Displaying publications 1 - 20 of 73 in total

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  1. Sachithanandan A, Nor Y
    Med J Malaysia, 2013 Apr;68(2):175-6.
    PMID: 23629571 MyJurnal
    Synchronous primary non-small cell lung cancers (NSCLC) are rare and may be discovered unexpectedly following lung resection. Discrimination from intrapulmonary metastases is important to guide treatment and prognosis but is difficult solely on clinical or radiological findings. Histopathological evaluation with immunohistochemistry (IHC) markers can prove decisive and should feature in the diagnostic algorithm of such patients. We report a rare case of two synchronous primary NSCLCs diagnosed post operatively following pathological examination of the resected lobe, highlighting the value of IHC and discuss the management of such patients.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung*
  2. Paudel KR, Mehta M, Yin GHS, Yen LL, Malyla V, Patel VK, et al.
    Environ Sci Pollut Res Int, 2022 Jul;29(31):46830-46847.
    PMID: 35171422 DOI: 10.1007/s11356-022-19158-2
    Non-small cell lung cancer (NSCLC) is reported to have a high incidence rate and is one of the most prevalent types of cancer contributing towards 85% of all incidences of lung cancer. Berberine is an isoquinoline alkaloid which offers a broad range of therapeutical and pharmacological actions against cancer. However, extremely low water solubility and poor oral bioavailability have largely restricted its therapeutic applications. To overcome these limitations, we formulated berberine-loaded liquid crystalline nanoparticles (LCNs) and investigated their in vitro antiproliferative and antimigratory activity in human lung epithelial cancer cell line (A549). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), trypan blue staining, and colony forming assays were used to evaluate the anti-proliferative activity, while scratch wound healing assay and a modified Boyden chamber assay were carried out to determine the anti-migratory activity. We also investigated major proteins associated with lung cancer progression. The developed nanoparticles were found to have an average particle size of 181.3 nm with spherical shape, high entrapment efficiency (75.35%) and have shown sustained release behaviour. The most remarkable findings reported with berberine-loaded LCNs were significant suppression of proliferation, inhibition of colony formation, inhibition of invasion or migration via epithelial mesenchymal transition, and proliferation related proteins associated with cancer progression. Our findings suggest that anti-cancer compounds with the problem of poor solubility and bioavailability can be overcome by formulating them into nanotechnology-based delivery systems for better efficacy. Further in-depth investigations into anti-cancer mechanistic research will expand and strengthen the current findings of berberine-LCNs as a potential NSCLC treatment option.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung*
  3. Loh LC, Chan LY, Tan RY, Govindaraju S, Ratnavelu K, Kumar S, et al.
    Asia Pac J Public Health, 2006;18(1):69-71.
    PMID: 16629441
    The prognosis of lung cancer remains poor with overall five year survival figures varying between five and 10% worldwide, However, it has been shown that surgery in patients with early stage disease in non-small cell lung cancer can achieve five year survival rates up to 80%, suggesting that early or delay diagnosis can influence prognosis. Nevertheless, studies addressing this have been inconclusive and mostly derived from Western countries.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/diagnosis*; Carcinoma, Non-Small-Cell Lung/mortality; Carcinoma, Non-Small-Cell Lung/surgery*
  4. Liam CK, Mallawathantri S, Fong KM
    Respirology, 2020 09;25(9):933-943.
