Analysis of Clinical Characteristics of Lung Cancer Combined with Multiple Primary Malignancies in Other Organs / 中国肺癌杂志

BACKGROUND@#With the popularization of chest computed tomography (CT) early screening for lung cancer, the detection rate of lung cancer combined with multiple primary malignancies (MPM) in other organs has been increasing. In this paper, the incidence, pathological characteristics, diagnosis and treatment characteristics and prognosis were discussed and analyzed to provide research basis for improving the clinical diagnosis and treatment of this disease.@*METHODS@#From September 2011 to September 2015, a total of 5,570 patients with lung cancer were treated in Jiangsu Cancer Hospital. The clinicopathological characteristics of 61 patients with lung cancer combined with MPM in other organs were retrospectively analyzed.@*RESULTS@#The incidence rate of lung cancer combined with MPM in other organs in this group was 1.1%, of which 15 cases were synchronous MPM (SMPM), 46 cases were metachronous MPM (MMPM). Colorectal cancer, breast cancer and thyroid cancer accounted for the top three of lung cancer combined with MPM in other organs. The overall 5-year survival rate was 39.3% and 71.4% of patients died from metastasis or recurrence of lung cancer. Multivariate analysis showed that the clinical stage of lung cancer patients, the order of occurrence of lung cancer and other tumors, the treatment status of patients with other organ tumors and the presence of epidermal growth factor receptor (EGFR) gene mutation were important factors for the survival of the patients.@*CONCLUSIONS@#The incidence rate of lung cancer combined with MPM in other organs is not uncommon. Lung cancer is the main cause of death compared with other organs tumors. Patients with advanced lung cancer, SMPM, lung cancer first, combined with tumor only receiving palliative treatment and without EGFR gene mutation had a poor prognosis.

Research Progress in Distinguishing Methods of Simultaneous Multiple Primary Lung Cancer and Intrapulmonary Metastasis / 中国肺癌杂志

Multiple primary lung cancer (MPLC) refers to lung cancer in which two or more primary lesions occurred simultaneously or successively in different parts of the same patient's lungs. The diagnosis interval is 6 months. MPLC is divided into synchronous MPLC (sMPLC) and metachronous MPLC (mMPLC). sMPLC and intrapulmonary metastasis (IM) are different in treatment strategies and prognosis. However, there are many controversies about the distinction between the two in clinical practice. This article summarizes the current main methods of diagnosing MPLC, and focuses on the latest research progress in distinguishing MPLC from IM. It aims to provide a theoretical basis for accurate diagnosis and treatment of patients with multifocal lung cancer.
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Cyclic RNA Molecule circ_0007766 Promotes the Proliferation of Lung Adenocarcinoma Cells by Up-regulating the Expression of Cyclin D1/CyclinE1/CDK4 / 中国肺癌杂志

BACKGROUND@#Cyclic RNA (circRNA) is a new type of non-coding RNA (ncRNA) which is different from traditional linear RNA. More and more studies suggest that circRNA can be used as a biological marker of many malignant tumors and becomes a potential target for treatment. Therefore, searching for new molecular targets of lung adenocarcinoma from the circRNA will help to reveal the new mechanism of the occurrence and development of lung adenocarcinoma, and provide new ideas for clinical diagnosis and treatment. In this study, the biological function of circ_0007766, a highly expressed circRNA found in a screen of lung adenocarcinoma tissue, was verified and analyzed in vitro, so as to preliminarily explore the mechanism of circ_0007766 in promoting the proliferation of lung adenocarcinoma.@*METHODS@#The expression level of circ_0007766 in lung adenocarcinoma cells was detected by qPCR. Then siRNA was used to knock down the expression of circ_0007766. The effects of knockdown of circ_0007766 on proliferation, cell cycle and apoptosis of lung adenocarcinoma cells were detected by CCK8, scratch test, PI staining and Annexin V/PI double staining. In addition, the biological mechanism of circ_0007766 in lung adenocarcinoma was preliminarily studied by qPCR and Western blots.@*RESULTS@#The expression of circ_0007766 in lung adenocarcinoma cell lines was detected by qPCR. The expression of circ_0007766 was interfered in SPCA-1 cells. The proliferation and migration abilities of cells were inhibited. The cell cycle was arrested in G0/G1 phase, but the apoptosis was not affected. The deletion of circ_0007766 did not affect the expression of ERBB2, but influenced the mRNA and protein expression of Cyclin D1/Cyclin E1/CDK4.@*CONCLUSIONS@#In vitro functional studies have shown that circ_0007766 may promote the proliferation and migration of lung adenocarcinoma cells. Further molecular mechanism studies have found that circ_0007766 can up-regulate the expression of Cyclin D1/Cyclin E1/CDK4, which are the key proteins of cell cycle, and thus promote the malignant proliferation of lung adenocarcinoma. From the perspective of circRNA, this study will provide new clues for the pathogenesis, development and prognosis of lung adenocarcinoma, and provide new target for clinical treatment.

