Log in

Relevant bibliographies by topics / Epidermal growth factor Mutation (Biology) Adenocarcinoma / Journal articles

To see the other types of publications on this topic, follow the link: Epidermal growth factor Mutation (Biology) Adenocarcinoma.

Journal articles on the topic 'Epidermal growth factor Mutation (Biology) Adenocarcinoma'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Epidermal growth factor Mutation (Biology) Adenocarcinoma.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Siegelin, Markus D., and Alain C. Borczuk. "Epidermal growth factor receptor mutations in lung adenocarcinoma." Laboratory Investigation 94, no. 2 (2013): 129–37. http://dx.doi.org/10.1038/labinvest.2013.147.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Suehisa, Hiroshi, Shinichi Toyooka, Katsuyuki Hotta, et al. "Epidermal Growth Factor Receptor Mutation Status and Adjuvant Chemotherapy With Uracil-Tegafur for Adenocarcinoma of the Lung." Journal of Clinical Oncology 25, no. 25 (2007): 3952–57. http://dx.doi.org/10.1200/jco.2007.11.8646.

Full text

Abstract:

Purpose Adjuvant chemotherapy with uracil-tegafur has been demonstrated to prolong survival among patients with resected lung adenocarcinomas. Epidermal growth factor receptor (EGFR) mutations have been reported to be present in lung adenocarcinomas. The present study evaluated whether the EGFR status could be used as a biologic predictor of the outcome of adjuvant chemotherapy with uracil-tegafur. Patients and Methods The EGFR mutational status of 187 patients with resected lung adenocarcinomas was determined using a polymerase chain reaction–based assay for EGFR exons 19 and 21; the results

APA, Harvard, Vancouver, ISO, and other styles

3

Ding, Meng, Haixiu Liao, Nannan Zhou, Ying Yang, Shihe Guan, and Liwen Chen. "B7-H3-Induced Signaling in Lung Adenocarcinoma Cell Lines with Divergent Epidermal Growth Factor Receptor Mutation Patterns." BioMed Research International 2020 (December 24, 2020): 1–8. http://dx.doi.org/10.1155/2020/8824805.

Full text

Abstract:

The cosignal molecule B7-H3 is gaining attention due to its abnormal expression and abundant signal transduction in many types of malignancies. B7-H3-induced signaling includes at least three cascades: PI3K/AKT, JAK2/STAT3, and Raf/MEK/ERK1/2, which are also involved in epidermal growth factor receptor- (EGFR-) triggered signaling in lung adenocarcinoma cells. However, the correlation between B7-H3-induced signaling and EGFR signaling, and between B7-H3-targeted immunotherapy and EGFR-targeted therapy in lung adenocarcinoma, remains to be elucidated. Herein we find that knockout of B7-H3 gene

APA, Harvard, Vancouver, ISO, and other styles

4

Peng, Min, Yi Ming Weng, Hua Li Liu, et al. "Clinical Characteristics and Survival Outcomes for Non-Small-Cell Lung Cancer Patients with Epidermal Growth Factor Receptor Double Mutations." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/7181368.

Full text

Abstract:

Multiple randomized clinical trials have demonstrated that epidermal growth factor receptor (EGFR) exon 19 deletion (19Del) and exon 21 L858R mutation (L858R) are highly correlated with sensitivity to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) treatment in non-small-cell lung cancer (NSCLC). A mutation in exon 20 (T790M) is reportedly associated with resistance to EGFR-TKIs. However, few studies have focused on patients harboring double mutations in these 3 mutation sites. In this retrospective study, forty-five patients (45/2546, 1.7%) harbored double mutations of 1

APA, Harvard, Vancouver, ISO, and other styles

5

Wang, Hexiang, Hongwei Guo, Zeguo Wang, Bao Shan, and Jizheng Lin. "The Diagnostic Value of Quantitative CT Analysis of Ground-Glass Volume Percentage in Differentiating Epidermal Growth Factor Receptor Mutation and Subtypes in Lung Adenocarcinoma." BioMed Research International 2019 (March 6, 2019): 1–8. http://dx.doi.org/10.1155/2019/9643836.

Full text

Abstract:

Objective. To retrospectively investigate computed tomographic (CT) quantitative analysis of ground-glass opacity (GGO) volume percentage and morphologic features of resected lung adenocarcinomas according to epidermal growth factor receptor (EGFR) mutation status and subtypes. Methods. Amplification refractory mutation system was used to detect mutations in the EGFR gene. Distribution of demographics and GGO volume percentage were performed according to EGFR mutation status and subtypes. Results. EGFR mutations were significantly more frequent in women (55.2% vs. 37.0%, p=0.001) and in never-

APA, Harvard, Vancouver, ISO, and other styles

6

Jänne, Pasi A., Jeffrey A. Engelman, and Bruce E. Johnson. "Epidermal Growth Factor Receptor Mutations in Non–Small-Cell Lung Cancer: Implications for Treatment and Tumor Biology." Journal of Clinical Oncology 23, no. 14 (2005): 3227–34. http://dx.doi.org/10.1200/jco.2005.09.985.

