Non–Small Cell Lung Cancer: Epidemiology, Screening, Diagnosis, and Treatment

Duma, Narjust; Santana-Dávila, Rafael; Molina, Julian R.

doi:10.1016/j.mayocp.2019.01.013

Cited by 1,429 publications

(1,272 citation statements)

References 144 publications

(153 reference statements)

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Section: Introductionmentioning

confidence: 99%

“…Lung cancer ranks the leading cause of cancer‐related death around the world, which causes around 1.8 million deaths in 2018, and the World Health Organization (WHO) estimates that the lung cancer mortality will continue to rise, mainly as a result of some unfavorable environmental and lifestyle factors . Non‐small cell lung cancer (NSCLC), which involves 3 main types including adenocarcinoma, squamous cell carcinoma, and large‐cell carcinoma, represents 85% of new diagnosed lung cancers . Although there are various treatment modalities including surgery, chemotherapy, targeted therapies as well as immunotherapy are applied either alone or in combination for NSCLC treatment, the prognosis is still poor; the 5‐year overall survival (OS) rate ranges from 68% in patients with stage IB disease to 0% to 10% in patients with stage IVA‐IVB disease, which is quite unsatisfactory .…”

Section: Introductionmentioning

confidence: 99%

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Circular RNA SMARCA5 may serve as a tumor suppressor in non‐small cell lung cancer

Tong

2020

Clinical Laboratory Analysis

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: This study aimed to investigate the correlation of circular RNA SMARCA5 (circ-SMARCA5) expression with clinicopathological characteristics and survival profiles, furthermore, to explore the function of circ-SMARCA5 on regulating cell proliferation and chemotherapy sensitivity in non-small cell lung cancer (NSCLC). Methods:A total of 460 NSCLC patients were retrospectively reviewed, and circ-SMARCA5 expressions in tumor tissue and adjacent tissue were detected by RT-qPCR. Clinical characteristics were collected. Disease-free survival (DFS) and overall survival (OS) were calculated. In vitro, circ-SMARCA5 overexpression and control overexpression plasmids were transfected into NCI-H1437 as well as NCI-H1299 cells, which were further treated with different concentrations of cisplatin and gemcitabine.Results: Circ-SMARCA5 expression was decreased in tumor tissues compared to adjacent tissues. Moreover, circ-SMARCA5 expression negatively correlated with tumor size, lymph node metastasis, and TNM stage, but positively correlated with DFS and OS. Subsequent analysis displayed that circ-SMARCA5 high expression independently predicted prolonged DFS and OS. In vitro, circ-SMARCA5 expression was reduced in NSCLC cell lines (NCI-H650, NCI-H1299, NCI-H1437, and A549) compared to human normal lung bronchus epithelial cell line (BEAS-2B). In NCI-H1437 and NCI-H1299 cells, cell proliferation was decreased by circ-SMARCA5 overexpression, furthermore, chemosensitivity to cisplatin and gemcitabine were enhanced in circ-SMARCA5 overexpression treated cells compared to the control cells. Conclusion:Circ-SMARCA5 may serve as a tumor suppressor in NSCLC, which provides insight to the exploration of novel strategies in NSCLC management. K E Y W O R D Scell proliferation, chemotherapy sensitivity, circular RNA SMARCA5, non-small cell lung cancer, survival

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Circular RNA SMARCA5 may serve as a tumor suppressor in non‐small cell lung cancer

Tong

2020

Clinical Laboratory Analysis

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“…Lung cancer is globally the leading cause of cancer death according to World Health Organization (WHO) [1]. Non-small cell lung cancer (NSCLC), a major subtype of lung cancer, accounts for about 85% of total diagnosed lung cancers [2]. Diverse risk factors, including smoking, exposure to asbestos and radon, and genetic mutations have been well identified.…”

Section: Introductionmentioning

confidence: 99%

EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway

Kim

Choi

Lim

et al. 2020

IJMS

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Non-small cell lung cancer (NSCLC) is a major subtype of lung cancer. Besides genetic and environmental factors, epigenetic alterations contribute to the tumorigenesis of NSCLC. Epigenetic changes are considered key drivers of cancer initiation and progression, and altered expression and activity of epigenetic modifiers reshape the epigenetic landscape in cancer cells. Euchromatic histone-lysine N-methyltransferase 2 (EHMT2) is a histone methyltransferase and catalyzes monoand di-methylation at histone H3 lysine 9 (H3K9me1 and H3K9me2, respectively), leading to gene silencing. EHMT2 overexpression has been reported in various types of cancer, including ovarian cancer and neuroblastoma, in relation to cell proliferation and metastasis. However, its role in NSCLC is not fully understood. In this study, we showed that EHMT2 gene expression was higher in NSCLC than normal lung tissue based on publicly available data. Inhibition of EHMT2 by BIX01294 (BIX) reduced cell viability of NSCLC cell lines via induction of autophagy. Through RNA sequencing analysis, we found that EHMT2 inhibition significantly affected the cholesterol biosynthesis pathway. BIX treatment directly induced the expression of SREBF2, which is a master regulator of cholesterol biosynthesis, by lowering H3K9me1 and H3K9me2 at the promoter. Treatment of a cholesterol biosynthesis inhibitor, 25-hydroxycholesterol (25-HC), partially recovered BIX-induced cell death by attenuating autophagy. Our data demonstrated that EHMT2 inhibition effectively induced cell death in NSCLC cells through altering cholesterol metabolism-dependent autophagy.

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“…Lung cancer is classified into small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC is further sub-classified into adenocarcinoma, large cell carcinoma, and squamous cell carcinoma [23]. Bronchioalveolar (BAC) and acinar carcinoma are two forms of adenocarcinoma.…”

Section: Classificationmentioning

confidence: 99%

Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells

Hamid

Petreaca

2020

Cancers

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Secondary resistant mutations in cancer cells arise in response to certain small molecule inhibitors. These mutations inevitably cause recurrence and often progression to a more aggressive form. Resistant mutations may manifest in various forms. For example, some mutations decrease or abrogate the affinity of the drug for the protein. Others restore the function of the enzyme even in the presence of the inhibitor. In some cases, resistance is acquired through activation of a parallel pathway which bypasses the function of the drug targeted pathway. The Catalogue of Somatic Mutations in Cancer (COSMIC) produced a compendium of resistant mutations to small molecule inhibitors reported in the literature. Here, we build on these data and provide a comprehensive review of resistant mutations in cancers. We also discuss mechanistic parallels of resistance.

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Non–Small Cell Lung Cancer: Epidemiology, Screening, Diagnosis, and Treatment

Cited by 1,429 publications

References 144 publications

Circular RNA SMARCA5 may serve as a tumor suppressor in non‐small cell lung cancer

Circular RNA SMARCA5 may serve as a tumor suppressor in non‐small cell lung cancer

EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway

Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells

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