ROS1-rearranged lung adenocarcinoma with peritoneal carcinomatosis on initial presentation

2020 ◽  
Vol 13 (3) ◽  
pp. e233864
Author(s):  
Vera Kazakova ◽  
Sylvia V Alarcon Velasco ◽  
Aleksandr Perepletchikov ◽  
Christopher S Lathan
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Peritoneal Carcinomatosis ◽  
Poor Prognosis ◽  
Primary Tumour ◽  
Small Cell ◽  
Small Cell Lung ◽  
Peritoneal Spread ◽  
New Onset

Peritoneal carcinomatosis (PC) is progression of the primary cancer to the peritoneum that is seen in only 1.2% of patients with lung cancer. It is associated with poor prognosis especially if present at the time of initial cancer diagnosis. The predisposing factors for peritoneal spread are not yet well understood. It has been suggested that the oncogene status of the tumour can influence the patterns of metastatic spread. There is not enough data about the role of c-ROS oncogene 1 (ROS1) mutation in the development of PC in non-small cell lung cancer. Here, we describe a case of a 56-year-old man who presented with new-onset ascites and was found to have PC. He was diagnosed with ROS1-rearranged lung adenocarcinoma. No obvious primary tumour was identified. Patient responded well to targeted therapy with crizotinib and remained 6 months free of disease progression.

scholarly journals Cell division cycle 20 overexpression predicts poor prognosis for patients with lung adenocarcinoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769223 ◽  
Author(s):  
Run Shi ◽  
Qi Sun ◽  
Jing Sun ◽  
Xin Wang ◽  
Wenjie Xia ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Division ◽  
Lung Adenocarcinoma ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Size ◽  
Poor Prognosis ◽  
Small Cell ◽  
Cell Division Cycle ◽  
Small Cell Lung

The cell division cycle 20, a key component of spindle assembly checkpoint, is an essential activator of the anaphase-promoting complex. Aberrant expression of cell division cycle 20 has been detected in various human cancers. However, its clinical significance has never been deeply investigated in non-small-cell lung cancer. By analyzing The Cancer Genome Atlas database and using some certain online databases, we validated overexpression of cell division cycle 20 in both messenger RNA and protein levels, explored its clinical significance, and evaluated the prognostic role of cell division cycle 20 in non-small-cell lung cancer. Cell division cycle 20 expression was significantly correlated with sex (p = 0.003), histological classification (p < 0.0001), and tumor size (p = 0.0116) in non-small-cell lung cancer patients. In lung adenocarcinoma patients, overexpression of cell division cycle 20 was significantly associated with bigger primary tumor size (p = 0.0023), higher MKI67 level (r = 0.7618, p < 0.0001), higher DNA ploidy level (p < 0.0001), and poor prognosis (hazard ratio = 2.39, confidence interval: 1.87–3.05, p < 0.0001). However, in lung squamous cell carcinoma patients, no significant association of cell division cycle 20 expression was observed with any clinical parameter or prognosis. Overexpression of cell division cycle 20 is associated with poor prognosis in lung adenocarcinoma patients, and its overexpression can also be used to identify high-risk groups. In conclusion, cell division cycle 20 might serve as a potential biomarker for lung adenocarcinoma patients.

scholarly journals High expression of Aurora-B is correlated with poor prognosis and drug resistance in non-small cell lung cancer

2018 ◽  
Vol 33 (2) ◽  
pp. 215-221 ◽  
Author(s):  
JingJing Yu ◽  
Jing Zhou ◽  
Fei Xu ◽  
Wei Bai ◽  
Wei Zhang
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Small Cell Lung Cancer ◽  
Poor Prognosis ◽  
Drug Response ◽  
Small Cell ◽  
Aurora B ◽  
Small Cell Lung ◽  
Nsclc Patients

Objective: Aurora kinase B (Aurora-B) is a crucial regulator of accurate mitosis. Abnormal Aurora-B expression is associated with aneuploidy and has been implicated in the pathogenesis and drug resistance in a variety of human cancers. However, little evidence is available regarding the role of Aurora-B in regulating drug response in non-small cell lung cancer (NSCLC), which is the most common type of lung cancer, and is characterized with poor prognosis and high mortality. Method: In the current study, we investigated the association of Aurora-B with the prognosis of NSCLC patients, and we also used the latest CRISPR/Cas9 system to explore the regulatory role of Aurora-B in NSCLC cells developing resistance to cisplatin (CDDP) and paclitaxel. Results: We found that Aurora-B was correlated with significantly reduced overall survival and disease-free survival in NSCLC patients. Aurora-B overexpression was also observed in NSCLC cells developing impaired response to both CDDP and paclitaxel. Moreover, we found, for the first time, that Aurora-B may impair NSCLC drug response by disturbing cell proliferation and inhibiting p53-related DNA damage response and apoptotic pathway, while the knockout of Aurora-B resensitized NSCLC cells to chemo drugs by ensuring correct chromosome segregation and restoring p53 expression. Conclusions: Our results demonstrated the association of Aurora-B with chemoresistance in NSCLC, which may finally contribute to the poor prognosis of NSCLC patients. We also suggested Aurora-B as a promising therapeutic target in NSCLC treatment.