Full text

Abstract:

The epidermal growth factor receptor (EGFR) has emerged as an attractive therapeutic target for patients with non–small-cell lung cancer (NSCLC). However, despite its almost universal presence in NSCLC tumors, therapeutic inhibition of EGFR has resulted in significant tumor regressions in only 10% to 20% of patients. Several investigations over the last 12 months have uncovered somatic mutations in EGFR that underlie the sensitivity to EGFR inhibitors. NSCLC tumors and cell lines with EGFR mutations are exquisitely sensitive to the EGFR tyrosine kinase inhibitors (TKIs), erlotinib and gefitini

APA, Harvard, Vancouver, ISO, and other styles

7

Zhu, Wang-Yu, Hai-Feng Li, Ke-Xin Fang, et al. "Epidermal Growth Factor Receptor Mutations and Their Prognostic Value with Carcinoembryonic Antigen in Pathological T1 Lung Adenocarcinoma." Disease Markers 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/2942618.

Full text

Abstract:

Aims. The prognostic value of epidermal growth factor receptor (EGFR) mutations in the context of serum carcinoembryonic antigen levels remains controversial in T1 lung adenocarcinoma. Methods. Clinical and pathological characteristics, preoperational carcinoembryonic antigen levels, EGFR mutations, and disease-free and overall survival were analysed retrospectively in 573 pathological T1 patients in East China. Results. EGFR mutations were detected in 220 of 573 patients (38.4%). Patients with serum carcinoembryonic antigen levels ≥ 2.12 ng/mL had worse disease-free (P<0.001) and overall s

APA, Harvard, Vancouver, ISO, and other styles

8

Riza, Nur Marleta, and Daniel Maranatha. "Triple Mutation Epidermal Growth Factor Receptor (EGFR) Exon 18 (G719S), 20 (T790M) and 21 (L858R) in a Male Patient with Lung Adenocarcinoma: A Case Report." Jurnal Respirasi 6, no. 1 (2020): 13. http://dx.doi.org/10.20473/jr.v6-i.1.2020.13-20.

Full text

Abstract:

Background: Lung cancer is one of the deadliest cancers in the world. The percentage of non small cell lung cancer (NSCLC) is about 80% of the incidence of lung cancer. The type of NSCLC, adenocarcinoma, is usually found in the presence of epidermal growth factor receptor (EGFR) mutations.Case. A male patient aged 70 years, an active smoker, works as a farmer. He has complained of shortness of breath, and chest pain for three months. There was no family history of suffering from malignancy. The cytology result of the right pleural fluid indicated adenocarcinoma. He was diagnosed with pulmonary

APA, Harvard, Vancouver, ISO, and other styles

9

Bell, Daphne W., Thomas J. Lynch, Sara M. Haserlat, et al. "Epidermal Growth Factor Receptor Mutations and Gene Amplification in Non–Small-Cell Lung Cancer: Molecular Analysis of the IDEAL/INTACT Gefitinib Trials." Journal of Clinical Oncology 23, no. 31 (2005): 8081–92. http://dx.doi.org/10.1200/jco.2005.02.7078.

Full text

Abstract:

Purpose Most cases of non–small-cell lung cancer (NSCLC) with dramatic responses to gefitinib have specific activating mutations in the epidermal growth factor receptor (EGFR), but the predictive value of these mutations has not been defined in large clinical trials. The goal of this study was to determine the contribution of molecular alterations in EGFR to response and survival within the phase II (IDEAL) and phase III (INTACT) trials of gefitinib. Patients and Methods We analyzed the frequency of EGFR mutations in lung cancer specimens from both the IDEAL and INTACT trials and compared it w

APA, Harvard, Vancouver, ISO, and other styles

10

Rybarczyk-Kasiuchnicz, Agnieszka, Rodryg Ramlau, and Katarzyna Stencel. "Treatment of Brain Metastases of Non-Small Cell Lung Carcinoma." International Journal of Molecular Sciences 22, no. 2 (2021): 593. http://dx.doi.org/10.3390/ijms22020593.

Full text

Abstract:

Lung cancer is one of the most common malignant neoplasms. As a result of the disease’s progression, patients may develop metastases to the central nervous system. The prognosis in this location is unfavorable; untreated metastatic lesions may lead to death within one to two months. Existing therapies—neurosurgery and radiation therapy—do not improve the prognosis for every patient. The discovery of Epidermal Growth Factor Receptor (EGFR)—activating mutations and Anaplastic Lymphoma Kinase (ALK) rearrangements in patients with non-small cell lung adenocarcinoma has allowed for the introduction

APA, Harvard, Vancouver, ISO, and other styles

11

Rybarczyk-Kasiuchnicz, Agnieszka, Rodryg Ramlau, and Katarzyna Stencel. "Treatment of Brain Metastases of Non-Small Cell Lung Carcinoma." International Journal of Molecular Sciences 22, no. 2 (2021): 593. http://dx.doi.org/10.3390/ijms22020593.

