نتایج جستجو برای: egfr

تعداد نتایج: 30143  

2015
Stefan Klingler Baofeng Guo Jun Yao Haiyan Yan Ling Zhang Angelina V. Vaseva Sida Chen Peter Canoll Ji-Hye Paik Haoqiang Ying Hongwu Zheng

Epidermal growth factor receptor (EGFR) is highly amplified, mutated, and overexpressed in human malignant gliomas. Despite its prevalence and growth-promoting functions, therapeutic strategies to inhibit EGFR kinase activity have not been translated into profound beneficial effects in glioma clinical trials. To determine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintena...

Journal: :Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1993
L L Chen B Gansbacher E Gilboa R Taetle J Oval M S Hibbs C K Huang M L Clawson S Bilgrami J Schlessinger

HL60 cells are devoid of endogenous epidermal growth factor receptor (EGFR). They respond to retinoic acid and undergo terminal granulocytic differentiation. EGFR complementary DNA was introduced into HL60 cells by retroviral gene transfer. Scatchard plot showed that the binding characteristics are identical to those of A431 cells. HL60-EGFR cells were estimated to express 34,000 EGFR/cell (Kd ...

Journal: :Journal of cell science 2002
Morten P Oksvold Henrik S Huitfeldt Anne Carine Østvold Ellen Skarpen

We have compared the activation and trafficking of epidermal growth factor receptor (EGFR) induced by UV light and EGF. Tyrosine phosphorylation of EGFR was not detected in UV-exposed cells by immunoblotting of whole cell lysates or EGFR immunoprecipitates with antibodies specific for each of the five activated autophosphorylation sites of EGFR. In addition, EGFR of UV-irradiated cells did not ...

Journal: :Cancer research 2005
Joseph Amann Shailaja Kalyankrishna Pierre P Massion Joyce E Ohm Luc Girard Hisayuki Shigematsu Michael Peyton Denise Juroske Yuhui Huang J Stuart Salmon Young H Kim Jonathan R Pollack Kiyoshi Yanagisawa Adi Gazdar John D Minna Jonathan M Kurie David P Carbone

Epidermal growth factor receptor (EGFR) is occasionally amplified and/or mutated in non-small cell lung cancer (NSCLC) and can be coexpressed with other members of the HER receptor family to form functional heterodimers. We therefore investigated lung cancer cell lines for alterations in EGFR gene copy number, enhanced expression of EGFR and other HER family members, and EGFR coding sequence mu...

2017
Dan Zhao Xuejing Chen Na Qin Dan Su Lijuan Zhou Quan Zhang Xi Li Xinyong Zhang Mulan Jin Jinghui Wang

Clinical trials have shown that epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) did not improve the survival of patients with EGFR-mutated non-small cell lung cancer (NSCLC) because of the high crossover of treatments. Realistically, the role of EGFR-TKIs in NSCLC with mutated EGFR is not well known. We retrospectively analysed data from patients with recurrent or metast...

Journal: :Cancer research 2015
Margaret Soucheray Marzia Capelletti Inés Pulido Yanan Kuang Cloud P Paweletz Jeffrey H Becker Eiki Kikuchi Chunxiao Xu Tarun B Patel Fatima Al-Shahrour Julián Carretero Kwok-Kin Wong Pasi A Jänne Geoffrey I Shapiro Takeshi Shimamura

Non-small cell lung cancers (NSCLC) that have developed resistance to EGF receptor (EGFR) tyrosine kinase inhibitor (TKI), including gefitinib and erlotinib, are clinically linked to an epithelial-to-mesenchymal transition (EMT) phenotype. Here, we examined whether modulating EMT maintains the responsiveness of EGFR-mutated NSCLCs to EGFR TKI therapy. Using human NSCLC cell lines harboring muta...

Journal: :Cancer research 2001
G S Akerman W H Tolleson K L Brown L L Zyzak E Mourateva T S Engin A Basaraba A L Coker K E Creek L Pirisi

Epidermal growth factor receptor (EGFR) levels are dramatically increased in human keratinocytes (HKc) immortalized with full-length human papillomavirus type 16 (HPV16) DNA (HKc/HPV16), but increases in EGFR levels actually precede immortalization. In some normal HKc strains, acute expression of HPV16 E6 (but not HPV16 E5, HPV16 E7, or HPV6 E6) from LXSN retroviral vectors produced an increase...

Journal: :Molecular pharmacology 2007
Hans H Schiffer Esther C Reding Stephen R Fuhs Qing Lu Fabrice Piu Steven Wong Pey-Lih H Littler Dave M Weiner William Keefe Phil K Tan Norman R Nash Anne E Knapp Roger Olsson Mark R Brann

We have developed a new assay for measuring epidermal growth factor receptor (EGFR) activation using the bioluminescence resonance energy transfer (BRET) technology, which directly measures the recruitment of signaling proteins to activated EGFR. Our results demonstrate that EGFR BRET assays precisely measure the pharmacology and signaling properties of EGFR expressed in human embryonic kidney ...

2017
Jian Qu Ya-Nan Wang Ping Xu Da-Xiong Xiang Rui Yang Wei Wei Qiang Qu

Icotinib is a novel and the third listed epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), which exerts a good anti-tumor efficacy on non-small cell lung cancer (NSCLC). The efficacy of EGFR-TKIs has been shown to be associated with the EGFR mutation status, especially exon 19 deletion (19Del) and exon 21 L858R mutation. Therefore, a meta-analysis was performed to assess ...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2005
Miguel Taron Yukito Ichinose Rafael Rosell Tony Mok Bartomeu Massuti Lurdes Zamora Jose Luis Mate Christian Manegold Mayumi Ono Cristina Queralt Thierry Jahan Jose Javier Sanchez Maria Sanchez-Ronco Victor Hsue David Jablons Jose Miguel Sanchez Teresa Moran

PURPOSE Activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) confer a strong sensitivity to gefitinib, a selective tyrosine kinase inhibitor of EGFR. EXPERIMENTAL DESIGN We examined EGFR mutations at exons 18, 19, and 21 in tumor tissue from 68 gefitinib-treated, chemorefractory, advanced non-small cell lung cancer patients from the United States, ...

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