As predictive markers for anti-EGFR therapy, KRAS and BRAF mutations are routinely detected in primary and metastatic colorectal tumor (CRC) cells, but rarely in circulating tumor cells (CTCs). (buyresearchchemicalss.net)
Epidermal growth factor receptor (EGFR)‐activating mutations confer sensitivity to tyrosine kinase inhibitor (TKI) treatment for non‐small‐cell lung cancer (NSCLC). (tokushima-u.ac.jp)
ASP8273 is a highly specific, irreversible, once‐daily, oral, EGFR TKI that inhibits both activating and resistance mutations. (tokushima-u.ac.jp)
ASP8273 300 mg was generally well tolerated and showed antitumor activity in Asian patients with both EGFR‐activating and T790M mutations. (tokushima-u.ac.jp)
Activating Mutations in the Epidermal Growth Factor Receptor Underlying Responsiveness of Non-Small-Cell Lung Cancer to Gefitinib" (PDF). (wikipedia.org)
Structural analyses and computational modeling indicate that EGFR G724S mutations may induce a conformation of the glycine-rich loop, which is incompatible with the binding of third-generation TKIs. (nature.com)
The identification of EGFR mutations and the discovery of their exquisite sensitivity to epidermal growth factor receptor (EGFR) inhibitors dramatically changed the therapeutic routine for lung adenocarcinoma (LADC) patients 1 , 2 , 3 . (nature.com)
First-generation EGFR TKIs, binding competitively and reversibly to the ATP-binding site of the EGFR tyrosine kinase domain, have resulted in a significant improvement in outcome for NSCLC patients with activating EGFR mutations (L858R and Del19). (researchgate.net)
The second-generation EGFR/HER TKIs were developed to treat resistant disease, targeting not only T790M but EGFR-activating mutations and wild-type EGFR. (researchgate.net)
The third-generation EGFR TKIs selectively and irreversibly target EGFR T790M and activating EGFR mutations, showing promising efficacy in NSCLC resistant to the first- and second-generation EGFR TKIs. (researchgate.net)
Currently, the first-generation gefitinib and erlotinib and second-generation afatinib have been approved for first-line treatment of metastatic NSCLC with activating EGFR mutations. (researchgate.net)
In this review, we summarize the available post-progression therapies including third-generation EGFR inhibitors and combination treatment strategies for treating patients with NSCLC harboring EGFR mutations and address the known mechanisms of resistance. (researchgate.net)
As we entered 2010, thoracic medical oncologists were moving away from a histology-agnostic approach and increasingly testing for activating mutations in EGFR . (medscape.com)
We also saw new and improved treatment options for EGFR- and ALK-positive disease and a growing array of new driver mutations with paired targeted therapies. (medscape.com)
In the past decade, applicability of targeted therapy expanded from EGFR and ALK to now include six other actionable mutations- RET , BRAF , ROS1 , MET exon 14, NTRK , and KRAS -with strong enough data to be included in National Comprehensive Cancer Network guidelines . (medscape.com)
With emerging targets, such as EGFR exon 20 and HER2 , we are hopeful this trend of newly recognized driver mutations and therapies will continue in the current decade. (medscape.com)
Somatic mutations in the TP53 , EGFR , and KRAS genes are common in lung cancers. (medlineplus.gov)
Mutations in epidermal growth factor receptor ( EGFR ), KRAS, and anaplastic lymphoma kinase ( ALK ) are mutually exclusive in patients with NSCLC, and the presence of one mutation in lieu of another can influence response to targeted therapy. (medscape.com)
[ 4 ] Further investigation demonstrated that the highest response rates to these TKIs were seen in patients with somatic mutations within the EGFR-TK domain, particularly exon 19 deletion, exon 21 L858R, and exon 18 G719X. (medscape.com)
In general, activating EGFR mutations are more commonly observed in patients with adenocarcinomas and no prior history of smoking, as well as in females and those of Asian descent. (medscape.com)
[ 7 ] researchers identified EGFR mutations in 50.5% of surgically resected lung adenocarcinomas. (medscape.com)
[ 8 ] These data support estimates from clinical trial evidence that activating EGFR mutations are seen in approximately 50% of Asians and 10% of non-Asians. (medscape.com)
Use of the EGFR-TKIs gefitinib, erlotinib, and afatinib is limited to patients with adenocarcinomas who have known activating EGFR mutations. (medscape.com)