Full text

Abstract:

Lung cancer is one of the most common malignant neoplasms. As a result of the disease’s progression, patients may develop metastases to the central nervous system. The prognosis in this location is unfavorable; untreated metastatic lesions may lead to death within one to two months. Existing therapies—neurosurgery and radiation therapy—do not improve the prognosis for every patient. The discovery of Epidermal Growth Factor Receptor (EGFR)—activating mutations and Anaplastic Lymphoma Kinase (ALK) rearrangements in patients with non-small cell lung adenocarcinoma has allowed for the introduction

APA, Harvard, Vancouver, ISO, and other styles

12

Kim, Jung Soo, Jeong-Seon Ryu, Sang Hoon Jeon, et al. "Dramatic response of acute disseminated intravascular coagulation to erlotinib in a patient with lung adenocarcinoma with activating EGFR mutation." Journal of International Medical Research 46, no. 1 (2017): 533–37. http://dx.doi.org/10.1177/0300060517720099.

Full text

Abstract:

Disseminated intravascular coagulation (DIC) is a commonly encountered clinical situation characterized by thrombotic occlusion or bleeding in patients with lung cancer. DIC in patients with cancer is usually asymptomatic, taking a chronic form as a compensatory mechanism. Although acute DIC in patients with lung cancer is rarely reported, it can be fatal. We herein describe a patient with lung adenocarcinoma with an activating mutation of the epidermal growth factor receptor (EGFR) gene who developed acute DIC after minor surgical excision. The patient’s condition dramatically improved immedi

APA, Harvard, Vancouver, ISO, and other styles

13

Takeuchi, Toshiyuki, Shuta Tomida, Yasushi Yatabe, et al. "Expression Profile–Defined Classification of Lung Adenocarcinoma Shows Close Relationship With Underlying Major Genetic Changes and Clinicopathologic Behaviors." Journal of Clinical Oncology 24, no. 11 (2006): 1679–88. http://dx.doi.org/10.1200/jco.2005.03.8224.

Full text

Abstract:

Purpose This study was conducted to gain insight into the relationship between expression profiles and underlying genetic changes, which are known to be important for the pathogenesis of lung cancers. Methods Expression profiles of 18,175 unique genes and three major targets for genetic changes, p53, epidermal growth factor receptor (EGFR), and K-ras, were investigated in 149 patients with non–small-cell lung cancer, including 90 patients with adenocarcinoma to determine their relationships with various clinicopathologic features and Gene Ontology (GO) terms. Results This study successfully es

APA, Harvard, Vancouver, ISO, and other styles

14

Chung, Fu-Tsai, Ming-Yun Ho, Yueh-Fu Fang, et al. "The Impact of Sequence of Chemotherapy and EGFR-TKI Treatment on DifferentEGFRMutation Lung Adenocarcinoma." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/948267.

Full text

Abstract:

Objectives. Chemotherapy as first-/second-line treatment in different epidermal growth factor receptor (EGFR) mutation lung adenocarcinoma remains controversial.Methods. Consecutive patients were collected between 2009 and 2012. Patients were divided into two groups (1st-line chemotherapy:n= 56 and 2nd-line chemotherapy:n= 55). Their outcomes profiles were analyzed.Results. The overall survival (OS) of all patients (390 versus 662 days,p< 0.0001), as well as both progression-free survival (PFS, 151 versus 252 days,p= 0.0001) and OS (308 versus 704 days,p= 0.0001) of patients withL858Rmutati

APA, Harvard, Vancouver, ISO, and other styles

15

Ren, Xiaohui, Xinfeng Cai, Jing Li, et al. "Histological transformation of lung adenocarcinoma to small cell lung cancer with mutant C797S conferring acquired resistance to osimertinib." Journal of International Medical Research 48, no. 6 (2020): 030006052092791. http://dx.doi.org/10.1177/0300060520927918.

Full text

Abstract:

Epidermal growth factor receptor (EGFR) gene-mutated non-small cell lung cancer may initially respond to EGFR tyrosine kinase inhibitors (TKIs), but may subsequently become resistant; however, the resistance mechanisms remain unclear. We report a rare case of acquired resistance to osimertinib associated with transformation to small cell lung cancer (SCLC) with cis-C797S mutation. A man with recurrent lung adenocarcinoma harboring an EGFR exon 19 deletion received erlotinib for 10 months following curative surgery and adjuvant chemotherapy. However, he switched to osimertinib after repeat biop

APA, Harvard, Vancouver, ISO, and other styles

16

de Langen, Adrianus J., and Egbert F. Smit. "Therapeutic approach to treating patients with BRAF-mutant lung cancer: latest evidence and clinical implications." Therapeutic Advances in Medical Oncology 9, no. 1 (2016): 46–58. http://dx.doi.org/10.1177/1758834016670555.

