Decreased Expression of Decorin and p57(KIP2) Correlates with Poor Survival and Lymphatic Metastasis in Lung Cancer Patients

2011 ◽  
Vol 26 (1) ◽  
pp. 9-21 ◽  
Author(s):  
Rong Biaoxue ◽  
Cai Xiguang ◽  
Liu Hua ◽  
Ma Hui ◽  
Yang Shuanying ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Lymphatic Metastasis ◽  
Expression Level ◽  
Normal Lung ◽  
Tgf Beta ◽  
Expression Levels ◽  
Lung Cancer Patients ◽  
Normal Tissues ◽  
Tumor Tissues

Purpose Decorin, p57(KIP2), and TGF-beta 1 have been investigated as prognostic factors because they appear to be associated with tumorigenesis; however, the effect of decorin and p57(KIP2) in lung cancer remains poorly understood. The purpose of this study was to examine the expression of decorin, p57(KIP2), and TGF-beta 1 in 64 lung cancer specimens and 36 normal lung specimens, and to analyze the relationships with respect to clinicopathological features and patient survival in lung cancer. Methods The expression levels of decorin, p57(KIP2), and TGF-beta 1 were examined by in situ hybridization and immunohistochemistry. Results Normal tissues exhibited a higher expression level of decorin than tumor tissues (P<0.05) and tumor tissues exhibited a higher expression level of TGF-beta 1 than normal tissues (P<0.05). The expression levels of p57(KIP2) and TGF-beta 1 were significantly associated with histological types of lung cancer (P<0.05), and the expression levels of decorin and p57(KIP2) were significantly associated with lymphatic invasion (P<0.05). Moreover, increased expression of decorin and p57(KIP2) correlated with increased survival (decorin, p=0.018; p57(KIP2), p=0.012). Conclusion Decreased expression levels of decorin and p57(KIP2) were associated with poor postsurgical survival time and lymphatic metastasis in lung cancer patients; moreover, low expression was an adverse prognostic factor.

scholarly journals Single-Cell Expression Landscape of SARS-CoV-2 Receptor ACE2 and Host Proteases in Normal and Malignant Lung Tissues from Pulmonary Adenocarcinoma Patients

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1250
Author(s):  
Guangchun Han ◽  
Ansam Sinjab ◽  
Kieko Hara ◽  
Warapen Treekitkarnmongkol ◽  
Patrick Brennan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Single Cell ◽  
Cancer Patients ◽  
Expression Profiles ◽  
Lung Cells ◽  
Alveolar Type ◽  
Specific Expression ◽  
Lung Cancer Patients ◽  
Normal Tissues ◽  
Cell Expression

The novel coronavirus SARS-CoV-2 is the causative agent of the COVID-19 pandemic. Severely symptomatic COVID-19 is associated with lung inflammation, pneumonia, and respiratory failure, thereby raising concerns of elevated risk of COVID-19-associated mortality among lung cancer patients. Angiotensin-converting enzyme 2 (ACE2) is the major receptor for SARS-CoV-2 entry into lung cells. The single-cell expression landscape of ACE2 and other SARS-CoV-2-related genes in pulmonary tissues of lung cancer patients remains unknown. We sought to delineate single-cell expression profiles of ACE2 and other SARS-CoV-2-related genes in pulmonary tissues of lung adenocarcinoma (LUAD) patients. We examined the expression levels and cellular distribution of ACE2 and SARS-CoV-2-priming proteases TMPRSS2 and TMPRSS4 in 5 LUADs and 14 matched normal tissues by single-cell RNA-sequencing (scRNA-seq) analysis. scRNA-seq of 186,916 cells revealed epithelial-specific expression of ACE2, TMPRSS2, and TMPRSS4. Analysis of 70,030 LUAD- and normal-derived epithelial cells showed that ACE2 levels were highest in normal alveolar type 2 (AT2) cells and that TMPRSS2 was expressed in 65% of normal AT2 cells. Conversely, the expression of TMPRSS4 was highest and most frequently detected (75%) in lung cells with malignant features. ACE2-positive cells co-expressed genes implicated in lung pathobiology, including COPD-associated HHIP, and the scavengers CD36 and DMBT1. Notably, the viral scavenger DMBT1 was significantly positively correlated with ACE2 expression in AT2 cells. We describe normal and tumor lung epithelial populations that express SARS-CoV-2 receptor and proteases, as well as major host defense genes, thus comprising potential treatment targets for COVID-19 particularly among lung cancer patients.