    PMID: 32335992 DOI: 10.1111/resp.13823
    Molecular biomarker testing of advanced-stage NSCLC is now considered standard of care and part of the diagnostic algorithm to identify subsets of patients for molecular-targeted treatment. Tumour tissue biopsy is essential for an accurate initial diagnosis, determination of the histological subtype and for molecular testing. With the increasing use of small biopsies and cytological specimens for diagnosis and the need to identify an increasing number of predictive biomarkers, proper management of the limited amount of sampling materials available is important. Many patients with advanced NSCLC do not have enough tissue for molecular testing and/or do not have a biopsy-amenable lesion and/or do not want to go through a repeat biopsy given the potential risks. Molecular testing can be difficult or impossible if the sparse material from very small biopsy specimens has already been exhausted for routine diagnostic purposes. A limited diagnostic workup is recommended to preserve sufficient tissue for biomarker testing. In addition, tumour biopsies are limited by tumour heterogeneity, particularly in the setting of disease resistance, and thus may yield false-negative results. Hence, there have been considerable efforts to determine if liquid biopsy in which molecular alterations can be non-invasively identified in plasma cell-free ctDNA, a potential surrogate for the entire tumour genome, can overcome the issues with tissue biopsies and replace the need for the latter.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/drug therapy; Carcinoma, Non-Small-Cell Lung/genetics*; Carcinoma, Non-Small-Cell Lung/metabolism; Carcinoma, Non-Small-Cell Lung/pathology
  5. Kho SS, Chan SK, Ismail AM, Tie ST
    Diagn Cytopathol, 2022 Dec;50(12):583-585.
    PMID: 36135808 DOI: 10.1002/dc.25056
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung*
  6. Rohilla S, Singh M, Priya S, Almalki WH, Haniffa SM, Subramaniyan V, et al.
    PMID: 36734949 DOI: 10.1615/JEnvironPatholToxicolOncol.2022042088
    Melatonin is a serotonin-derived pineal gland hormone with many biological functions like regulating the sleep-wake cycle, circadian rhythm, menstrual cycle, aging, immunity, and antioxidants. Melatonin synthesis and release are more pronounced during the night, whereas exposure to light decreases it. Evidence is mounting in favor of the therapeutic effects of melatonin in cancer prevention, treatment and delayed onset in various cancer subtypes. Melatonin exerts its anticancer effect through modification of its receptors such as melatonin 1 (MT1), melatonin 2 (MT2), and inhibition of cancer cell proliferation, epigenetic alterations (DNA methylation/demethylation, histone acetylation/deacetylation), metastasis, angiogenesis, altered cellular energetics, and immune evasion. Melatonin performs a significant function in immune modulation and enhances innate and cellular immunity. In addition, melatonin has a remarkable impact on epigenetic modulation of gene expression and alters the transcription of genes. As an adjuvant to cancer therapies, it acts by decreasing the side effects and boosting the therapeutic effects of chemotherapy. Since current treatments produce drug-induced unwanted toxicities and side effects, they require alternate therapies. A recent review article attempts to summarize the mechanistic perspective of melatonin in different cancer subtypes like skin cancer, breast cancer, hepatic cancer, renal cell cancer, non-small cell lung cancer (NSCLC), colon oral, neck, and head cancer. The various studies described in this review will give a firm basis for the future evolution of anticancer drugs.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung*
  7. Ramachandran S, Verma AK, Dev K, Goyal Y, Bhatt D, Alsahli MA, et al.