Full text

Abstract:

Lung adenocarcinoma is known for its high rate of somatic mutations and genomic rearrangements. The identification of epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase (ALK) rearrangements that sensitize tumors to specific drugs has changed the therapeutic approach and prognosis in these molecularly-defined subgroups. Several other key genetic alterations have been identified, of which BRAF mutations are found in 4% of non-small cell lung cancer (NSCLC) cases. Targeted drugs against BRAF and downstream MEK were recently approved for the treatment of BRAF-positive

APA, Harvard, Vancouver, ISO, and other styles

17

Michalaki, Vasiliki, Andreas Polydorou, Theodosios Theodosopoulos, et al. "Microsatellite instability and mutations in BRAF and KRAS in small bowel adenocarcinoma." Journal of Clinical Oncology 37, no. 15_suppl (2019): e15037-e15037. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e15037.

Full text

Abstract:

e15037 Background: Small-bowel adenocarcinomas (SBAs) are rare cancers with a significantly lower incidence, later stage at diagnosis, and worse overall survival than other intestinal-derived cancers. Activating KRAS and/or BRAF mutations have been identified as predictors of resistance to anti-epidermal growth factor receptor (EGFR) The aim of this study was to perform a comprehensive immunohistochemical.analysis of KRAS, NRAS, V600E BRAF mutations and microsatellite instability using a cohort of surgically resected cases in our institution. Methods: A total of 17 patients (10 males and 7 fem

APA, Harvard, Vancouver, ISO, and other styles

18

Chen, Hung-Jen, Chih-Yen Tu, Kuo-Yang Huang, Chun-Ru Chien, and Te-Chun Hsia. "Early serum tumor marker levels after fourteen days of tyrosine kinase inhibitor targeted therapy predicts outcomes in patients with advanced lung adenocarcinoma." PLOS ONE 15, no. 12 (2020): e0240736. http://dx.doi.org/10.1371/journal.pone.0240736.

Full text

Abstract:

Objective Image evaluation strategy for lung cancer patients has difficulty obtaining the appropriate quantity of diffuse lung nodules and bone metastases. The study was to demonstrate whether early variations in the levels of serum 4-tumor markers (4-TMs)(carcinoembryonic antigen [CEA], cancer antigen [CA]125, CA19-9, and CA15-3) after TKI targeted therapy were associated with treatment response in patients with lung adenocarcinoma. Methods Patients with stage IIIB-IV lung adenocarcinoma taking epidermal growth factor receptor (EGFR) TKIs or anaplastic lymphoma kinase (ALK) inhibitors were en

APA, Harvard, Vancouver, ISO, and other styles

19

Stewart, Erin L., Celine Mascaux, Nhu-An Pham, et al. "Clinical Utility of Patient-Derived Xenografts to Determine Biomarkers of Prognosis and Map Resistance Pathways in EGFR-Mutant Lung Adenocarcinoma." Journal of Clinical Oncology 33, no. 22 (2015): 2472–80. http://dx.doi.org/10.1200/jco.2014.60.1492.

Full text

Abstract:

Purpose Although epidermal growth factor receptor (EGFR) –mutated adenocarcinomas initially have high response rates to EGFR tyrosine kinase inhibitors (TKIs), most patients eventually develop resistance. Patient-derived xenografts (PDXs) are considered preferred preclinical models to study the biology of patient tumors. EGFR-mutant PDX models may be valuable tools to study the biology of these tumors and to elucidate mechanisms of resistance to EGFR-targeted therapies. Methods Surgically resected early-stage non–small-cell lung carcinoma (NSCLC) tumors were implanted into nonobese diabetic se

APA, Harvard, Vancouver, ISO, and other styles

20

Chen, Yu-Hung, Tso-Fu Wang, Sung-Chao Chu, et al. "Incorporating radiomic feature of pretreatment 18F-FDG PET improves survival stratification in patients with EGFR-mutated lung adenocarcinoma." PLOS ONE 15, no. 12 (2020): e0244502. http://dx.doi.org/10.1371/journal.pone.0244502.

Full text

Abstract:

Background To investigate the survival prognostic value of the radiomic features of 18F-FDG PET in patients who had EGFR (epidermal growth factor receptor) mutated lung adenocarcinoma and received targeted TKI (tyrosine kinase inhibitor) treatment. Methods Fifty-one patients with stage III-IV lung adenocarcinoma and actionable EGFR mutation who received first-line TKI were retrospectively analyzed. All patients underwent pretreatment 18F-FDG PET/CT, and we calculated the PET-derived radiomic features. Cox proportional hazard model was used to examine the association between the radiomic featur

APA, Harvard, Vancouver, ISO, and other styles

21

Nanamiya, Ren, Ryoko Saito-Koyama, Yasuhiro Miki, et al. "EphB4 as a Novel Target for the EGFR-Independent Suppressive Effects of Osimertinib on Cell Cycle Progression in Non-Small Cell Lung Cancer." International Journal of Molecular Sciences 22, no. 16 (2021): 8522. http://dx.doi.org/10.3390/ijms22168522.

