scholarly journals Expression of inflammatory interleukins and selected miRNAs in non-small cell lung cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Agata Dutkowska ◽  
Bartosz Szmyd ◽  
Marcin Kaszkowiak ◽  
Daria Domańska-Senderowska ◽  
Dorota Pastuszak-Lewandoska ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Strong Influence ◽  
Small Cell ◽  
Tumour Tissue ◽  
Small Cell Lung ◽  
Tissue Samples ◽  
Primary Nsclc ◽  
Inflammatory Processes ◽  
History Of ◽  
Immune Destruction

AbstractTumours are characterised by an ability to avoid immune destruction and the presence of cancer-associated inflammation. Better understanding of the link between lung cancer and such inflammation is vital for early detection and personalized treatment. Thus, we examined the mRNA expression of interleukins IL-1β, IL-6, IL-17 and miR-9, miR-122 as potential useful biomarkers of NSCLC. Tumour tissues, non-cancerous tissue and blood samples were collected from 39 patients with primary NSCLC undergoing surgical treatment. The selected RNA was isolated from tissue samples and selected miRNAs from peripheral blood exosomes. This RNA was transcribed to cDNA and quantified using RT-qPCR. Significantly higher expression of the selected interleukins was observed in non-cancerous than tumour tissue, and IL-6 was significantly higher in the tumour tissue of patients with a history of ≤ 40 pack-years (PYs) (2.197, IQR: 0.821–4.415) than in those with > 40 PYs (0.461, IQR: 0.372–0.741; p = 0.037). It is clear that inflammatory processes play a role in NSCLC, as indicated by the upregulation of IL-1β and IL-6 in tumour and adjacent tissue, and that smoking has a strong influence on inflammation in tumourigenesis, demonstrated by the upregulation of IL-6 in tumour samples among patients with ≤ 40 PYs compared to > 40 PYs.

scholarly journals History of Extensive Disease Small Cell Lung Cancer Treatment: Time to Raise the Bar? A Review of the Literature

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 998
Author(s):  
Chiara Lazzari ◽  
Aurora Mirabile ◽  
Alessandra Bulotta ◽  
Maria Grazia Viganó ◽  
Francesca Rita Ogliari ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Treatment Time ◽  
Small Cell ◽  
Review Of The Literature ◽  
Small Cell Lung ◽  
Extensive Disease ◽  
History Of ◽  
Line Standard

Several trials have tried for decades to improve the outcome of extensive disease small cell lung cancer (ED-SCLC) through attempts to modify the standard treatments. Nevertheless, platinum/etoposide combination and topotecan have remained respectively the first and the second line standard treatments for the last 40 years. With the advent of immunotherapy, this scenario has finally changed. Our review aims to provide an overview of the primary studies on the actual therapeutic strategies available for ED-SCLC patients, and to highlight emerging evidence supporting the use of immunotherapy in SCLC patients.

Cytogenetic Findings in Primary Non-Small Cell Lung Cancer

1994 ◽  
Vol 80 (2) ◽  
pp. 151-156
Author(s):  
Elvira D'Alessandro ◽  
Maria Luisa Lo Re ◽  
Roberto Crisci ◽  
Claudio Ligas ◽  
Giorgio Furio Coloni
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Chromosome Loss ◽  
Small Cell Lung ◽  
Primary Nsclc ◽  
Cytogenetic Analyses ◽  
Triploid Clone

Non-small cell lung cancer (NSCLC) shows a complex cytogenetic heterogeneity and up to now no particular chromosomal aberration seems to characterize its malignant evolution. We therefore performed cytogenetic analyses of 20 primary NSCLC, 8 adenocarcinomas and 12 squamous cell carcinomas on direct preparations or short-term cultures. Only 1 case was analyzed after long-term culture. Results were obtained from 11 samples and clonal rearrangements were found in 3 cases, a diploid and a near-triploid clone with several aberrations such as i (9q), rob (14; 15) and rob (21; 21) in 1 case, a near-triploid clone in 1 case, and Y chromosome loss in 1 case. Other aberrations found were sporadic, but + 7 aneuploidy and translocations involving 1p were detected in 2 and 3 samples respectively. Although to date it has been very difficult to recognize primary changes in NSCLC, nevertheless a literature review and our results indicate that i(9q) and robertsonian translocations are relevant findings.

Predictive Factors for Interstitial Lung Disease, Antitumor Response, and Survival in Non–Small-Cell Lung Cancer Patients Treated With Gefitinib

2006 ◽  
Vol 24 (16) ◽  
pp. 2549-2556 ◽  
Author(s):  
Masahiko Ando ◽  
Isamu Okamoto ◽  
Nobuyuki Yamamoto ◽  
Koji Takeda ◽  
Kenji Tamura ◽  
...  
Keyword(s):  
Risk Factors ◽  
Lung Cancer ◽  
Adverse Effect ◽  
Interstitial Lung Disease ◽  
Small Cell Lung Cancer ◽  
Predictive Factors ◽  
Small Cell ◽  
Small Cell Lung ◽  
Antitumor Response ◽  
History Of

