scholarly journals Acute Abdomen: A Rare Presentation of Lung Cancer Metastasis

2009 ◽  
Vol 2009 ◽  
pp. 1-3
Author(s):  
E. Guérin ◽  
O. Gilbert ◽  
D. Dequanter
Keyword(s):  
Lung Cancer ◽  
Gastric Ulcer ◽  
Cell Carcinoma ◽  
Acute Abdomen ◽  
Cancer Metastasis ◽  
Small Cell ◽  
Current Management ◽  
Rare Presentation ◽  
Lung Cancer Metastasis ◽  
Surgical Emergencies

Surgical emergencies caused by bowel metastases from carcinoma of the lung are very rare. We describe two cases of symptomatic gastrointestinal metastatic small cell carcinoma: the first one concerns a 69-year-old man with an acute abdomen and the second is a 72-year-old man complaining of a gastric ulcer symptoms. We also discuss the current management and the prognosis of these patients.

A Case and Review of Bowel Perforation Secondary to Metastatic Lung Cancer

2005 ◽  
Vol 71 (2) ◽  
pp. 110-116 ◽  
Author(s):  
Robert A. Garwood ◽  
Mark D. Sawyer ◽  
E.J. Ledesma ◽  
Eugene Foley ◽  
Jeffrey A. Claridge
Keyword(s):  
Lung Cancer ◽  
Small Bowel ◽  
Cell Carcinoma ◽  
Cancer Metastasis ◽  
Bowel Perforation ◽  
Large Cell Carcinoma ◽  
Metastatic Lung Cancer ◽  
Small Bowel Perforation ◽  
Lung Cancer Metastasis ◽  
Metastatic Lung

Gastrointestinal tract perforation (GITP) secondary to metastatic lung cancer is extremely rare. We present a case of small bowel perforation secondary to metastatic lung cancer. The objective of this study was to review the current literature and further characterize the incidence, histology, and risk of GITP secondary to lung cancer metastasis. A Medline search was done to identify all the cases of GITP attributed to metastatic lung cancer reported in the literature. Data was collected and analyzed from a collection of cases in the medical literature since 1960. We identified 98 cases of perforated lung cancer metastasis to the small intestine. Four gastric perforations, three colonic perforations, and one appendiceal perforation were also identified but not analyzed. The mean age was 64.5 years. There was a male predominance of 89 per cent versus 11 per cent female. Perforations occurred most often in the jejunum (53%) followed by ileum (28%). Combined jejunum-ileum lesions accounted for 4 per cent of perforations. No duodenal perforations were reported, though a specific site was not determined in 13 per cent of cases. Small bowel perforations were most often caused by adenocarcinoma (23.7%), squamous cell carcinoma (22.7%), large cell carcinoma (20.6%), and small cell carcinoma (19.6%). The prevalence of small bowel perforation secondary to a given primary lung cancer histology varied by region. The mean survival was 66 days with 50 per cent of patients not surviving past 30 days. Despite a high incidence of lung cancer, small bowel perforation secondary to lung cancer metastasis remains relatively rare. Perforated metastases occur more often in men and are found more commonly in the jejunum. Small bowel perforations are caused most often by adenocarcinoma; however, squamous cell and large cell carcinoma metastases are more likely to result in perforation. Small bowel perforation in this setting has a significant impact on mortality, decreasing 1-year survival to less than 3 per cent.