scholarly journals Increased KIF15 Expression Predicts a Poor Prognosis in Patients with Lung Adenocarcinoma

2018 ◽  
Vol 51 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Yuan Qiao ◽  
Jingtao Chen ◽  
Chao Ma ◽  
Yingmin Liu ◽  
Peitong Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Lung Adenocarcinoma ◽  
Small Cell Lung Cancer ◽  
Messenger Rna ◽  
Poor Prognosis ◽  
Human Lung ◽  
Small Cell ◽  
Small Cell Lung ◽  
Protein Levels

Background/Aims: Lung cancer is the leading cause of cancer-related deaths worldwide. The outcome of patients with non-small cell lung cancer remains poor; the 5-year survival rate for stage IV non-small cell lung cancer is only 1.0%. KIF15 is a tetrameric kinesin spindle motor that has been investigated for its regulation of mitosis. While the roles of kinesin motor proteins in the regulation of mitosis and their potentials as therapeutic targets in pancreatic cancer have been described previously, the role of KIF15 in lung cancer development remains unknown. Methods: Paired lung carcinoma specimens and matched adjacent normal tissues were used for protein analysis. Clinical data were obtained from medical records. We first examined KIF15 messenger RNA expression in The Cancer Genome Atlas database, and then determined KIF15 protein levels using immunohistochemistry and western blotting. Differences between the groups were analyzed using repeated measures analysis of variance. Overall survival was analyzed using the Kaplan–Meier method. Cell-cycle and proliferation assays were conducted using A549, NCI-H1299, and NCI-H226 cells. Results: KIF15 was significantly upregulated at both the messenger RNA and protein levels in human lung tumor tissues. In patients with lung adenocarcinoma, KIF15 expression was positively associated with disease stages; high KIF15 expression predicted a poor prognosis. KIF15 knockdown using short hairpin RNA in two human lung adenocarcinoma cell lines induced G1/S phase cell cycle arrest and inhibited cell growth, but there was no effect in human lung squamous cell carcinoma. Conclusion: Our findings show that KIF15 is involved in lung cancer carcinogenesis. KIF15 could therefore serve as a specific prognostic marker for patients with lung adenocarcinoma.

scholarly journals MiR-27a-3p Promotes Non-Small Cell Lung Cancer Through SLC7A11-Mediated-Ferroptosis

2021 ◽  
Vol 11 ◽  
Author(s):  
Xuan Lu ◽  
Ningning Kang ◽  
Xinxin Ling ◽  
Ming Pan ◽  
Wenjing Du ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Small Cell ◽  
Small Cell Lung ◽  
Adenocarcinoma Cell ◽  
Qrt Pcr ◽  
Nsclc Patients

BackgroundFerroptosis is a newly generated regulatory cell death promoted by the accumulated lipid-based reactive oxygen species (ROS). Solute carrier family 7 member 11 (SLC7A11), the cystine/glutamate antiporter, is known as a ferroptosis executor that exhibits a positive correlation with carcinoma progression because of antioxidant function. Nonetheless, it is yet unclear on the understanding of ferroptosis regulation in lung cancer.MethodsDatabase, qRT-PCR, Western-blot (WB), and immunohistochemistry were utilized to determine SLC7A11 expression and function, as well as gene iron related to necrosis in clinical tissue specimens and cells; a ferroptosis inducer, inhibitors, and SLC7A11 lentivirus were used to confirm SLC7A11’s biological activity in cell viability, oxidative stress, lipid peroxidation, and iron ion enrichment in non-small cell lung cancer (NSCLC) in different cells; lentivirus was used to infect lung adenocarcinoma cell lines to acquire miR-27a-3p overexpression and knockdown cell lines, and to detect SLC7A11 level through qRT-PCR and WB. The influence of upregulated/downregulated miR-27a-3p on ferroptosis and other related biological characteristics of lung adenocarcinoma cell lines was detected.ResultsUpregulated SLC7A11 was shown in NSCLC patients and cells, and increased SLC7A11 had a relation to the poorly prognostic status of NSCLC patients. Besides, a novel miRNA, miR-27a-3p, was an essential modulator of ferroptosis via directly targeting SLC7A11 in NSCLC cells. Overexpressing miR-27a-3p led to SLC7A11 suppression via directly binding to its 3’-UTR, followed by the reduction of erastin-caused ferroptosis. In contrast, inhibited miR-27a-3p resulted in an increase in NSCLC cells’ sensitivity to erastin. Of importance, the accumulated lipid ROS and cell death of iron peptide mediated by anti-miR-27a-3p can be eliminated by impeding the glutamylation process. Our literature collectively uncovered that miR-27a-3p modulated ferroptosis by targeting SLC7A11 in NSCLC cells, illustrating the important role of miRNA in ferroptosis.ConclusionMiR-27a-3p modulates ferroptosis via targeting SLC7A11 in NSCLC cells, implying the significant role of miR-27a-3p/SLC7A11 in ferroptosis.

