Correlation Of Lung Cancer Research Articles

Research Progress of the Effect of Mediterranean Diet on the Correlation of Lung Cancer

Lung cancer is one of the top 10 causes of death in the world today, and it is a great concern worldwide for its high mortality rate. Currently, the researchers are digging into various factors influencing the occurrence and development of lung cancer in order to increase the odds for curing lung cancer, improve the prognosis of lung cancer patients as well as reduce its morbidity. The Mediterranean diet (MD) is a special dietary structure that is based on eating vegetables, fruits, coarse grains, legumes and low-fat fish, which have anti-inflammatory, antioxidant and lipid-lowering effects. Recent studies have revealed that the MD may prevent lung cancer occurrence to some extent and inhibit its development. The purpose of this paper is to summarize and analytically discuss the effects of the MD on the oncogenesis and development of lung cancer through a review of the relevant literatures, thus to provide references for MD to prevent and treat lung cancer. .

THSD7A Positivity Predicts Poor Survival and Is Linked to High FAK Expression and FGFR1-Wildtype in Female Patients with Squamous Cell Carcinoma of the Lung.

Lung cancer is the leading cause of cancer-related deaths in the western world, with squamous cell carcinoma being one of the most common histological subtypes. Prognostic and predictive markers are still largely missing for squamous cell carcinoma of the lung (LSCC). Several studies indicate that THSD7A might at least play a role in the prognosis of different tumors. FAK seems to play an important role in lung cancer and is discussed as a potential therapeutic target. In addition, there is evidence that FAK-dependent signaling pathways might be affected by THSD7A. For that reason, we investigated the role of THSD7A as a potential tumor marker in LSCC and whether THSD7A expression has an impact on the expression level of FAK. A total of 101 LSCCs were analyzed by immunohistochemistry using tissue microarrays. THSD7A positivity was associated with poor overall survival in female patients and showed a relation to high FAK expression in this subgroup. To our knowledge, we are the first to report these correlations in lung cancer. The results might be proof of the assumed activation of FAK-dependent signaling pathways by THSD7A and that as a membrane-associated protein, THSD7A might serve as a putative therapeutic target in LSCC.

LINC01342 silencing upregulates microRNA-508-5p to inhibit progression of lung cancer by reducing cysteine-rich secretory protein 3

Long noncoding RNAs (lncRNAs) are critical players during cancer progression. Nevertheless, the effect of most lncRNAs in lung cancer (LC) remains unclear. We aimed to explore the role of LINC01342 in LC development through the microRNA-508-5p (miR-508-5p)/cysteine-rich secretory protein 3 (CRISP3) axis. LINC01342, miR-508-5p, and CRISP3 expression in clinical samples and cell lines were determined, and their correlations in LC were analyzed. The prognostic role of LINC01342 in LC patients was evaluated. LC cells were screened and, respectively, transfected to alter the expression of LINC01342, miR-508-5p, and CRISP3. Then, proliferation, migration, invasion, and apoptosis of transfected LC cells were determined, and the in vivo tumor growth was observed as well. Binding relationships between LINC01342 and miR-508-5p, and between miR-508-5p and CRISP3 were identified. LINC01342 and CRISP3 were upregulated and miR-508-5p was downregulated in LC tissues and cells. High LINC01342 expression indicated a poor prognosis of LC patients. The LINC01342/CRISP3 silencing or miR-508-5p elevation inhibited proliferation, migration, and invasion of LC cells and promoted LC cell apoptosis, and also suppressed the in vivo tumor growth. LINC01342 bound to miR-508-5p and miR-508-5p targeted CRISP3. LINC01342 plays a prognostic role in LC and LINC01342 silencing upregulates miR-508-5p to inhibit the progression of LC by reducing CRISP3.

Rapid diagnosis of lung cancer and glioma based on serum Raman spectroscopy combined with deep learning

AbstractLung cancer and glioma are common malignancies worldwide and pose a serious threat to human health. There may be a certain correlation between lung cancer patients and glioma patients in serum composition, but to date, no study on the classification and correlation of lung cancer and glioma is available. In this paper, the differences and relationships between lung cancer and glioma were analyzed from serum Raman spectra. The existing detection methods of lung cancer and glioma are time consuming and expensive, so we propose a method based on patient serum Raman spectra combined with deep learning, which can screen lung cancer and glioma accurately with speed and low cost. In this study, features were extracted from the original spectral data of patients with lung cancer, glioma, and control subjects. By adding different decibels of white Gaussian noise to the training set for data enhancement, the enhanced training set data were imported into a multilayer perceptron (MLP), recursive neural network (RNN), convolutional neural network (CNN), and AlexNet using fivefold cross‐validation to build the diagnostic model. The results show that PLS‐AlexNet is the best model. The accuracy of this model in the binary classification experiment of lung cancer and control subjects, lung cancer and glioma, and glioma and control subjects were 99%, 95.2%, and 100%, respectively, and the experimental accuracy of the AlexNet triclassification algorithm is also above 85%. This method has great potential in clinical diagnosis of diseases.

Advances in lung cancer biomarkers: The role of (metal-) metabolites and selenoproteins.

Lung cancer (LC) is the second most common cause of death in men after prostate cancer, and the third most recurrent type of tumor in women after breast and colon cancers. Unfortunately, when LC symptoms begin to appear, the disease is already in an advanced stage and the survival rate only reaches 2%. Thus, there is an urgent need for early diagnosis of LC using specific biomarkers, as well as effective therapies and strategies against LC. On the other hand, the influence of metals on more than 50% of proteins is responsible for their catalytic properties or structure, and their presence in molecules is determined in many cases by the genome. Research has shown that redox metal dysregulation could be the basis for the onset and progression of LC disease. Moreover, metals can interact between them through antagonistic, synergistic and competitive mechanisms, and for this reason metals ratios and correlations in LC should be explored. One of the most studied antagonists against the toxic action of metals is selenium, which plays key roles in medicine, especially related to selenoproteins. The study of potential biomarkers able to diagnose the disease in early stage is conditioned by the development of new analytical methodologies. In this sense, omic methodologies like metallomics, proteomics and metabolomics can greatly assist in the discovery of biomarkers for LC early diagnosis.