Microarray analyses reveal genes related to progression and prognosis of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma is a high morbidity and mortality cancer in China. Here are few biomarkers and therapeutic targets. Our study was aimed to identify candidate genes correlated to ESCC. Oncomine, The Cancer Genome Atlas, Gene Expression Omnibus were retrieved for eligible ESCC data. Deregulated genes were identified by meta-analysis and validated by an independent dataset. Survival analyses and bioinformatics analyses were used to explore potential mechanisms. Copy number variant analyses identified upstream mechanisms of candidate genes. In our study, top 200 up/down-regulated genes were identified across two microarrays. A total of 139 different expression genes were validated in GSE53625. Survival analysis found that nine genes were closely related to prognosis. Furthermore, Gene Ontology analyses and Kyoto Encyclopedia of Genes and Genomes analyses showed that different expression genes were mainly enriched in cell division, cell cycle and cell-cell adhesion pathways. Copy number variant analyses indicated that overexpression of ECT2 and other five genes were correlated with copy number amplification. The current study demonstrated that ECT2 and other eight candidate genes were correlated to progression and prognosis of esophageal squamous cell carcinoma, which might provide novel insights to the mechanisms.

The expression levels of CYP3A4 and CYP3A5 serve as potential prognostic biomarkers in lung adenocarcinoma.

Lung adenocarcinoma remains to be a high-mortality disease with few effective prognostic biomarkers. Novel biomarkers are urgently demanded to supplement the current prognostic biomarkers. Here, we explored the prognostic value of CYP3A4 and CYP3A5 in lung adenocarcinoma. The tissue microarray was made up of lung adenocarcinoma samples and corresponding normal lung tissues from Nanjing Medical University affiliated Cancer Hospital Tissue Bank. The expression of CYP3A4, together with CYP3A5, was detected by the chip data from Gene Expression Omnibus datasets and immunohistochemistry staining of the tissue microarray. Then, we assessed the relationships between CYP3A4 or CYP3A5 expression level and clinicopathological factors to estimate the clinical significance. Kaplan-Meier curves were applied to analyze the prognosis. Univariate and multivariate Cox analyses were subsequently applied to identify the independent prognostic factors. Immunohistochemistry staining results showed that by comparison with matched normal tissues, CYP3A4 was frequently hyper-expressed in lung adenocarcinoma tissues while CYP3A5 was hypo-expressed, which was consistent with the Gene Expression Omnibus analysis. Kaplan-Meier analysis indicated that high-CYP3A4 or low-CYP3A5 expression level predicted poor survival in lung adenocarcinoma patients. Multivariate Cox analysis found that hypo-expression of CYP3A5 was an independent prognostic factor. Further study revealed that combination of these two markers exhibited a more powerful predictor of poor prognosis, which could target to more accurate survival of lung adenocarcinoma. Our findings indicate that combination of CYP3A4 and CYP3A5 may serve as a novel prognostic biomarker in lung adenocarcinoma, which contribute to the precision of predicting the survival in lung adenocarcinoma.

Predictive Value of Ercc1 and Xpd Polymorphisms for Clinical Outcomes of Patients Receiving Neoadjuvant Therapy: A Prisma-Compliant Meta-Analysis.

Excision repair cross complementing 1 (ERCC1) and xeroderma pigmentosum group D (XPD) play important roles in the nucleotide excision repair (NER) pathway. The correlation between ERCC1 polymorphisms (rs11615 and rs3212986) and XPD polymorphisms (rs13181 and rs1799793) with the response rate and overall survival of cancer patients who accept neoadjuvant therapy has been extensively investigated. However, the results are inconclusive. In this study, we performed a meta-analysis to determine the strength of this correlation. A comprehensive literature search was conducted in Medline, PubMed, and Embase up to February 2015. A review of all titles and abstracts was performed by 2 of the authors to screen the articles based on the eligibility criteria. Clinical trials, observational studies, and epidemiological studies describing ERCC polymorphisms and neoadjuvant treatment were considered for review. The response rate was analyzed using pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs). Overall survival was assessed using the hazard ratio (HR) with corresponding 95% confidence intervals. In the present meta-analysis, we demonstrated that the ERCC1 rs3212986 polymorphism was significantly correlated with the response rate of esophageal cancer patients to neoadjuvant therapy (OR =  .49, 95% CI = 0.31-0.76, heterogeneity P = 0.480). Furthermore, a considerable correlation was observed between ERCC1 rs11615 and the response rate of esophageal cancer patients to neoadjuvant therapy (OR = 0.228, 95% CI = 0.125-0.418, heterogeneity P = 0.291). No correlation was observed in the meta-analysis of overall survival. The individual studies included in our study differed in their patient selection and therapeutic protocols, which might lead to some bias in the results. These findings indicate that the ERCC1 rs11615 and ERCC1 rs312986 polymorphisms may be candidate pharmacogenomic factors capable of predicting the response rate of esophageal cancer patients who accept neoadjuvant therapy. Further studies are warranted.