochem. 2014 Jun;3...
- PubMed ID: 22126621, Achmad A, Hanaoka H, Yoshioka H, Yamamoto S, Tominaga H, Araki T, Ohshima Y, Ori...
*Showing only the more recent 20. More publications can be found for each product on its corresponding product page