Full text

Abstract:

Osimertinib is the latest generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor used for patients with EGFR-mutated non-small cell lung cancer (NSCLC). We aimed to explore the novel mechanisms of osimertinib by particularly focusing on EGFR-independent effects, which have not been well characterized. We explored the EGFR-independent effects of osimertinib on cell proliferation using NSCLC cell lines, an antibody array analysis, and the association between the action of osimertinib and the ephrin receptor B4 (EphB4). We also studied the clinicopathological significance of

APA, Harvard, Vancouver, ISO, and other styles

22

Lin, Liping, Fuxi Huang, Fang Chen, Yan He, Jiazhu Hu, and Xiaolong Cao. "Anaplastic lymphoma kinase (ALK)-rearranged pulmonary pleomorphic carcinoma successfully treated with crizotinib." Journal of International Medical Research 46, no. 8 (2018): 3491–97. http://dx.doi.org/10.1177/0300060517748262.

Full text

Abstract:

Pulmonary pleomorphic carcinoma (PPC) is rare, and the response of patients to conventional chemotherapy is very poor. Here we present a patient with anaplastic lymphoma kinase (ALK)-rearranged advanced PPC treated with crizotinib. Computed tomography revealed a mass in the left upper lung of a nonsmoking 60-year-old woman. Pathological findings using resected tissue were consistent with PPC stage 1A, T1bN0M0. Although the patient received adjuvant radiotherapy, the disease relapsed, quickly progressed, and remained PPC according to analysis of biopsied tissue. Although negative for epidermal

APA, Harvard, Vancouver, ISO, and other styles

23

Buder, Anna, Ellen Heitzer, Julie Waldispühl-Geigl, et al. "Somatic Copy-Number Alterations in Plasma Circulating Tumor DNA from Advanced EGFR-Mutated Lung Adenocarcinoma Patients." Biomolecules 11, no. 5 (2021): 618. http://dx.doi.org/10.3390/biom11050618.

Full text

Abstract:

Background: To assess the clinical relevance of genome-wide somatic copy-number alterations (SCNAs) in plasma circulating tumor DNA (ctDNA) from advanced epidermal growth factor receptor (EGFR)-mutated lung adenocarcinoma patients. Methods: We included 43 patients with advanced EGFR T790M-positive lung adenocarcinoma who were treated with osimertinib after progression under previous EGFR-TKI therapy. We performed genomic profiling of ctDNA in plasma samples from each patient obtained pre-osimertinib and after patients developed resistance to osimertinib. SCNAs were detected by shallow whole-ge

APA, Harvard, Vancouver, ISO, and other styles

24

Takeda, Masayuki, and Kazuhiko Nakagawa. "First- and Second-Generation EGFR-TKIs Are All Replaced to Osimertinib in Chemo-Naive EGFR Mutation-Positive Non-Small Cell Lung Cancer?" International Journal of Molecular Sciences 20, no. 1 (2019): 146. http://dx.doi.org/10.3390/ijms20010146.

Full text

Abstract:

Activating mutations of the epidermal growth factor receptor gene (EGFR) are a driving force for some lung adenocarcinomas. Several randomized phase III studies have revealed that treatment with first- or second-generation EGFR tyrosine kinase inhibitors (TKIs) results in an improved progression-free survival (PFS) compared to standard chemotherapy in chemonaive patients with advanced non–small cell lung cancer (NSCLC), selected based on the presence of EGFR mutations. Patients treated with second-generation EGFR-TKIs have also shown an improved PFS relative to those treated with first-generat

APA, Harvard, Vancouver, ISO, and other styles

25

Kharbanda, Akriti, David M. Walter, Andrea A. Gudiel, Nancy Schek, David M. Feldser, and Eric S. Witze. "Blocking EGFR palmitoylation suppresses PI3K signaling and mutant KRAS lung tumorigenesis." Science Signaling 13, no. 621 (2020): eaax2364. http://dx.doi.org/10.1126/scisignal.aax2364.

Full text

Abstract:

Non–small cell lung cancer (NSCLC) is often characterized by mutually exclusive mutations in the epidermal growth factor receptor (EGFR) or the guanosine triphosphatase KRAS. We hypothesized that blocking EGFR palmitoylation, previously shown to inhibit EGFR activity, might alter downstream signaling in the KRAS-mutant setting. Here, we found that blocking EGFR palmitoylation, by either knocking down the palmitoyltransferase DHHC20 or expressing a palmitoylation-resistant EGFR mutant, reduced activation of the kinase PI3K, the abundance of the transcription factor MYC, and the proliferation of

APA, Harvard, Vancouver, ISO, and other styles

26

Chang, Jer-Hwa, Tsung-Ching Lai, Po-Jen Yang, et al. "Associations of TIMP-3 Genetic Polymorphisms with EGFR Statuses and Cancer Clinicopathologic Development in Lung Adenocarcinoma Patients." International Journal of Molecular Sciences 21, no. 21 (2020): 8023. http://dx.doi.org/10.3390/ijms21218023.

Full text

Abstract:

Lung adenocarcinoma (LADC) is a major subtype of lung cancer, particularly among populations of East Asia. The epidermal growth factor receptor (EGFR) is the most frequently mutated oncogene promoting LADC progression and can serve as a therapeutic target in LADC. The tissue inhibitor of metalloproteinases (TIMP)-3 is a major regulator of extracellular matrix turnover via targeting of matrix metalloproteinases (MMPs), and thus, plays a critical role in tumor development and progression. The purpose of this study was to investigate potential associations among TIMP-3 genetic polymorphisms, EGFR

APA, Harvard, Vancouver, ISO, and other styles

27

Ferrara, Miriam Grazia, Vincenzo Di Noia, Ettore D’Argento, et al. "Oncogene-Addicted Non-Small-Cell Lung Cancer: Treatment Opportunities and Future Perspectives." Cancers 12, no. 5 (2020): 1196. http://dx.doi.org/10.3390/cancers12051196.