scholarly journals Screening prognostic markers for non-small cell lung cancer based on data mining and bioinformatics analysis

2020 ◽  
Author(s):  
Bin Han ◽  
Kaushik Chandra Aman ◽  
Dongqing Wei ◽  
Shulin Zhang ◽  
Minjie Meng
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Small Cell Lung Cancer ◽  
Differentially Expressed Genes ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Prognostic Markers ◽  
Small Cell ◽  
Differentially Expressed ◽  
Small Cell Lung

Abstract Background At present, non-small cell lung cancer has a high morbidity and mortality, and the recurrence and metastasis situation is serious. It is impossible to accurately predict the prognosis of cancer patients clinically. Biomarker is a kind of biomolecule with wide application prospects, and its potential in cancer prognosis is gradually revealed, and it is expected to be applied clinically. Results We integrated four gene expression profiles (GSE19188, GSE19804, GSE101929 and GSE18842) from the GEO database and screened the commonly differentially expressed genes using the GEO2R online tool. We screened 952 commonly differentially expressed genes. Gene ontology analysis showed that CDEGs were mainly enriched in biological processes such as cell adherin, angiogenesis and positive regulation of angiogenesis, and KEGG pathways such as ECM-receptor interaction and cell adherin molecules (CAMs). Up-regulation of G2 and S phase-expressed protein 1(GTSE1) expression is associated with poor prognosis of lung adenocarcinoma(LADE) and lung squamous cell carcinoma(LUSC). Up-regulation of Neuromedin-U(NMU) expression, down-regulation of Proto-oncogene c-Fos(FOS) and Cyclin-dependent kinase inhibitor 1C(CDKN1C) is only associated with poor prognosis of LADE. Conclusions We believe that GTSE1, NMU, FOS, and CDKN1C have potential application value as prognostic markers for lung adenocarcinoma, and are of great significance for lung adeno carcinoma efficacy evaluation and relapse monitoring. At the same time, GTSE1 may also be used as a new target for cancer treatment New ways.

LIFE SPAN PREDICTION AT METASTATIC NON-SMALL CELL LUNG CANCER

2018 ◽  
Vol 64 (4) ◽  
pp. 522-527
Author(s):  
Aleksey Shutko ◽  
Viktor Mus
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Small Cell Lung Cancer ◽  
Life Span ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Hemopoietic Stem Cells ◽  
Small Cell Lung ◽  
Individual Life

Individual parameters of circulating hemopoietic stem cells (HSC) lymphoid origin were measured by cytofluorometry before treatment of patients with metastatic non-small cell lung cancer and were retrospectively compared with individual life span's (LS). The possibility of poor prognosis of treatment's results (LS

Do we Need Maintenance Chemotherapy in Advanced NSCLC in the Era of Immune and Targeted Therapy?

2019 ◽  
Vol 15 (1) ◽  
pp. 50-55
Author(s):  
Ahmed Nagy ◽  
Omar Abdel Rahman ◽  
Heba Abdullah ◽  
Ahmed Negida
Keyword(s):  
Lung Cancer ◽  
Maintenance Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Statistical Significance ◽  
Small Cell ◽  
Maintenance Chemotherapy ◽  
Small Cell Lung ◽  
The Impact

Background: Although well established for the effective management of hematologic cancers, maintenance chemotherapy has only been recently incorportated as a treatment paradigm for advanced non–small-cell lung cancer. Maintenance chemotherapy aims to prolong a clinically favorable response state achieved after finishing induction therapy which is usually predefined in number before startng treatment. There are 2 modalities for maintenance therapy; continuation maintenance (involving a non-platinum component which was a part of the induction protocol or a targeted agent) and switch maintenance therapy (utilizing a new agent which was not a part of the induction regimen). Methods: The purpose of this article is to review the role of maintenance therapy in the treatment of advanced Non-Small Cell Lung Cancer (NSCLC) and provide a brief overview about induction chemotherapy in NSCLC to address the basis of maintenance therapy as a treatment option. We will also compare the impact of maintenance chemotherapy with the now evolving role of immunotherapy in NSCLC. Results: There have been 4 maintenance studies to date showing prolonged PFS and OS with statistical significance. However, Three out of the four studies (ECOG4599, JMEN, and PARAMOUNT) did not report tumor molecular analysis. As regard Immunotherapy, current data is in favour of strongly an increasing role for immunotherapy in NSCLC. Conclusion: Maintenance therapy in NSCLC continues to be an important therapeutic line to improve outcome in patients with metastatic and recurrent disease.

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