scholarly journals P1.06-012 Non-Small Cell Lung Cancer (NSCLC) Patient Characteristics and Clinical Care Insights in Sweden: The SCAN-LEAF Study

2017 ◽  
Vol 12 (11) ◽  
pp. S1990 ◽  
Author(s):  
M. Sandelin ◽  
M. Planck ◽  
J.B. Sørensen ◽  
O.T. Brustugun ◽  
J. Rockberg ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Clinical Care ◽  
Nsclc Patient ◽  
Patient Characteristics ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Possible involvement of the Hedgehog and PDPK1–Akt pathways in the growth and migration of small-cell lung cancer

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110165
Author(s):  
Naiwang Tang ◽  
Bin Hu ◽  
Yin Zhang ◽  
Zhiwei Chen ◽  
Ronghuan Yu
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Molecular Mechanisms ◽  
Patient Characteristics ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancers ◽  
And Migration ◽  
Proliferation And Migration

Background Small-cell lung cancer (SCLC) accounts for approximately 15% to 20% of all lung cancers, and it is the leading cause of tumor-related deaths globally. This study explored the molecular mechanisms underlying the development of SCLC. Methods The correlations of phosphoinositide-dependent kinase-1 (PDPK1), p-Akt, and Hedgehog expression with patient characteristics were analyzed using SCLC specimens, and their expression was measured in BEAS-2B cells (control) and the SCLC cell lines H82, H69, H446, H146, and H526. Transfection experiments were performed to inhibit or activate gene expression in cells. We then measured the proliferation and migration of H146 cells. Results PDPK1, p-Akt, and Hedgehog expression was significantly higher in SCLC tissues, and their expression was correlated with patient characteristics. p-Akt expression was significantly correlated with Hedgehog expression. In H146 cells, PDPK1 and p-Akt were significantly upregulated. Silencing of PDPK1 or Akt and inhibition of Hedgehog significantly inhibited the proliferation and migration of H146 cells. PDPK1 and Akt affected Hedgehog expression, but Hedgehog did not affect PDPK1 or p-Akt expression. Conclusions The interaction between the PDPK1–Akt pathway and the Hedgehog pathway influences the prognosis, growth, and migration of SCLC.

scholarly journals STAT3: Versatile Functions in Non-Small Cell Lung Cancer

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1107 ◽  
Author(s):  
Julian Mohrherr ◽  
Iris Z. Uras ◽  
Herwig P. Moll ◽  
Emilio Casanova
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Nsclc Patient ◽  
Small Cell ◽  
Janus Kinase ◽  
Small Cell Lung ◽  
Solid Malignancies ◽  
Janus Kinase 1

Signal Transducer and Activator of Transcription 3 (STAT3) activation is frequently found in non-small cell lung cancer (NSCLC) patient samples/cell lines and STAT3 inhibition in NSCLC cell lines markedly impairs their survival. STAT3 also plays a pivotal role in driving tumor-promoting inflammation and evasion of anti-tumor immunity. Consequently, targeting STAT3 either directly or by inhibition of upstream regulators such as Interleukin-6 (IL-6) or Janus kinase 1/2 (JAK1/2) is considered as a promising treatment strategy for the management of NSCLC. In contrast, some studies also report STAT3 being a tumor suppressor in a variety of solid malignancies, including lung cancer. Here, we provide a concise overview of STAT3‘s versatile roles in NSCLC and discuss the yins and yangs of STAT3 targeting therapies.

scholarly journals Profile of alectinib for the treatment of ALK-positive non-small cell lung cancer (NSCLC): patient selection and perspectives

2019 ◽  
Vol Volume 12 ◽  
pp. 4567-4575 ◽  
Author(s):  
Niki Karachaliou ◽  
Manuel Fernandez Bruno ◽  
Jillian Wilhelmina Paulina Bracht ◽  
Rafael Rosell
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Patient Selection ◽  
Cell Lung Cancer ◽  
Nsclc Patient ◽  
Small Cell ◽  
Small Cell Lung ◽  
Alk Positive

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 RB1 loss induced small cell lung cancer transformation as acquired resistance to pembrolizumab in an advanced NSCLC patient

Lung Cancer ◽  
2021 ◽  
Vol 151 ◽  
pp. 101-103
Author(s):  
Sayaka Arakawa ◽  
Tatsuya Yoshida ◽  
Masayuki Shirasawa ◽  
Daisuke Takayanagi ◽  
Shigehiro Yagishita ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Advanced Nsclc ◽  
Nsclc Patient ◽  
Acquired Resistance ◽  
Small Cell ◽  
Small Cell Lung ◽  
Advanced Nsclc Patient

Clinical significance of the EML4-ALK fusion gene and association with EGFR and KRASgene mutation in 208 Chinese patients with non-small cell lung cancer.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e17514-e17514 ◽  
Author(s):  
JUN Chen ◽  
Hongyu Liu ◽  
Tong Yang ◽  
Sen Wei ◽  
Qinghua Zhou
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Fusion Gene ◽  
Nsclc Patient ◽  
Small Cell ◽  
Chinese Patients ◽  
Small Cell Lung ◽  
Kras Mutations ◽  
Female Patients

e17514 Background: EML4-ALK fusion gene is a potentially relevant oncogenic event in lung cancer, which represents a new subgroup of non-small cell lung cancer (NSCLC) patients who respond positively to ALK inhibitors. The characteristics of EML4-ALK fusion gene in Chinese Patients with NSCLC are poorly understood. In this study, we aimed to analyze the prevalence of EML4-ALK fusion gene and their correlation to epidermal growth factor receptor (EGFR) status, KRAS mutation, and clinico-pathological data in Chinese patients with NSCLC. Methods: Genes were detected by nested RT-PCR and confirmed by sequencing. Results: 208 cases of NSCLC were evaluated. There were 24.5% (51/208 cases of mutations in EGFR at exons 18-21, and EGFR mutations occur predominantly (92%) in exons 19 and 21. In concordance with previous reports, these mutations are identified at high frequencies in females (47.5%, 29/61 vs 15.0%, 22/147 in males; P = 0.000); never-smokers (42.3%, 33/78 vs 13.9%, 18/130 in smokers; P = 0.000), and adenocarcinoma patients (44.2%, 42/95 vs 8.0%, 9/113 in non-adenocarcinoma patients; P = 0.000). There were only 6 cases (6/208, 2.88%) of KRAS mutations in our study group. We identified 7 patients who harbored the EML4-ALK fusion gene (3.37%, 7/208) which all confirmed by DNA sequencing. Of these 7 patients, 2 cases displayed the EML4-ALK variant 1 (28.6%), 1 case exhibited variant 2 (14.3%) and 4 cases carried variant 3 (57.1%). All of the positive cases corresponded to female patients (11.5%, 7/61). Six of the positive cases were non-smokers (7.69%, 6/78). The incidence of EML4-ALK translocation in female non-smoking adenocarcinoma patients is as high as 15.2% (5/33). No EGFR/KRAS mutations were detected among EML4-ALK positive patients. The meta-analysis demonstrated that EML4-ALK translocation was 4.71% (125/2652) in unselected patients with NSCLC, and was also predominant in female patients with adenocarcinoma. Conclusions: EML4-ALK translocations are infrequent in the entire NSCLC patient population, but are frequent in the NSCLC patient subgroup of female, nonsmokers, and adenocarcinoma patients.

Sign in / Sign up

Export Citation Format

Share Document