Full text

Abstract:

Before the introduction of tyrosine kinase inhibitors (TKIs) for a particular subgroup of patients, despite platinum-based combination chemotherapy, the majority of patients affected by non-small-cell lung cancer (NSCLC) did not live longer than one year. With deeper understanding of tumor molecular biology, treatment of NSCLC has progressively entered the era of treatment customization according to tumor molecular characteristics, as well as histology. All this information allowed the development of personalized molecular targeted therapies. A series of studies have shown that, in some cases,

APA, Harvard, Vancouver, ISO, and other styles

28

Omerovic, Jasminka, Michael J. Clague, and Ian A. Prior. "Phosphatome profiling reveals PTPN2, PTPRJ and PTEN as potent negative regulators of PKB/Akt activation in Ras-mutated cancer cells." Biochemical Journal 426, no. 1 (2010): 65–72. http://dx.doi.org/10.1042/bj20091413.

Full text

Abstract:

Oncogenic Ras mutations render the protein constitutively active and promote tumorigenesis via chronic stimulation of effector pathways. In A549 lung adenocarcinoma approx. 50% of the total Ras population is constitutively active, yet these cells display only weak activation of the effectors: ERK1/2 (extracellular-signal-regulated kinase 1/2) and Akt. In order to identify key negative regulators of oncogenic Ras signalling we performed a phosphatome RNAi (RNA interference) screen in A549 cells and ranked their effects on phosphorylation of Ser473 of Akt. As expected, the tumour suppressor PTEN

APA, Harvard, Vancouver, ISO, and other styles

29

Drilon, Alexander, Michael Duruisseaux, Ji-Youn Han, et al. "Clinicopathologic Features and Response to Therapy of NRG1 Fusion–Driven Lung Cancers: The eNRGy1 Global Multicenter Registry." Journal of Clinical Oncology 39, no. 25 (2021): 2791–802. http://dx.doi.org/10.1200/jco.20.03307.

Full text

Abstract:

PURPOSE Although NRG1 fusions are oncogenic drivers across multiple tumor types including lung cancers, these are difficult to study because of their rarity. The global eNRGy1 registry was thus established to characterize NRG1 fusion–positive lung cancers in the largest and most diverse series to date. METHODS From June 2018 to February 2020, a consortium of 22 centers from nine countries in Europe, Asia, and the United States contributed data from patients with pathologically confirmed NRG1 fusion–positive lung cancers. Profiling included DNA-based and/or RNA-based next-generation sequencing

APA, Harvard, Vancouver, ISO, and other styles

30

Miller, Vincent A., Fred R. Hirsch, and David H. Johnson. "Systemic Therapy of Advanced Bronchioloalveolar Cell Carcinoma: Challenges and Opportunities." Journal of Clinical Oncology 23, no. 14 (2005): 3288–93. http://dx.doi.org/10.1200/jco.2005.19.240.

Full text

Abstract:

Bronchioloalveolar cell carcinoma (BAC) has fascinated physicians with its unique epidemiology, pathology, clinical manifestations, and natural history when compared with other non–small-cell lung cancer (NSCLC) subtypes. However, the relative rarity of pure BAC as defined by the WHO, and the inconsistent definitions used in various series, has limited systematic study of this entity. Retrospective and prospective studies suggest that patients with BAC treated with cytotoxic chemotherapy have a longer median survival than those with other subtypes of NSCLC. However, the widely accepted view th

APA, Harvard, Vancouver, ISO, and other styles

31

Zhao, Jing, Julien Dinkel, Arne Warth, et al. "CT characteristics in pulmonary adenocarcinoma with epidermal growth factor receptor mutation." PLOS ONE 12, no. 9 (2017): e0182741. http://dx.doi.org/10.1371/journal.pone.0182741.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Allo, Ghassan, Bizhan Bandarchi, Naoki Yanagawa, et al. "Epidermal growth factor receptor mutation-specific immunohistochemical antibodies in lung adenocarcinoma." Histopathology 64, no. 6 (2014): 826–39. http://dx.doi.org/10.1111/his.12331.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Kwon, Oh Jung, Min Hyeok Lee, Sung Ju Kang, et al. "Double primary lung adenocarcinoma diagnosed by epidermal growth factor receptor mutation status." Yeungnam University Journal of Medicine 34, no. 2 (2017): 270–74. http://dx.doi.org/10.12701/yujm.2017.34.2.270.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Poh, Mau-Ern, Chong-Kin Liam, Jiunn-Liang Tan, Yong-Kek Pang, Chee-Kuan Wong, and Ken-Siong Kow. "Acrometastasis from an epidermal-growth-factor-receptor (EGFR) mutation-positive lung adenocarcinoma." Cancer Treatment Communications 2, no. 2-3 (2014): 21–23. http://dx.doi.org/10.1016/j.ctrc.2014.08.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Li, Baoping, and Lei Zhang. "Gefitinib combined biologic therapy for advanced lung adenocarcinoma." Journal of Clinical Oncology 31, no. 15_suppl (2013): e19098-e19098. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e19098.

