First-line treatment of advanced epidermal growth factor receptor (EGFR) mutation positive non-squamous non-small cell lung cancer

Greenhalgh, J; Dwan, Kerry; Boland, Angela; Bates, Victoria; Vecchio, Fabio Maria; Dündar, Yenal; Jain, Pooja; Green, John A.

doi:10.1002/14651858.cd010383.pub2

Cited by 169 publications

(133 citation statements)

References 106 publications

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“…6,15 Further pooled analysis indicated a significant improvement in OS in the 19del subgroup. 17,18 These outcomes may lead to a tendency in clinical practice to prescribe afatinib to patients with 19del mutations. Several real-world studies have also demonstrated this tendency and reported longer median PFS in common EGFR mutation groups.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and safety of afatinib in a Chinese population with advanced lung adenocarcinoma with sensitive EGFR mutations

et al. 2019

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Background Afatinib is an irreversible ErbB family blocker that improves progression‐free survival (PFS) of advanced EGFR ‐mutant lung adenocarcinoma compared to chemotherapy. However, afatinib leads to more adverse events than first‐generation EGFR inhibitors. Hence, exploration of the optimal afatinib initial dose and its efficacy and safety in Asian patients has drawn extensive attention. Methods We retrospectively evaluated demographic and clinical information, survival data, and adverse events in advanced non‐small cell lung cancer patients treated with afatinib from 27 February 2017 to 30 October 2018. Results A total of 60 patients were included in the study. Thirty‐nine (65%) patients received afatinib as first‐line treatment. The median PFS was 12.3 months (95% confidence internal 7.6–17.0). Multivariate Cox regression analysis revealed that age, gender, smoking history, baseline brain metastasis status, afatinib starting dose, and mutation type did not significantly influence PFS. No significant difference in median PFS between patients treated with an initial dose of afatinib of 40 mg or 30 mg, either in the first‐line (14.5 vs. 5.2 months; P = 0.101) or in a second or later‐line setting (3.0 vs. 5.0 months; P = 0.375) was observed. The incidence of all grades of rash/acne (92.5% vs. 61.1%; P = 0.011) and paronychia (82.5% vs. 50.0%; P = 0.010) in the 40 mg group was significantly higher than in the 30 mg group. Conclusion First‐line afatinib treatment is beneficial for advanced lung adenocarcinoma patients with sensitive EGFR mutations. Initial dose and baseline brain metastasis status do not significantly impact PFS.

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Section: Discussionmentioning

confidence: 99%

Efficacy and safety of afatinib in a Chinese population with advanced lung adenocarcinoma with sensitive EGFR mutations

et al. 2019

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“…EGFR mutation-positive NSCLC is emerging as an important biologic subtype of lung cancer, with an estimated prevalence of 10–15% in patients with non-squamous NSCLC [39]. Given the selective effectiveness seen with use of tyrosine-kinase inhibitors (TKIs) in prolonging progression-free survival, especially within specific mutant subtypes, it follows that further investigation and stratification of NSCLC patients, not only by histologic subtype but also by molecular profile, will prove invaluable for the future management of these patients [39]. With overexpression in epithelial-derived malignancies, such as NSCLC and its association with tumorigenesis and metastasis, EGFR has become a promising therapeutic target for adoptive T-cell therapy.…”

Section: Target Antigens For Carsmentioning

confidence: 99%

CAR T-cell therapy for lung cancer and malignant pleural mesothelioma

Zeltsman

Dozier

McGee

et al. 2017

Translational Research

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Immunotherapy is a promising field that harnesses the power of the immune system as a therapeutic agent for cancer treatment. Beneficial outcomes shown in patients with non-small cell lung cancer (NSCLC) and malignant pleural mesothelioma (MPM) with relatively higher tumor-infiltrating T cells, combined with impressive responses obtained in a cohort of patients with NSCLC following checkpoint blockade therapy, lays a strong foundation to promote effector immune responses in these patients. One such approach being investigated is administration of tumor antigen-targeted T cells with transduction of a chimeric antigen receptor (CAR). CARs are synthetic receptors that enhance T-cell antitumor effector function and have gained momentum to investigate in solid tumors based on recent successes of clinical trials treating patients with B-cell hematologic malignancies. This review summarizes target antigens for CAR T-cell therapy that are being investigated in preclinical studies as well as clinical trials for both NSCLC and MPM patients., We discuss the rationale for combination immunotherapies for NSCLC and MPM patients. Additionally, we have highlighted the challenges and strategies for overcoming the obstacles facing translation of CAR T-cell therapy to solid tumors.

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“…Lung adenocarcinoma (LAD) is the most common histological type of NSCLC, and because of its tendency to form haematogenous metastasis, patients often die of relapse and metastasis [2]. Although advanced detection measures and treatments including surgery, chemotherapy, radiotherapy, and targeted therapy are widely used, the likelihood of a complete cure is slim [3, 4]. Therefore, a thorough understanding of the molecular mechanisms involved in the development and progression of LAD could provide more effective diagnostic markers and targets for LAD patient therapy [5].…”

Section: Introductionmentioning

confidence: 99%

Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression

et al. 2017

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BackgroundNumerous studies have shown that long non-coding RNAs (lncRNAs) behave as a novel class of transcript during multiple cancer processes, such as cell proliferation, apoptosis, migration, and invasion. LINC00152 is located on chromosome 2p11.2, and has a transcript length of 828 nucleotides. The biological role of LINC00152 in LAD(lung adenocarcinoma) remains unknown.MethodsQuantitative reverse transcription PCR(qRT-PCR) was used to detect LINC00152 expression in 60 human LAD tissues and paired normal tissues. In vitro and in vivo studies showed the biological function of LINC00152 in tumour progression. RNA transcriptome sequencing technology was performed to identify the downstream suppressor IL24(interleukin 24) which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation (RIP), RNA pulldown, and Chromatin immunoprecipitation (ChIP) assays were carried out to reveal the interaction between LINC00152, EZH2 and IL24.ResultsLINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. High levels of LINC00152 expression were correlated with advanced TNM stage, larger tumor size, and lymph node metastasis, as well as shorter survival time. Silencing of LINC00152 suppressed cell growth and induced cell apoptosis. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. Moreover, the ectopic expression of IL24 repressed cell proliferation and partly reversed LINC00152 overexpression-induced promotion of cell growth in LAD.ConclusionsOur study reveals an oncogenic role for LINC00152 in LAD tumorigenesis, suggesting that it could be used as a therapeutic target in LAD treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0581-3) contains supplementary material, which is available to authorized users.

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First-line treatment of advanced epidermal growth factor receptor (EGFR) mutation positive non-squamous non-small cell lung cancer

Cited by 169 publications

References 106 publications

Efficacy and safety of afatinib in a Chinese population with advanced lung adenocarcinoma with sensitive EGFR mutations

Efficacy and safety of afatinib in a Chinese population with advanced lung adenocarcinoma with sensitive EGFR mutations

CAR T-cell therapy for lung cancer and malignant pleural mesothelioma

Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression

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