    Oxid Med Cell Longev, 2021;2021:5563746.
    PMID: 34336101 DOI: 10.1155/2021/5563746
    With over a million deaths every year around the world, lung cancer is found to be the most recurrent cancer among all types. Nonsmall cell lung carcinoma (NSCLC) amounts to about 85% of the entire cases. The other 15% owes it to small cell lung carcinoma (SCLC). Despite decades of research, the prognosis for NSCLC patients is poorly understood with treatment options limited. First, this article emphasises on the part that tumour microenvironment (TME) and its constituents play in lung cancer progression. This review also highlights the inflammatory (pro- or anti-) roles of different cytokines (ILs, TGF-β, and TNF-α) and chemokine (CC, CXC, C, and CX3C) families in the lung TME, provoking tumour growth and subsequent metastasis. The write-up also pinpoints recent developments in the field of chemokine biology. Additionally, it covers the role of extracellular vesicles (EVs), as alternate carriers of cytokines and chemokines. This allows the cytokines/chemokines to modulate the EVs for their secretion, trafficking, and aid in cancer proliferation. In the end, this review also stresses on the role of these factors as prognostic biomarkers for lung immunotherapy, apart from focusing on inflammatory actions of these chemoattractants.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/immunology*
  8. Lee SS, Cheah YK
    J Immunol Res, 2019;2019:3046379.
    PMID: 30944831 DOI: 10.1155/2019/3046379
    Cellular components of the tumour microenvironment (TME) are recognized to regulate the hallmarks of cancers including tumour proliferation, angiogenesis, invasion, and metastasis, as well as chemotherapeutic resistance. The linkage between miRNA, TME, and the development of the hallmarks of cancer makes miRNA-mediated regulation of TME a potential therapeutic strategy to complement current cancer therapies. Despite significant advances in cancer therapy, lung cancer remains the deadliest form of cancer among males in the world and has overtaken breast cancer as the most fatal cancer among females in more developed countries. Therefore, there is an urgent need to develop more effective treatments for NSCLC, which is the most common type of lung cancer. Hence, this review will focus on current literature pertaining to antitumour or protumourigenic effects elicited by nonmalignant stromal cells of TME in NSCLC through miRNA regulation as well as current status and future prospects of miRNAs as therapeutic agents or targets to regulate TME in NSCLC.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/genetics; Carcinoma, Non-Small-Cell Lung/pathology*; Carcinoma, Non-Small-Cell Lung/therapy
  9. How SH, Ng TH, Kuan YC, Jamalludin AR, Fauzi AR
    Asia Pac J Clin Oncol, 2015 Sep;11(3):221-7.
    PMID: 24575820 DOI: 10.1111/ajco.12179
    Data on lung cancer survival are lacking in developing countries. Our objectives were to describe the survival of our lung cancer patients and to determine independent prognostic factors affecting survival.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/mortality*; Carcinoma, Non-Small-Cell Lung/pathology
  10. Shi Yeen TN, Pathmanathan R, Shiran MS, Ahmad Zaid FA, Cheah YK
    J Biomed Sci, 2013 Apr 16;20:22.
    PMID: 23590575 DOI: 10.1186/1423-0127-20-22
    BACKGROUND: Somatic mutations of the epidermal growth factor receptor (EGFR) are reportedly associated with various responses in non-small cell lung cancer (NSCLC) patients receiving the anti-EGFR agents. Detection of the mutation therefore plays an important role in therapeutic decision making. The aim of this study was to detect EGFR mutations in formalin fixed paraffin embedded (FFPE) samples using both Scorpion ARMS and high resolution melt (HRM) assay, and to compare the sensitivity of these methods.