scholarly journals miRNA-486 and miRNA-499 in human plasma evaluate the clinical stages of lung cancer and play a role as a tumor suppressor in lung tumorigeneisis not pathogenesis

2016 ◽  
Vol 11 (1) ◽  
pp. 264 ◽  
Author(s):  
Youchao Jia ◽  
Aimin Zang ◽  
Yanguang Feng ◽  
Xiao-Fang Li ◽  
Ke Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Cell Lung Cancer ◽  
Statistical Significance ◽  
Small Cell ◽  
Expression Level ◽  
Control Group ◽  
Small Cell Lung ◽  
Lung Cancer Patients

<p class="Abstract">It was aimed to explore the expression level of miRNA-486 and miRNA-499 in the plasma of lung cancer patients and analysis their differences in expre-ssion. The expression level of both miRNA-486 and miRNA-499 in the plasma of non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) were lower than that of the control group (p&lt;0.05) and the decrease was more obvious in NSCLC. Compare with the miRNA-499，expression quantity in NSCLC patients plasma. There was statistical significance difference (p&lt;0.05) between III～Ⅳstage and I～II stage. The expression quantity of miRNA in plasma of patients with extensive-stage SCLC was lower than that of patients with limited-stage SCLC (p&lt;0.05). The sensitivity and specificity of plasms miRNA-486 respectively were 88.5% and 83.3%. The expression of miRNA-499 and miRNA-486 in lung cancer patients were up-regulated, and might be closely related to the occurrence and prognosis of lung cancer, and might be used as potential screening and prognosis index for lung cancer.</p><p> </p>

scholarly journals Characterization of Distinct T Cell Receptor Repertoires in Tumor and Distant Non-tumor Tissues from Lung Cancer Patients

2019 ◽  
Vol 17 (3) ◽  
pp. 287-296 ◽  
Author(s):  
Xiang Wang ◽  
Botao Zhang ◽  
Yikun Yang ◽  
Jiawei Zhu ◽  
Shujun Cheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cell ◽  
Cancer Patients ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Lung Cancer Patients ◽  
Tumor Tissues

scholarly journals Methyl DNA phosphate adduct formation in lung tumor tissue and adjacent normal tissue of lung cancer patients

2019 ◽  
Vol 40 (11) ◽  
pp. 1387-1394 ◽  
Author(s):  
Bin Ma ◽  
Peter W Villalta ◽  
J Bradley Hochalter ◽  
Irina Stepanov ◽  
Stephen S Hecht
Keyword(s):  
Lung Cancer ◽  
Dna Adducts ◽  
Human Lung ◽  
Lung Tumor ◽  
Normal Lung ◽  
Lung Cancer Patients ◽  
Normal Tissues ◽  
Phosphate Backbone ◽  
Limit Of Quantitation ◽  
Methylating Carcinogens

Abstract The formation of methyl DNA adducts is a critical step in carcinogenesis initiated by the exposure to methylating carcinogens. Methyl DNA phosphate adducts, formed by methylation of the oxygen atoms of the DNA phosphate backbone, have been detected in animals treated with methylating carcinogens. However, detection of these adducts in human tissues has not been reported. We developed an ultrasensitive liquid chromatography–nanoelectrospray ionization–high resolution tandem mass spectrometry method for detecting methyl DNA phosphate adducts. Using 50 μg of human lung DNA, a limit of quantitation of two adducts/1010 nucleobases was achieved. Twenty-two structurally unique methyl DNA phosphate adducts were detected in human lung DNA. The adduct levels were measured in both tumor and adjacent normal tissues from 30 patients with lung cancer, including 13 current smokers and 17 current non-smokers, as confirmed by measurements of urinary cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol. Levels of total methyl DNA phosphate adducts in normal lung tissues were higher in smokers than non-smokers, with an average of 13 and 8 adducts/109 nucleobases, respectively. Methyl DNA phosphate adducts were also detected in lung tissues from untreated rats with steady-state levels of 5–7 adducts/109 nucleobases over a period of 70 weeks. This is the first study to report the detection of methyl DNA phosphate adducts in human lung tissues. The results provide new insights toward using these DNA adducts as potential biomarkers to study human exposure to environmental methylating carcinogens.

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