[ 9 ] Most importantly, patients with KRAS mutations seem to have a poorer prognosis and seem to be resistant to EGFR-TKIs, although the extent to which this might influence treatment selection remains somewhat unclear. (medscape.com)
Because EGFR and ALK mutations are mutually exclusive, patients with ALK rearrangements are not thought to benefit from EGFR-targeting TKIs. (medscape.com)
By introducing random mutations into EGFRs and starving cells of IL-3, only those with EGFR-activating mutations survived. (asbmb.org)
Patients with EGFR activating mutations and ALK translocations were excluded from recruitment. (esmo.org)
However, 25% to 30% of patients with EGFR -activating mutations show intrinsic resistance, and the responders invariably acquire resistance to gefitinib. (aacrjournals.org)
Here, we showed that hepatocyte growth factor (HGF), a ligand of MET oncoprotein, induces gefitinib resistance of lung adenocarcinoma cells with EGFR -activating mutations by restoring the phosphatidylinositol 3-kinase/Akt signaling pathway via phosphorylation of MET, but not EGFR or ErbB3. (aacrjournals.org)
Lung cancers that harbor activating EGFR mutations and ALK fusions are exquisitely sensitive to small molecule EGFR and ALK tyrosine kinase inhibitors, respectively. (massgeneral.org)
There will be five patient cohorts and eligible patients will be enrolled into each cohort in parallel based on EGFR or HER2 exon 20 mutation status and prior treatment status: - Cohort 1: Patients that have HER2- positive or HER2-negative breast cancer with HER2 activating mutations. (mycancergenome.org)
Patient is positive for EGFR or HER2 mutations based on DNA genetic testing of either tumor tissue or plasma samples, but tissue is preferred. (mycancergenome.org)
Patients with documented EGFR or HER2 mutations are identified by local testing from participating sites using next generation sequencing (NGS) test. (mycancergenome.org)
We searched for mutations in the EGFR gene in primary tumors from patients with non-small-cell lung cancer who had a response to gefitinib, those who did not have a response, and those who had not been exposed to gefitinib. (nih.gov)
A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene, which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib. (nih.gov)
Yet, despite EGFR mutations occurring in approximately 24% of GBM cases, treatment with EGFR inhibitors has not been successful in this cancer. (yale.edu)
In the new study, the research team showed that the most common extracellular mutations that occur in GBM prevent the EGFR from discriminating between the seven different growth factors that normally activate it. (yale.edu)
It was first thought that these mutations just activate the EGF receptor, much like the mutations seen in lung cancer, but our results show that they also change the type of signal given by the receptor," said Mark Lemmon, PhD , co-director of the Yale Cancer Biology Institute, deputy director of Yale Cancer Center, the David A. Sackler Professor of Pharmacology, and senior author of the study. (yale.edu)
Our results provide new insight into how the EGF receptor differentiates one activating growth factor from another-and with these mutations, that ability to distinguish is lost. (yale.edu)
In a collaborative effort across the Lemmon and Ferguson labs in the institute, Anatoly Kiyatkin, PhD, a research scientist at Yale, found that GBM mutations reduce the ability of EGFR to distinguish between EGF and epiregulin (EREG), another growth factor that binds to the EGF receptor in cellular assays. (yale.edu)
Graduate student Chun Hu, who is first author on the study, showed that the mutations allow EGFR to form strong dimers in response to EREG and other low-affinity ligands. (yale.edu)
It was first thought that these mutations just activate the EGF receptor, much like the mutations seen in lung cancer, but our results show that they also change the type of signal given by the receptor. (yale.edu)
In vitro studies have shown that EGFR tyrosine kinase inhibitors (TKIs) greatly inhibit cellular growth and induced apoptosis in the ATC cell lines, while somatic mutations in the tyrosine kinase domain or an increased gene copy number are associated with increased sensitivity to TKIs in non-small cell lung cancer. (bmj.com)
These agents show great promise in patients who harbor epidermal growth factor receptor (EGFR) activating mutations or EML4-ALK, said Antonio Passaro, MD , from the European Institute of Oncology in Milan, and colleagues, writing in a recent article in OncoTargets and Therapy . (medpagetoday.com)
