Analysis ofEGFR,EML4-ALK,KRAS, andc-METmutations in Chinese lung adenocarcinoma patients

Xia, Ning; An, Jian; Jiang, Qixia; Li, Min; Tan, Jun

doi:10.3109/01902148.2013.819535

Cited by 54 publications

(49 citation statements)

References 44 publications

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“…The mutation rates in Chinese population were much higher in adenocarcinomas, females, or never-smokers, ranging from 45% to 61% [1,32,44,46]. Similar to these reports, we have found that EGFR mutations were more frequently observed in females (63.5% vs. 28.1% in males), never-smokers (55.7% vs. 26.2% in ever smokers), and adenocarcinomas (49.5% vs. 2.6% in squamous cell carcinomas) in our cohort.…”

Section: Discussionmentioning

confidence: 99%

Characterization of common and rare mutations in EGFR and associated clinicopathological features in a large population of Chinese patients with lung cancer

Wei

Ren

Zhang

et al. 2017

Pathology - Research and Practice

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Section: Discussionmentioning

confidence: 99%

Characterization of common and rare mutations in EGFR and associated clinicopathological features in a large population of Chinese patients with lung cancer

Wei

Ren

Zhang

et al. 2017

Pathology - Research and Practice

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“…EML4-ALK rearrangement was reported as a relatively low frequent rearrangement ranging from 1.5% to 6.7% among unselected Caucasian NSCLC patients (14)(15)(16)(17). It seems to have higher frequency in Asian population, and was reported as high as 5.1-10% (18)(19)(20)(21). Part of the explanation was that in those studies, patients were selected from EGFR wild population.…”

Section: Discussionmentioning

confidence: 99%

High concordance of ALK rearrangement between primary tumor and paired metastatic lymph node in patients with lung adenocarcinoma

Hou

Ren

Su³

et al. 2016

J. Thorac. Dis.

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Background: Lung cancer has heterogeneous features. It remains unclear whether ALK rearrangement was distributed heterogeneously in tumor from different anatomic sites. To address this issue, we investigate the concordance of ALK rearrangement between primary tumors and paired metastatic lymph nodes in pulmonary adenocarcinoma patients. Results: A total of 101 patients were enrolled into this study with a median age of 60 years old (range, 35-78 years). ALK rearrangement was found in 20 primary lesions, while in 18 paired metastatic lymph nodes. ALK rearrangement was more frequently happened in younger (P<0.001), Nonsmokers (P=0.012), high-stage disease (P=0.021) and predominantly solid growth pattern (P=0.024). The concordance rate between primary tumor and paired metastatic lymph nodes was 98%. Two patients with ALK rearrangement on primary tumor didn't show ALK gene fusion on paired metastatic lymph nodes. Sixty-eight cases had more than two stations of metastatic lymph nodes. ALK rearrangement in the different station of metastatic lymph nodes of the same patient was consistent.Conclusions: High concordant rate of ALK rearrangement between primary tumors and paired metastatic lymph nodes were found in this study. The authors concluded that specimens from metastatic lesions and primary tumors are equally suitable for detection ALK rearrangement.

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“…In this respect, it will be important in future studies to assess the occurrence of the Δ7–8 mutation in paired samples of primary and recurrent tumors after MET antibody-based therapies, but also anti-EGFR therapies since cells may use MET Δ7–8 to bypass EGFR signaling [3, 53]. With this in mind, the use of specific tyrosine kinase inhibitors of MET may have preference over antibody-based therapy for resistant tumors, at least in the ones that are KRAS and RAF wild type, [3, 21, 57, 61] since MET Δ7–8 is sensitive to these inhibitors [42]. Such inhibitors have already shown to improve overall survival of patients with non-small cell lung carcinoma with MET amplification and renal papillary carcinoma with MET mutations [11, 45].…”

Section: Discussionmentioning

confidence: 99%

Identification of a novel MET mutation in high-grade glioma resulting in an auto-active intracellular protein

et al. 2015

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MET has gained interest as a therapeutic target for a number of malignancies because of its involvement in tumorigenesis, invasion and metastasis. At present, a number of inhibitors, both antibodies against MET or its ligand hepatocyte growth factor, and small molecule MET tyrosine kinase inhibitors are in clinical trials. We here describe a novel variant of MET that is expressed in 6 % of high-grade gliomas. Characterization of this mutation in a glioma cell line revealed that it consists of an intronic deletion, resulting in a splice event connecting an intact splice donor site in exon 6 with the next splice acceptor site being that of exon 9. The encoded protein lacks parts of the extracellular IPT domains 1 and 2, encoded by exons 7 and 8, resulting in a novel pseudo-IPT and is named METΔ7−8. METΔ7−8 is located predominantly in the cytosol and is constitutively active. The auto-activating nature of METΔ7−8, in combination with a lack of transmembrane localization, renders METΔ7−8 not targetable using antibodies, although the protein is efficiently deactivated by MET-specific tyrosine kinase inhibitors. Testing of MET-expressing tumors for the presence of this variant may be important for treatment decision making.

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Analysis ofEGFR,EML4-ALK,KRAS, andc-METmutations in Chinese lung adenocarcinoma patients

Cited by 54 publications

References 44 publications

Characterization of common and rare mutations in EGFR and associated clinicopathological features in a large population of Chinese patients with lung cancer

Characterization of common and rare mutations in EGFR and associated clinicopathological features in a large population of Chinese patients with lung cancer

High concordance of ALK rearrangement between primary tumor and paired metastatic lymph node in patients with lung adenocarcinoma

Identification of a novel MET mutation in high-grade glioma resulting in an auto-active intracellular protein

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