Full text

Abstract:

e19098 Background: Gefitinib is an effective treatment for non-small cell lung cancer patients with epidermal growth factor receptor (EGFR) mutations. However, due to the limited genetic testing methods and other constraints, a large proportion of patients did not benefit from it. In order to overcome the limitation of genetic testing and other constraints, we use gefitinib with the immune-biotherapy to treatment advanced lung adenocarcinoma. Methods: From February 2011 to December 2012, we use gefitinib combined with immune-therapy to treat 59 cases with advanced lung adenocarcinoma. These pa

APA, Harvard, Vancouver, ISO, and other styles

36

Hayasaka, Kazuki, Satoshi Shiono, Yuki Matsumura, et al. "Epidermal Growth Factor Receptor Mutation as a Risk Factor for Recurrence in Lung Adenocarcinoma." Annals of Thoracic Surgery 105, no. 6 (2018): 1648–54. http://dx.doi.org/10.1016/j.athoracsur.2018.01.052.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Fujiwara, Takumi, Tetsu Kobayashi, Taro Yasuma, et al. "De Novo T790M Mutation in an L858R Epidermal Growth Factor Receptor Mutant-Associated Lung Adenocarcinoma." Cancers 12, no. 10 (2020): 3074. http://dx.doi.org/10.3390/cancers12103074.

Full text

Abstract:

Background: Lung cancer is the leading cause of mortality for cancer worldwide. A point mutation in exon 21 of the epidermal growth factor receptor resulting in the substitution of arginine for leucine at position 858 (L858R) is a frequent cause of lung adenocarcinoma. Tyrosine kinase inhibitors are effective for treating patients with lung cancer associated with mutant epidermal growth factor receptors but most tumors become resistant shortly after treatment. The substitution of methionine for threonine at position 790 (T790M) on exon 20 is the most frequently acquired mutation leading to res

APA, Harvard, Vancouver, ISO, and other styles

38

Chang, Huang-Chih, Yu-Mu Chen, Chia-Cheng Tseng, et al. "Impact of epidermal growth factor receptor gene expression level on clinical outcomes in epidermal growth factor receptor mutant lung adenocarcinoma patients taking first-line epidermal growth factor receptor–tyrosine kinase inhibitors." Tumor Biology 39, no. 3 (2017): 101042831769593. http://dx.doi.org/10.1177/1010428317695939.

Full text

Abstract:

Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are first-choice treatments for advanced non-small-cell lung cancer patients harboring EGFR mutations. Although EGFR mutations are strongly predictive of patients’ outcomes and their response to treatment with EGFR-TKIs, early failure of first-line therapy with EGFR-TKIs in patients with EGFR mutations is not rare. Besides several clinical factors influencing EGFR-TKI efficacies studied earlier such as the Eastern Cooperative Oncology Group performance status or uncommon mutation, we would like to see whether semi-quanti

APA, Harvard, Vancouver, ISO, and other styles

39

Sharma, Saniya, Nalini Gupta, Navneet Singh, Rini Chaturvedi, Digambar Behera, and Arvind Rajwanshi. "Cytomorphological features as predictors of epidermal growth factor receptor mutation status in lung adenocarcinoma." CytoJournal 15 (April 2, 2018): 11. http://dx.doi.org/10.4103/cytojournal.cytojournal_45_17.

Full text

Abstract:

Background: Epidermal growth factor receptor mutation-positive (EGFR-p) lung adenocarcinomas are sensitive to tyrosine kinase inhibitors. Although histopathological subtype is an independent predictor of mutation status, there is a paucity of data on the cytomorphological features correlating with the EGFR mutation status. Therefore, the aim of this study was to determine whether certain cytomorphological features correlate with EGFR mutation in lung adenocarcinoma. Materials and Methods: A retrospective analysis of 48 lung adenocarcinoma cases diagnosed on fine needle aspiration cytology with

APA, Harvard, Vancouver, ISO, and other styles

40

Kawata, Natsuki, Miyo Inoue, Nobuyuki Horita, et al. "Multiple nodular pulmonary metastases of lung adenocarcinoma with epidermal growth factor receptor mutation." Respiratory Investigation 54, no. 2 (2016): 133–35. http://dx.doi.org/10.1016/j.resinv.2015.09.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Amanda, Gina, AgusDwi Susanto, Dicky Soehardiman, et al. "Adenocarcinoma of the lung with positive epidermal growth factor receptor mutation in pregnancy." Lung India 34, no. 6 (2017): 548. http://dx.doi.org/10.4103/0970-2113.217574.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Wang, Pei, and Cuiying Zhang. "Epidermal Growth Factor Receptor Gene Mutation in Pulmonary Adenocarcinoma Patients in Inner Mongolia." Chest 149, no. 4 (2016): A279. http://dx.doi.org/10.1016/j.chest.2016.02.291.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Normawati, Normawati, Suryanti Dwi Pratiwi, and Nanik Setijowati. "EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) AND CARCINOEMBRYONIC ANTIGEN (CEA) RELATIONSHIP OF LUNG ADENOKARSINOMA IN SAIFUL ANWAR HOSPITA MALANG." Berkala Kedokteran 13, no. 2 (2017): 173. http://dx.doi.org/10.20527/jbk.v13i2.4073.