    RESULTS: All of the mutations were found in adenocarcinoma, except one that was in squamous cell carcinoma. The mutation rate was 45.7% (221/484). Complex mutations were also observed, wherein 8 tumours carried 2 mutations and 1 tumour carried 3 mutations.

    CONCLUSIONS: Both methods detected EGFR mutations in FFPE samples. HRM assays gave more EGFR positive results compared to Scorpion ARMS.

    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/genetics*; Carcinoma, Non-Small-Cell Lung/pathology
  11. Halim NHA, Zakaria N, Satar NA, Yahaya BH
    Methods Mol Biol, 2016;1516:371-388.
    PMID: 27032945 DOI: 10.1007/7651_2016_326
    Cancer is a major health problem worldwide. The failure of current treatments to completely eradicate cancer cells often leads to cancer recurrence and dissemination. Studies have suggested that tumor growth and spread are driven by a minority of cancer cells that exhibit characteristics similar to those of normal stem cells, thus these cells are called cancer stem cells (CSCs). CSCs are believed to play an important role in initiating and promoting cancer. CSCs are resistant to currently available cancer therapies, and understanding the mechanisms that control the growth of CSCs might have great implications for cancer therapy. Cancer cells are consist of heterogeneous population of cells, thus methods of identification, isolation, and characterisation of CSCs are fundamental to obtain a pure CSC populations. Therefore, this chapter describes in detail a method for isolating and characterizing a pure population of CSCs from heterogeneous population of cancer cells and CSCs based on specific cell surface markers.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/genetics; Carcinoma, Non-Small-Cell Lung/pathology*
  12. Liam CK, Leow HR, Pang YK
    J Thorac Oncol, 2013 Dec;8(12):e114.
    PMID: 24389448 DOI: 10.1097/JTO.0b013e3182a4e111
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/diagnosis*; Carcinoma, Non-Small-Cell Lung/genetics
  13. Liam CK, Lim KH, Wong CM
    Chest, 2002 Jan;121(1):309-10.
    PMID: 11796481
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/epidemiology*; Carcinoma, Non-Small-Cell Lung/pathology
  14. Rajadurai P, Cheah PL, How SH, Liam CK, Annuar MAA, Omar N, et al.
    Lung Cancer, 2019 10;136:65-73.
    PMID: 31446227 DOI: 10.1016/j.lungcan.2019.08.005
    In the recent years, increased understanding of the molecular profiles of non-small cell lung cancer (NSCLC) has allowed for targeted treatment of actionable genetic mutations. The management of NSCLC now requires multiple molecular tests to guide the treatment strategy. In the light of this, there is a need to establish a molecular testing consensus statement for advanced NSCLC patients in Malaysia. This Malaysian consensus statement was developed by a panel of experts, chaired by a pathologist and composed of three other pathologists, four respiratory physicians and three oncologists. It reflects currently available scientific data and adaptations of recommendations from international guidelines to the local landscape. Expert recommendations on different aspects of molecular testing agreed upon by the panel are provided as structured discussions. These recommendations address the appropriate patients and samples to be tested, as well as when and how these tests should be performed. The algorithms for molecular testing in metastatic NSCLC, in the first line setting and upon disease progression beyond first line therapy, were developed.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/diagnosis*; Carcinoma, Non-Small-Cell Lung/etiology*
  15. Paudel KR, Wadhwa R, Tew XN, Lau NJX, Madheswaran T, Panneerselvam J, et al.
    Life Sci, 2021 Jul 01;276:119436.
    PMID: 33789146 DOI: 10.1016/j.lfs.2021.119436
    Non-small cell lung cancer (NSCLC) is one of the major causes of cancer-related mortality globally. Despite the availability of therapeutic options, the improvement in patient survival is yet to be achieved. Recent advances in natural product (e.g., Rutin) research, therapeutic nanotechnology and especially the combination of both could aid in achieving significant improvements in the treatment or management of NSCLC. In this study, we explore the anti-cancer activity of Rutin-loaded liquid crystalline nanoparticles (LCNs) in an in vitro model where we have employed the A549 human lung epithelial carcinoma cell line. The anti-proliferative activity was determined by MTT and Trypan blue assays, whereas, the anti-migratory activity was evaluated by the scratch wound healing assay and a modified Boyden chamber assay. We also evaluated the anti-apoptotic activity by Annexin V-FITC staining, and the colony formation activity was studied using crystal violet staining. Here, we report that Rutin-LCNs showed promising anti-proliferative and anti-migratory activities. Furthermore, Rutin-LCNs also induced apoptosis in the A549 cells and inhibited colony formation. The findings warrant further detailed and in-depth anti-cancer mechanistic studies of Rutin-LCNs with a focus towards a potential therapeutic option for NSCLC. LCNs may help to enhance the solubility of Rutin used in the treatment of lung cancer and hence enhance the anticancer effect of Rutin.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/drug therapy*; Carcinoma, Non-Small-Cell Lung/pathology
  16. Wu YL, Lu S, Lu Y, Zhou J, Shi YK, Sriuranpong V, et al.
    J Thorac Oncol, 2018 10;13(10):1539-1548.
    PMID: 29966800 DOI: 10.1016/j.jtho.2018.06.012
    INTRODUCTION: The phase III randomized PROFILE 1014 study demonstrated superiority of crizotinib to first-line chemotherapy in prolonging progression-free survival (PFS) in previously untreated patients with ALK receptor tyrosine kinase gene (ALK)-positive advanced nonsquamous NSCLC. This result was consistent with that in the smaller subset of East Asian patients in PROFILE 1014. The subsequent study reported here prospectively evaluated crizotinib in a larger East Asian patient population.

    METHODS: In this open-label phase III study (PROFILE 1029), patients were randomized 1:1 to receive orally administered crizotinib 250 mg twice daily continuously (3-week cycles) or intravenously administered chemotherapy (pemetrexed 500 mg/m2, plus cisplatin 75 mg/m2, or carboplatin [at a dose to produce area under the concentration-time curve of 5-6 mg·min/mL]) every 3 weeks for a maximum of six cycles. PFS confirmed by independent radiology review was the primary end point.