Epidermal15
AXL dimerizes with and phosphorylates epidermal growth factor receptor (EGFR), resulting in activation of phospholipase Cγ (PLCγ)-protein kinase C (PKC), which, in turn, activates mTOR. (iucc.ac.il)
Tyrosine kinase inhibitors (TKIs) against the human epidermal growth factor receptor (EGFR) are now standard treatment in the clinic for patients with advanced EGFR mutant non-small-cell lung cancer (NSCLC). (researchgate.net)
This family, which includes epidermal growth factor receptor (EGFR), plays a pivotal role in normal cell growth, lineage determination, repair, and functional differentiation. (medscape.com)
They used the ability of Ba/F3 lymphoid cells to overcome their dependence on interleukin 3 with activated epidermal growth factor receptors, or EGFRs, which are perennially turned on in many cancers. (asbmb.org)
Renal epidermal growth factor receptor (EGFR) signaling is activated in models of diabetic nephropathy (DN), and inhibition of the EGFR signaling pathway protects against the development of DN. (diabetesjournals.org)
Most patients with non-small-cell lung cancer have no response to the tyrosine kinase inhibitor gefitinib, which targets the epidermal growth factor receptor (EGFR). (nih.gov)
In vitro, EGFR mutants demonstrated enhanced tyrosine kinase activity in response to epidermal growth factor and increased sensitivity to inhibition by gefitinib. (nih.gov)
The epidermal growth factor receptor (EGFR) is frequently mutated in cancers and is an important and successful therapeutic target, especially in lung cancer. (yale.edu)
To mediate these processes, the extracellular ligand binding region of EGFR senses environmental cues via interactions with one of its 7 known ligands, of which epidermal growth factor (EGF) is the most well characterized ( 2 , 3 ). (biorxiv.org)
We previously reported that the epidermal growth factor receptor (EGFR) is required for stimulation of IL-6 and IL-8 secretion by cultured airway epithelial cells in response to an aqueous extract of settled dust from these facilities (HDE, hogbarn dust extract) [AmJRespCritCareMed,177,A158,2008]. (cdc.gov)
MIAMI BEACH-Drugs that block epidermal growth factor receptor (EGFR) tyrosine kinase activity may represent a new option for patients whose non-small-cell lung cancer (NSCLC) has progressed despite standard chemotherapy, Jose Baselga, MD, reported at the Molecular Targets and Cancer Therapeutics meeting (abstract 630A). (cancernetwork.com)
The epidermal growth factor receptor (EGFR) has been reported to be overexpressed in anaplastic thyroid carcinoma (ATC). (bmj.com)
KRAS3
The EGFR and KRAS genes each provide instructions for making a protein that is embedded within the cell membrane. (medlineplus.gov)
Metformin and salinomycin as the best combination for the eradication of NSCLC monolayer cells and their alveospheres (cancer stem cells) irrespective of EGFR, KRAS, EML4/ALK and LKB1 status. (mpg.de)
Our focus is on understanding biological mechanisms that dictate drug sensitivity and resistance in oncogene-addicted lung cancers (those with activating genetic alterations EGFR, ALK, KRAS, etc. (massgeneral.org)
NSCLC6
In phase I, Japanese patients (aged ≥20 years) with NSCLC previously treated with ≥1 EGFR TKI received escalating ASP8273 doses (25‐600 mg) to assess safety/tolerability and to determine the maximum tolerated dose (MTD) and/or the recommended phase II dose (RP2D) by the Bayesian Continual Reassessment Method. (tokushima-u.ac.jp)
Efficacy of Second-Line Pemetrexed-Carboplatin in EGFR-Activating Mutation-Positive NSCLC: Does Exon 19 Deletion Differ from Exon 21 Mutation? (hindawi.com)
Although they exhibited promising anti-T790M activity in the laboratory, their clinical activity among T790M+ NSCLC was poor mainly because of dose-limiting toxicity due to simultaneous inhibition of wild-type EGFR. (researchgate.net)
Among the third-generation EGFR TKIs, osimertinib is today the only drug approved by the Food and Drug Administration and the European Medicines Agency to treat metastatic EGFR T790M NSCLC patients who have progressed on or after EGFR TKI therapy. (researchgate.net)
Dr. Baselga, of Vall D'Hebron University Hospital, Barcelona, Spain, reported phase II data from a multicenter, international, randomized, double-blind, parallel-group study of two different dosages of the investigational EGFR tyrosine kinase inhibitor ZD-1839 (Iressa) as salvage monotherapy for patients with advanced NSCLC. (cancernetwork.com)