Nm23-H1 inhibits hypoxia induced epithelial-mesenchymal transition and stemness in non-small cell lung cancer cells

2019 ◽  
Vol 400 (6) ◽  
pp. 765-776 ◽  
Author(s):  
Cun-en Wu ◽  
Yu-wen Zhuang ◽  
Jin-yong Zhou ◽  
Shen-lin Liu ◽  
Xi Zou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Small Cell ◽  
Small Cell Lung ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis ◽  
Allelic Deletion

Abstract The Nm23 gene has been acknowledged to play a crucial role in lung cancer metastasis inhibitory cascades controlled by multiple factors. Low expression or allelic deletion of nm23-H1 is strongly linked to widespread metastasis and poor differentiation of non-small cell lung cancer (NSCLC). In this study, nm23-H1 was down regulated in epithelial-mesenchymal transition (EMT) and stemness enhancement under cobalt chloride (CoCl2)-induced hypoxia in NSCLC cells. Moreover, knocking down of nm23-H1 by shRNA apparently promoted hypoxia induced EMT and stemness, which was entirely suppressed via over expression of nm23-H1. Mechanistically, the Wnt/β-catenin signaling pathway was found to participate in the nm23-H1-mediated process. Besides, XAV939 prohibited cell EMT and stemness which could be impaired by knocking down of nm23-H1, while stable transfection of nm23-H1 attenuated hypoxia phonotype induced by lithium chloride (LiCl). Generally, our experiment provided evidence that nm23-H1 can reverse hypoxia induced EMT and stemness through the inhibition of the Wnt/β-catenin pathway, which may furnish a deeper perspective into the better treatment or prognosis for NSCLC.

scholarly journals miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Tangwei Wu ◽  
Hui Hu ◽  
Tianzhu Zhang ◽  
Liyuan Jiang ◽  
Xiaoyi Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cancer Metastasis ◽  
Small Cell ◽  
Nsclc Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Lung Cancer Metastasis ◽  
Nsclc Patients

Metastasis is the leading cause of high mortality in lung cancer patients, and metastatic lung cancer is difficult to treat. miRNAs are involved in various biological processes of cancer, including metastasis. Our previous studies revealed that miR-25 promoted non-small-cell lung cancer (NSCLC) cell proliferation and suppressed cell apoptosis by directly targeting TP53 and MOAP1. In this work, we further explored the miR-25 expression in NSCLC patients in the Cancer Genome Atlas (TCGA) database and measured the miR-25 expression levels in the tissues of NSCLC patients and cell lines. miR-25 was overexpressed in both NSCLC tissues and cell lines. NSCLC patients who expressed a higher level of miR-25 exhibited worse overall survival than those with a lower level of miR-25. Overexpression of miR-25 enhanced NSCLC cell migration and invasion, while the inhibition of miR-25 exhibited the opposite effects. We identified the large tumor suppressor homology 2 (LATS2) as a new target gene of miR-25 in lung cancer. The effects of miR-25 on promoting NSCLC cell migration and invasion were at least partially due to activation of the Hippo signaling pathway. Additionally, miR-25 antagomir inhibited xenograft tumor growth and metastasis by the upregulation of LATS2. Taken together, our findings demonstrate that miR-25 contribute to lung cancer cell proliferation and metastasis by targeting the LATS2/YAP signaling pathway, which implicate miR-25 as a promising therapeutic target for lung cancer metastasis. Given that oxidative stress induces the overexpression of miR-25 and plays a critical role in cancer progression, this study establishes miR-25 as an intermediate between oxidative stress and lung cancer metastasis.

scholarly journals Cyclophilin A promotes non-small cell lung cancer metastasis via p38 MAPK

2017 ◽  
Vol 9 (1) ◽  
pp. 120-128 ◽  
Author(s):  
Yinan Guo ◽  
Mei Jiang ◽  
Xiaoting Zhao ◽  
Meng Gu ◽  
Ziyu Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
P38 Mapk ◽  
Cell Lung Cancer ◽  
Cancer Metastasis ◽  
Cyclophilin A ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancer Metastasis

scholarly journals Integrin αvβ5 as a biomarker for the assessment of non‐small cell lung cancer metastasis and overall survival

2014 ◽  
Vol 9 (4) ◽  
pp. 457-467 ◽  
Author(s):  
Sally Yan Bai ◽  
Nuo Xu ◽  
Cuicui Chen ◽  
Yuan‐lin Song ◽  
Jie Hu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cancer Metastasis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancer Metastasis
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