Full text

Abstract:

Abstract: EGFR mutations is associated with sensitivity to tyrosine kinase inhibitors (TKI’s) therapy which are found in Lung Adenocarcinoma. There are some limitations in detecting EGFR mutation. CEA is also expected to predict treatment efficiency of EGFR-TKI's therapy. In this study, we investigated the relationship between serum Carcinoembryonic antigen (CEA) and Epidermal Growth Factor Receptor (EGFR) Mutations in Lung Adenocarcinoma patient. Methods : The research was conducted in Dr. Saiful Anwar General Hospital Malang. From May 2014 to November 2015, 54 lung adenocarcinoma patients wh

APA, Harvard, Vancouver, ISO, and other styles

44

Shah, Niharika, Helmut Popper, Smriti Karki, and Deebya Raj Mishra. "Use of immunohistochemistry for detection of Epidermal growth factor receptor mutation status in lung adenocarcinoma." Journal of Pathology of Nepal 10, no. 2 (2020): 1706–10. http://dx.doi.org/10.3126/jpn.v10i2.30170.

Full text

Abstract:

Background: Since the advent of targeted therapy in lung cancer, in settings where it is not possible to send for molecular testing of lung adenocarcinoma, immunohistochemistry for EGFR mutation-specific antibodies can be used as an alternative for detection of EGFR mutation. Materials and methods: 50 lung adenocarcinoma cases were screened at the Medical University of Graz. 19 cases in which molecular test as well as immunohistochemistry were positive for EGFR mutation. Cases where immunohistochemistry results and molecular test for the E-746-A750 deletion and the L858 mutation were pos

APA, Harvard, Vancouver, ISO, and other styles

45

AlGharras, Abdulaziz, Bojan Kovacina, Zhe Tian, et al. "Imaging-Based Surrogate Markers of Epidermal Growth Factor Receptor Mutation in Lung Adenocarcinoma: A Local Perspective." Canadian Association of Radiologists Journal 71, no. 2 (2020): 208–16. http://dx.doi.org/10.1177/0846537119888387.

Full text

Abstract:

Purpose: To identify computed tomography (CT) features of epidermal growth factor receptor (EGFR) mutation-positive lung adenocarcinoma in Canadian population and whether imaging-based surrogate markers of EGFR mutation in our population were similar to those found in the Asian population. Materials and Methods: Pretreatment CT scans of 223 patients with adenocarcinoma of the lung (112 with EGFR mutation and 111 without mutation) were retrospectively assessed for 20 specific CT features by 2 radiologists, who were blinded to the status of EGFR mutation. Univariate and multivariate logistic reg

APA, Harvard, Vancouver, ISO, and other styles

46

Doval, DineshChandra, KumardeepDutta Choudhury, Vineet Talwar, et al. "Epidermal growth factor receptor mutation in lung adenocarcinoma in India: A single center study." Journal of Carcinogenesis 12, no. 1 (2013): 12. http://dx.doi.org/10.4103/1477-3163.114970.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

D'Haene, Nicky, Marie Le Mercier, Isabelle Salmon, Zita Mekinda, Myriam Remmelink, and Thierry Berghmans. "SMAD4 Mutation in Small Cell Transformation of Epidermal Growth Factor Receptor Mutated Lung Adenocarcinoma." Oncologist 24, no. 1 (2018): 9–13. http://dx.doi.org/10.1634/theoncologist.2018-0016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Yano, Motoki, Hidefumi Sasaki, Yoshihiro Kobayashi, et al. "Epidermal Growth Factor Receptor Gene Mutation and Computed Tomographic Findings in Peripheral Pulmonary Adenocarcinoma." Journal of Thoracic Oncology 1, no. 5 (2006): 413–16. http://dx.doi.org/10.1016/s1556-0864(15)31604-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Chen, Wenhui, Yingxiang Lin, Yanxia Yu, Ping Wei, and Huaping Dai. "Recurrent bilateral spontaneous pneumothorax secondary to lung adenocarcinoma with epidermal growth factor receptor mutation." Thoracic Cancer 7, no. 2 (2015): 257–60. http://dx.doi.org/10.1111/1759-7714.12292.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Yano, Motoki, Hidefumi Sasaki, Yoshihiro Kobayashi, et al. "Epidermal Growth Factor Receptor Gene Mutation and Computed Tomographic Findings in Peripheral Pulmonary Adenocarcinoma." Journal of Thoracic Oncology 1, no. 5 (2006): 413–16. http://dx.doi.org/10.1097/01243894-200606000-00006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!