In a subgroup of these patients we identified an association between selection of EGFR T790M -negative but EGFR G724S -positive subclones and osimertinib resistance. (nature.com)
Third-generation EGFR inhibitors such as osimertinib have been designed to overcome acquired resistance induced by the EGFR T790M gatekeeper mutation 10 . (nature.com)
Clinical results show that patients treated with osimertinib respond in up to 71% in the background of an acquired EGFR T790M mutation 11 , 12 . (nature.com)
Patient P1 (UICC stage IIIA, 59 years old, female) received osimertinib within the AURA trial (NCT01802632) after progression on erlotinib and the detection of an acquired EGFR T790M mutation (T1) (Fig. 1a ). (nature.com)
Even though progression occurred after 8.2 months with the growth of target lesions and a new EGFR T790M -negative and EGFR G724S -positive pleural effusion with a molecular fraction (MF, estimate of allelic fraction without calculating the purity and ploidy) of 6.3% (T2) (Supplementary Table 1C ). (nature.com)
However, after a median duration of response of ~12 months, all patients develop tumor resistance, and in over half of these patients this is due to the emergence of the EGFR T790M resistance mutation. (researchgate.net)
It is unclear how the presence of an acquired EGFR mutation such as T790M should influence therapeutic decisions. (medscape.com)
Approximately 60% of acquired resistance to these agents is driven by a single secondary mutation within the EGFR kinase domain, specifically substitution of the gatekeeper residue threonine-790 with methionine (T790M). (rcsb.org)
Due to dose-limiting toxicities associated with inhibition of wild-type EGFR (wtEGFR), we sought inhibitors of T790M-containing EGFR mutants with selectivity over wtEGFR. (rcsb.org)
X-ray crystal structures revealed two distinct binding modes and enabled the design of a selective series of novel diaminopyrimidine-based inhibitors with good potency against T790M-containing mutants of EGFR, high selectivity over wtEGFR, broad kinase selectivity, and desirable physicochemical properties. (rcsb.org)
Inhibitors10
Combined treatment with PI3Kα and either EGFR, AXL, or PKC inhibitors reverts this resistance. (iucc.ac.il)
We demonstrate that EGFR G724S limits the activity of third-generation EGFR inhibitors both in vitro and in vivo. (nature.com)
Systematic inhibitor screening and in-depth kinetic profiling validate these findings and show that second-generation EGFR inhibitors retain kinase affinity and overcome EGFR G724S -mediated resistance. (nature.com)
Our data provide a mechanistic basis for the osimertinib-induced selection of EGFR G724S -mutant clones and a rationale to treat these patients with clinically approved second-generation EGFR inhibitors. (nature.com)
Alternative by-pass mechanisms involving MET amplification or activation of the MAPK pathway may also play a role in the development of resistance to third-generation EGFR inhibitors 14 , 15 , 17 . (nature.com)
Within our LADC re-biopsy program we performed targeted sequencing of lesions that progressed under treatment with third-generation EGFR inhibitors. (nature.com)
Selective compounds have been developed that target either the extracellular ligand-binding region of the EGFR (including a number of monoclonal antibodies [MAbs], immunotoxins, and ligand-binding cytotoxic agents) or the intracellular tyrosine kinase region (including various small-molecule inhibitors). (medscape.com)
Initial studies with the EGFR tyrosine kinase inhibitors (TKIs) gefitnib (Iressa) and erlotinib (Tarceva) demonstrated biologic and clinical activity in only a relatively limited subset of lung cancers. (medscape.com)
We describe the evolution of HTS hits derived from Jak2/Tyk2 inhibitors into selective EGFR inhibitors. (rcsb.org)
Methods: Beas-2B human bronchial epithelial cells were treated with HDE in the absence or presence of signaling pathway inhibitors, and EGFR and ERK1/2 phosphorylation were then assessed by immunoblotting. (cdc.gov)
Pathway5
Using protein-sensitive fluorescent markers, the research team revealed that when a cell dies, the EGFR-ERK pathway - a cell activation signaling pathway known for its involvement in the regulation of cell survival - is temporarily activated in the neighboring cells. (pasteur.fr)
The scientists observed that the activation of the EGFR-ERK pathway protected neighboring cells from cell death for approximately one hour, thereby preventing the simultaneous elimination of a group of cells. (pasteur.fr)