Purpose Interstitial lung disease (ILD) is a serious adverse effect of gefitinib, but its prevalence and risk factors remain largely unknown. We examined the prevalence of and risk factors for gefitinib-induced ILD associated with practical use of the drug in Japanese with non–small-cell lung cancer (NSCLC). Patients and Methods Clinical information was retrospectively assembled for NSCLC patients who started gefitinib treatment at affiliated institutions of the West Japan Thoracic Oncology Group between August 31 and December 31, 2002. Medical records of patients who developed pulmonary infiltrates were reviewed by a central committee of extramural experts for identification of patients with gefitinib-induced ILD. Multivariate logistic or Cox regression analysis was performed to identify independent predictive factors for ILD, antitumor response, and survival. Results Seventy cases of and 31 deaths from gefitinib-induced ILD were identified among 1,976 consecutively treated patients at 84 institutions, corresponding to a prevalence of 3.5% and mortality of 1.6%. Gefitinib-induced ILD was significantly associated with male sex, a history of smoking, and coincidence of interstitial pneumonia (odds ratios = 3.10, 4.79, and 2.89, respectively). Predictive factors for response were female sex, no history of smoking, adenocarcinoma histology, metastatic disease, and good performance status (PS), whereas predictive factors for survival were female sex, no history of smoking, adenocarcinoma histology, nonmetastatic disease, good PS, and previous chest surgery. Conclusion ILD is a serious adverse effect of gefitinib in the clinical setting that cannot be ignored. However, patient selection based on sex and smoking history can minimize ILD risk and maximize the clinical benefit of gefitinib.

scholarly journals miR-196b-5p–mediated downregulation of TSPAN12 and GATA6 promotes tumor progression in non-small cell lung cancer

2020 ◽  
Vol 117 (8) ◽  
pp. 4347-4357 ◽  
Author(s):  
Guang Liang ◽  
Wei Meng ◽  
Xiangjie Huang ◽  
Wangyu Zhu ◽  
Changtian Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Rna Binding ◽  
Nsclc Patient ◽  
Small Cell ◽  
Small Cell Lung ◽  
Tissue Samples ◽  
Underlying Mechanisms

Lung cancer is the leading cause of cancer-related deaths worldwide and non-small cell lung cancer (NSCLC) accounts for over 80% of lung cancer cases. The RNA binding protein, QKI, belongs to the STAR family and plays tumor-suppressive functions in NSCLC. QKI-5 is a major isoform of QKIs and is predominantly expressed in NSCLC. However, the underlying mechanisms of QKI-5 in NSCLC progression remain unclear. We found that QKI-5 regulated microRNA (miRNA), miR-196b-5p, and its expression was significantly up-regulated in NSCLC tissues. Up-regulated miR-196b-5p promotes lung cancer cell migration, proliferation, and cell cycle through directly targeting the tumor suppressors, GATA6 and TSPAN12. Both GATA6 and TSPAN12 expressions were down-regulated in NSCLC patient tissue samples and were negatively correlated with miR-196b-5p expression. Mouse xenograft models demonstrated that miR-196b-5p functions as a potent onco-miRNA, whereas TSPAN12 functions as a tumor suppressor in NSCLC in vivo. QKI-5 bound to miR-196b-5p and influenced its stability, resulting in up-regulated miR-196b-5p expression in NSCLC. Further analysis showed that hypomethylation in the promoter region enhanced miR-196b-5p expression in NSCLC. Our findings indicate that QKI-5 may exhibit novel anticancer mechanisms by regulating miRNA in NSCLC, and targeting the QKI5∼miR-196b-5p∼GATA6/TSPAN12 pathway may enable effectively treating some NSCLCs.

scholarly journals Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets

2019 ◽  
Vol 20 (3) ◽  
pp. 593 ◽  
Author(s):  
Beatriz Ballester ◽  
Javier Milara ◽  
Julio Cortijo
Keyword(s):  
Lung Cancer ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Current Knowledge ◽  
Molecular Targets ◽  
Small Cell ◽  
Small Cell Lung ◽  
Mesenchymal Transition ◽  
Cellular Processes ◽  
History Of

Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial pulmonary disease with a median survival of 2–4 years after diagnosis. A significant number of IPF patients have risk factors, such as a history of smoking or concomitant emphysema, both of which can predispose the patient to lung cancer (LC) (mostly non-small cell lung cancer (NSCLC)). In fact, IPF itself increases the risk of LC development by 7% to 20%. In this regard, there are multiple common genetic, molecular, and cellular processes that connect lung fibrosis with LC, such as myofibroblast/mesenchymal transition, myofibroblast activation and uncontrolled proliferation, endoplasmic reticulum stress, alterations of growth factors expression, oxidative stress, and large genetic and epigenetic variations that can predispose the patient to develop IPF and LC. The current approved IPF therapies, pirfenidone and nintedanib, are also active in LC. In fact, nintedanib is approved as a second line treatment in NSCLC, and pirfenidone has shown anti-neoplastic effects in preclinical studies. In this review, we focus on the current knowledge on the mechanisms implicated in the development of LC in patients with IPF as well as in current IPF and LC-IPF candidate therapies based on novel molecular advances.

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