Correlation between p-STAT3 overexpression and prognosis in lung cancer: A systematic review and meta-analysis.

ObjectivePrevious studies have shown the correlation between p-STAT3 overexpression and prognosis in a variety of human tumors. However, their correlation in lung cancer remains controversial. We performed a systematic review and meta-analysis to explore the correlation between p-STAT3 overexpression and prognosis in lung cancer patients.MethodsWe searched PubMed, Embase, Web of Science, CNKI, VIP, and WanFang Data to identify relevant studies. Two reviewers independently screened the literature search results, extracted data, and assessed the methodological quality of the included studies. Then, meta-analysis was performed by using Review Manager 5.3 and STATA 14 software. A random-effect model was employed to evaluate all related pooled results. Statistical heterogeneity of each study was assessed by I2. Publication bias was determined by funnel plot and the Begg’s or Egger’s tests.ResultsEventually, 13 studies were included in present meta-analysis. Among these 13 studies, 8 studies were associated with the overall survival of lung cancer and 10 studies with other clinicopathological characteristics. The results of this meta-analysis suggested that p-STAT3 overexpression may be a poor prognosis biomarker in lung cancer (HR: 1.23; 95% CI: 1.04–1.46; P = 0.02). In terms of other clinicopathological characteristics, p-STAT3 overexpression was more frequent to advanced TNM stages ranging from III to IV (OR: 1.92; 95% CI: 1.13–3.27; P = 0.02) and lymphatic node metastasis (OR: 1.81; 95% CI: 1.20–2.72; P = 0.004). But, it was not associated with tumor differentiation (OR: 0.82; 95% CI: 0.44–1.53; P = 0.54).Conclusionp-STAT3 overexpression has significant correlation with poorer overall survival of lung cancer patients, as well as with more advanced TNM stages and lymph node metastasis. Thus, it may serve a biomarker for poor prognosis in lung cancer. Nevertheless, our findings should be confirmed by large prospective studies.

Expressions of Frat and beta-catenin in lung cancer and their clinicopathological correlations.

Frat proteins are positive regulator of Wnt-signal transduction.By binding to GSK3,Frat prevents the phosphorylation and concomitant degradation of beta-catenin and allows the activation of downstream targetgenes by beta-catenin/TCF complexes. The aim of this study is to investigate the protein expression of Frat and beta-catenin and their clinicopathological correlations in lung cancer. By means of tissue chip technique and immunohistochemical method, 52 cases of lung carcinoma were examed to detect the expression of Frat and beta-catenin. The positive expression rate of Frat was 75% . The positive expression rate of Frat in well,moderately and poorly differentiated NSCLCs were 41.67%(5/12), 83.33%(15/18) and 88.24%(15/17). There was a significant difference in Frat expression among well,moderately and poorly differentiated NSCLCs (Chi-Square=9.229, P=0.01). The abnormal cell expression rate of beta-catenin was 71.15%. The abnormal cell expression rate of beta-catenin in well,moderately and poorly differentiated NSCLCs were 41.67%(5/12), 61.11%(11/18) and 100%(17/17). There was a significant difference (Chi-Square=12.601, P=0.002). The abnormal cell expression of beta-catenin is associated with pooly differentiated NSCLCs. The expression of Frat is positively correlated with the degree of tumor differentiation and the abnormal cell expression of beta-catenin.

Tobacco-related cancer in relation to prevalence of drinking and smoking in eastern Austria.

Eastern Austrian regional mortality patterns of oral cancer (oral cavity, pharynx and larynx) and oesophageal, lung and urinary bladder cancer were compared to smoker rates and to liver cirrhosis mortality by type of residence: Vienna (1.7 x 10(6) inhabitants), middle towns (50,000-100,000 and 10,000-50,000 inhabitants), small towns (2000-10,000 inhabitants) and rural areas categorized by agrarian quota less than or equal to 10%, 10%-20% and greater than 20%. The study area (Vienna, Lower Austria and Burgenland) covers 23,600 km2 with 3.23 x 10(6) inhabitants. In men, liver cirrhosis correlated negatively with smoker rates (r = 0.74, P = 0.1). Deaths from oral cancer and oesophageal cancer correlated significantly with deaths from liver cirrhosis (r = 0.81, P = 0.03; r = 0.78, P = 0.04, respectively) but not with smoker rates; lung cancer and bladder cancer correlated significantly with smoker rates (r = 0.91, P = 0.01; r0.83, P = 0.04, respectively), but not with liver cirrhosis. In women, similar urban-rural gradients for all parameters resulted in a positive correlation between liver cirrhosis and smoker rates (r = 0.59, P = 0.22) and a significant correlation of lung cancer with liver cirrhosis (r = 0.75, P = 0.05). Oral cancer correlated significantly with liver cirrhosis (r = 0.83, P = 0.02), but not with smoker rates; lung cancer correlated more significantly with smoker rates (r = 0.92, P = 0.01) than with liver cirrhosis; bladder cancer correlated positively with smoker rates (r = 0.70, P = 0.12). Geographical distribution of oral and oesophageal cancer in Eastern Austria seems thus to be highly subject to the prevalence of heavy drinking. Sociocultural influences upon the occurrence of these cancers seem to be mediated through drinking habits rather than through smoking habits alone.