BRAF-mutant non-small cell lung cancer (NSCLC): Patient (pt) characteristics and outcomes by class of mutation.

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.

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P1.01-20 The Association Between BRAF Mutation Class and Clinical Features in BRAF-Mutant Chinese Non-Small Cell Lung Cancer Patients

Journal of Thoracic Oncology ◽

10.1016/j.jtho.2019.08.735 ◽

2019 ◽

Vol 14 (10) ◽

pp. S363

Author(s):

Q. Lin ◽

H. Zhu ◽

Y. Li ◽

H. Zhang ◽

H. Ding ◽

...

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cancer Patients ◽

Clinical Features ◽

Cell Lung Cancer ◽

Braf Mutation ◽

Small Cell ◽

Small Cell Lung ◽

Lung Cancer Patients ◽

Braf Mutant

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

OncoTargets and Therapy ◽

10.2147/ott.s174548 ◽

2019 ◽

Vol Volume 12 ◽

pp. 4567-4575 ◽

Cited By ~ 1

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

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LBA59 First-line nivolumab (NIVO) + ipilimumab (IPI) combined with 2 cycles of platinum-based chemotherapy (chemo) vs 4 cycles of chemo in advanced non-small cell lung cancer (NSCLC): Patient-reported outcomes (PROs) from CheckMate 9LA

Annals of Oncology ◽

10.1016/j.annonc.2020.08.2292 ◽

2020 ◽

Vol 31 ◽

pp. S1187-S1188

Author(s):

M. Reck ◽

T-E. Ciuleanu ◽

M. Cobo ◽

M. Schenker ◽

B. Zurawski ◽

...

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Patient Reported Outcomes ◽

Nsclc Patient ◽

Small Cell ◽

Small Cell Lung ◽

First Line ◽

Platinum Based Chemotherapy ◽

Patient Reported

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

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1917531117 ◽

2020 ◽

Vol 117 (8) ◽

pp. 4347-4357 ◽

Cited By ~ 9

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.

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

Lung Cancer ◽

10.1016/j.lungcan.2020.11.016 ◽

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

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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.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.15_suppl.e17514 ◽

2012 ◽

Vol 30 (15_suppl) ◽

pp. e17514-e17514 ◽

Cited By ~ 1

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.

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