    RESULTS: Crizotinib significantly prolonged PFS (hazard ratio, 0.402; 95% confidence interval [CI]: 0.286-0.565; p < 0.001). The median PFS was 11.1 months with crizotinib and 6.8 months with chemotherapy. The objective response rate was 87.5% (95% CI: 79.6-93.2%) with crizotinib versus 45.6% (95% CI: 35.8-55.7%) with chemotherapy (p < 0.001). The most common adverse events were increased transaminase levels, diarrhea, and vision disorders with crizotinib and leukopenia, neutropenia, and anemia with chemotherapy. Significantly greater improvements from baseline in patient-reported outcomes were seen in crizotinib-treated versus chemotherapy-treated patients.

    CONCLUSIONS: First-line crizotinib significantly improved PFS, objective response rate, and patient-reported outcomes compared with standard platinum-based chemotherapy in East Asian patients with ALK-positive advanced NSCLC, which is similar to the results from PROFILE 1014. The safety profiles of crizotinib and chemotherapy were consistent with those previously published.

    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/drug therapy*; Carcinoma, Non-Small-Cell Lung/pathology
  17. Othman N, Nagoor NH
    Int J Oncol, 2019 01;54(1):306-314.
    PMID: 30365047 DOI: 10.3892/ijo.2018.4602
    The silencing of Bcl‑xL in the nonsmall cell lung cancer (NSCLC) cell line, A549, downregulates miR‑361‑5p expression. This study aimed to determine the biological effects of miR‑361‑5p on NSCLC, and to elucidate the molecular mechanisms through which apoptosis is regulated. MicroRNA (miRNA or miR) functional analyses were performed via transfection of miR‑361‑5p mimics and inhibitors, demonstrating that the inhibition of miR‑361‑5p induced the apoptosis of NSCLC cells. To elucidate the function of miR‑361‑5p in vivo, cells transfected with miR‑361‑5p inhibitors were microinjected into zebrafish embryos, and immunostained using antibodies to detect the active form of caspase‑3. Co-transfection with siBcl‑xL and miR‑361‑5p mimics illustrated the association between Bcl‑xL, miR‑361‑5p and apoptosis; miR‑361‑5p mimics blocked the apoptosis initiated by siBcl‑xL. Luciferase reporter assays identified mothers against decapentaplegic homolog 2 (SMAD2) as a novel target of miR‑361‑5p and the reduction of its protein level was validated by western blot analysis. To confirm the molecular mechanisms through which apoptosis is regulated, gene rescue experiments revealed that the ectopic expression of SMAD2 attenuated the inhibitory effects on apoptosis induced by miR‑361‑5p. In this study, to the best of our knowledge, we provide the first evidence that miR‑361‑5p functions as an oncomiR in A549 and SK‑LU‑1 cells through the regulation of SMAD2, suggesting that miR‑361‑5p may be employed as a potential therapeutic target for the miRNA-based therapy of NSCLC.
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/genetics*; Carcinoma, Non-Small-Cell Lung/metabolism
  18. Shee-Chai C, Liam CK, Mun KS
    J Thorac Oncol, 2017 10;12(10):e171-e173.
    PMID: 28939153 DOI: 10.1016/j.jtho.2017.06.068
    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/drug therapy*; Carcinoma, Non-Small-Cell Lung/pathology
  19. Tang WH, Alip A, Saad M, Phua VC, Chandran H, Tan YH, et al.
    Asian Pac J Cancer Prev, 2015;16(5):1901-6.
    PMID: 25773842
    BACKGROUND: Brain metastases occur in about 20-40% of patients with non-small-cell lung carcinoma (NSCLC), and are usually associated with a poor outcome. Whole brain radiotherapy (WBRT) is widely used but increasingly, more aggressive local treatments such as surgery or stereotactic radiosurgery (SRS) or stereotactic radiotherapy (SRT) are being employed. In our study we aimed to describe the various factors affecting outcomes in NSCLC patients receiving local therapy for brain metastases.