The elimination of groups of neighboring cells is never observed in epithelial tissue in normal conditions, when the EGFR-ERK pathway is not deliberately inhibited, even if a large number of cells are eliminated. (pasteur.fr)
E1/E2 heterodimer binding on CD81 activates the epithelial growth factor receptor (EGFR) signaling pathway (PubMed:22855500). (proteopedia.org)
Further studies to identify the MMP-independent pathway by which HDE activates EGFRs and the roles of ERK1/2 in HDE effects may lead to new insights into disease mechanisms and possible new therapeutic approaches. (cdc.gov)
PI3K2
In HER2 positive breast tumours, HER2 activates the PI3K/AKT and the RAS/RAF/MAPK pathways, and stimulate cell growth, survival and differentiation. (genome.jp)
Effector proteins are then recruited to activate various cellular signaling pathways, including RAS/RAF/MEK, PI3K/AKT/mTOR, and JAK/STAT ( 1 ). (biorxiv.org)
Fast Activated Cell-based ELISA (FACE™) Kits provide a simple, sensitive method for detecting protein phosphorylation directly in the cell, without making extracts or performing electrophoresis and membrane blotting. (activemotif.com)
Flow chart of the FACE in cell Western method that uses a cell based ELISA to measure the levels of the native and phospho forms of signaling proteins and kinases that are activated by phosphorylation. (activemotif.com)
Thus we hypothesized that HDE would lead to EGFR phosphorylation and downstream activation of ERK/MAPK signaling. (cdc.gov)
Results: Exposure of cells to 5% HDE stimulated EGFR phosphorylation at 5 and 15 min, and this increased phosphorylation was sustained up to 18 hr. (cdc.gov)
EGFR phosphorylation induced by 10 ng/ml EGF was greater in magnitude at 5 and 15 min but the response was of shorter duration. (cdc.gov)
The EGFR tyrosine kinase inhibitor AG1478 (10 mM) prevented EGFR phosphorylation by both EGF and HDE, implicating autophosphorylation. (cdc.gov)
The matrix metalloproteinase (MMP) inhibitor GM6001 (25 mM) did not block HDE-induced EGFR phosphorylation, consistent with its failure to block HDE stimulation of IL-6 and IL-8 release. (cdc.gov)
this ERK phosphorylation was inhibited by AG1478, indicating EGFR involvement, and by the MEK inhibitor U0126 (10 mM). (cdc.gov)
Conclusions: HDE induces both rapid and sustained EGFR phosphorylation, and ERK1/2 is in turn activated downstream of EGFR activation. (cdc.gov)
Patients7
Here, we characterized the role of the acquired EGFR G724S mutation that was diagnosed in osimertinib-resistant lesions of four individual EGFR 19del -mutant LADC patients. (nature.com)
By way of background, patients with non-small cell who do not demonstrate actionable markers, either EGFR mutation or ALK or ROS1 translocations, are generally treated with first line platinum-based combination chemotherapy. (ecancer.org)
In patients suffering from TNBC, the deregulation of various signalling pathways (Notch and Wnt/beta-catenin), EGFR protein have been confirmed. (genome.jp)
Patients were not selected by tumor EGFR status. (cancernetwork.com)
The EGFR gene status and protein expression were investigated by direct DNA sequencing of the hot-spot regions in exons 18, 19 and 21, fluorescence in situ hybridisation (FISH), and immunohistochemistry in tumour tissues from 23 patients with ATC. (bmj.com)
Despite the low incidence of somatic EGFR gene mutation and amplification in the study samples, in view of the fact that high polysomy was often identified by FISH, as well as the current lack of therapeutic options, EGFR TKIs are worth investigating for treating the patients with ATC who have at least giant cell subtype. (bmj.com)
Autophagy1
We have now determined that in cultured podocytes, high glucose led to increases in activation of EGFR signaling but decreases in autophagy activity as indicated by decreased beclin-1 and inhibition of LC3B autophagosome formation as well as increased rubicon (an autophagy inhibitor) and SQSTM1 (autophagy substrate). (diabetesjournals.org)
Overexpression2
Although, ErbB-2 does not have any known high-affinity ligands, its kinase activity can be activated without ligand by either overexpression or heteroassociation with other members of the ErbB family. (activemotif.com)
Because of its essential roles in cell signaling, misregulation or overexpression of EGFR often causes a cancerous phenotype. (biorxiv.org)
Protein3