    MATERIALS AND METHODS: The case records of 125 patients with NSCLC and brain metastases consecutively treated with radiotherapy at two tertiary centres from January 2006 to June 2012 were analysed for patient, tumour and treatment-related prognostic factors. Patients receiving SRS/SRT were treated using Cyberknife. Variables were examined in univariate and multivariate testing.

    RESULTS: Overall median survival was 3.4 months (95%CI: 1.7-5.1). Median survival for patients with multiple metastases receiving WBRT was 1.5 months, 1-3 metastases receiving WBRT was 3.6 months and 1-3 metastases receiving surgery or SRS/SRT was 8.9 months. ECOG score (≤2 vs >2, p=0.001), presence of seizure (yes versus no, p=0.031), treatment modality according to number of brain metastases (1-3 metastases+surgery or SRS/SRT±WBRT vs 1-3 metastases+WBRT only vs multiple metastases+WBRT only, p=0.007) and the use of post-therapy systemic treatment (yes versus no, p=0.001) emerged as significant on univariate analysis. All four factors remained statistically significant on multivariate analysis.

    CONCLUSIONS: ECOG ≤2, presence of seizures, oligometastatic disease treated with aggressive local therapy (surgery or SRS/SRT) and the use of post-therapy systemic treatment are favourable prognostic factors in NSCLC patients with brain metastases.

    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/mortality; Carcinoma, Non-Small-Cell Lung/pathology*; Carcinoma, Non-Small-Cell Lung/therapy
  20. Ho GF, Chai CS, Alip A, Wahid MIA, Abdullah MM, Foo YC, et al.
    BMC Cancer, 2019 Sep 09;19(1):896.
    PMID: 31500587 DOI: 10.1186/s12885-019-6107-1
    BACKGROUND: This study aimed to evaluate the efficacy, side-effects and resistance mechanisms of first-line afatinib in a real-world setting.

    METHODS: This is a multicenter observational study of first-line afatinib in Malaysian patients with epidermal growth factor receptor (EGFR)-mutant advanced non-small cell lung cancer (NSCLC). Patients' demographic, clinical and treatment data, as well as resistance mechanisms to afatinib were retrospectively captured. The statistical methods included Chi-squared test and independent t-test for variables, Kaplan-Meier curve and log-rank test for survival, and Cox regression model for multivariate analysis.

    RESULTS: Eighty-five patients on first-line afatinib from 1st October 2014 to 30th April 2018 were eligible for the study. EGFR mutations detected in tumors included exon 19 deletion in 80.0%, exon 21 L858R point mutation in 12.9%, and rare or complex EGFR mutations in 7.1% of patients. Among these patients, 18.8% had Eastern Cooperative Oncology Group performance status of 2-4, 29.4% had symptomatic brain metastases and 17.6% had abnormal organ function. Afatinib 40 mg or 30 mg once daily were the most common starting and maintenance doses. Only one-tenth of patients experienced severe side-effects with none having grade 4 toxicities. The objective response rate was 76.5% while the disease control rate was 95.3%. At the time of analysis, 56 (65.9%) patients had progression of disease (PD) with a median progression-free survival (mPFS) of 14.2 months (95% CI, 11.85-16.55 months). Only 12.5% of the progressed patients developed new symptomatic brain metastases. The overall survival (OS) data was not mature. Thirty-three (38.8%) patients had died with a median OS of 28.9 months (95% CI, 19.82-37.99 months). The median follow-up period for the survivors was 20.0 months (95% CI, 17.49-22.51 months). Of patients with PD while on afatinib, 55.3% were investigated for resistance mechanisms with exon 20 T790 M mutation detected in 42.0% of them.

    CONCLUSIONS: Afatinib is an effective first-line treatment for patients with EGFR-mutant advanced NSCLC with a good response rate and long survival, even in patients with unfavorable clinical characteristics. The side-effects of afatinib were manageable and T790 M mutation was the most common resistance mechanism causing treatment failure.

    Matched MeSH terms: Carcinoma, Non-Small-Cell Lung/drug therapy*; Carcinoma, Non-Small-Cell Lung/genetics; Carcinoma, Non-Small-Cell Lung/metabolism
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