RNA-Seq analysis and the data from experimental models revealed that neutrophilic NCF1-dependent ROS promoted alcoholic hepatitis (AH) by inhibiting AMP-activated protein kinase (a key regulator of lipid metabolism) and microRNA-223 (a key antiinflammatory and antifibrotic microRNA). (jci.org)
Each well is then incubated with a primary antibody specific for the activated protein of interest. (activemotif.com)
FACE Kits also contain primary antibody specific for the native inactive protein, so you can monitor both native and activated protein levels in the same experiment. (activemotif.com)
Tumors1
Targeted molecular therapy against EGFR has shown promise as an adjuvant therapy in preliminary studies in several solid tumors, including head and neck cancer. (medscape.com)
Inhibits1
Our data indicated that PET1 inhibits EGFR-mediated cell migration. (biorxiv.org)
Ligand3
Based on these findings, the researchers suggest an important role of altered ligand discrimination by EGFR in development of glioblastoma multiforme, with potential implications for therapeutic targeting in this and other cancers. (yale.edu)
Ligand binding promotes EGFR oligomerization mediated by the extracellular region. (biorxiv.org)
Specifically, the TM of unliganded (inactive) EGFR dimerizes at the C-terminus (C t ), while the ligand bound form dimerizes N-terminally (N t ), and the two helices are also rotated by 180° between the conformations ( 4 , 5 ). (biorxiv.org)
Fusions1
Rearranged during transfection (RET), kinase alterations, which include fusions and activating point mutation, lead to overactive RET signaling and uncontrolled cell growth. (medscape.com)
Squamous1
Erk2 but not Erk1 regulates crosstalk between Met and EGFR in squamous cell carcinoma cell lines. (mpg.de)
Genes2
There is no longer a need for signals to activate these genes. (cancerquest.org)
10 Genes that, when activated, contribute to the carcinogenesis are generally termed proto-oncogenes. (bmj.com)
Monoclonal1
As discussed below, activity of the EGFR monoclonal antibody cetuximab seems to be independent of EGFR mutation status. (medscape.com)
Tumor2
In the case of afatinib this profile translates into a robust reduction of colony formation and tumor growth of EGFR G724S -driven cells. (nature.com)
Monocytes/macrophages support mammary tumor invasivity by co-secreting lineage-specific EGFR ligands and a STAT3 activator. (mpg.de)
STAT31
Activates STAT3 leading to cellular transformation (By similarity). (proteopedia.org)
Signaling1
When these proteins are turned on (activated) by binding to other molecules, signaling pathways are triggered within cells that promote cell proliferation. (medlineplus.gov)
Cellular3
We performed systematic biochemical, cellular, and structural analyses to determine the functional relevance of this mutation in the context of targeted EGFR inhibition. (nature.com)
Different growth factors normally stabilize EGFR dimers with distinct structures and activation kinetics, which signal differently to specify or bias cellular outcome. (yale.edu)
Activation of EGFR regulates essential cellular processes including cell migration, proliferation, and apoptosis ( 1 ). (biorxiv.org)
Cancerous1
This technique , presented in the Journal of Biological Chemistry , offers a simple means of identifying EGFR variants that potentially drive cancerous activity and merit further investigation. (asbmb.org)
Receptor2
The ErbB-2 proto-oncogene, also called Neu, EGFR-2 or HER-2, is a member of the transmembrane receptor tyrosine kinase family, which also includes EGF receptor and EGFR-3 (HER-3 or ErbB-3). (activemotif.com)
An electron density 'omit map' from X-ray crystallography showing a structural change in the EGFR dimerization site of the mutated receptor (indicated by green mesh), leading to enhanced EREG-driven dimerization. (yale.edu)
Cells4
AMPIVIEW™ EGFR (AS) Dig RNA Probes are digoxigenin-labeled RNA probes targeting EGFR nucleic acid (DNA/RNA or RNA) for in situ hybridization in tissues and cells. (enzolifesciences.com)
AMPIVIEW™ EGFR (AS) Dig RNA probes have been designed to target the EGFR or HER-1 DNA and RNA in tissues and cells. (enzolifesciences.com)
AMPIVIEW™ EGFR (AS) Dig RNA Probes are optimized for detection of EGFR RNA or RNA/DNA in FFPE tissues or cells with DIGX ® anti-digoxigenin linker, POLYVIEW® PLUS detection reagents combined with HIGHDEF ® chromogens and counterstains (linker and detection solutions not inlcuded). (enzolifesciences.com)
FACE is a highly sensitive high-throughput assay designed for detecting activated proteins within mammalian cells. (activemotif.com)