HapMap-based study on the association between MPO and GSTP1 gene polymorphisms and lung cancer susceptibility in Chinese Han population.

AIM: Myeloperoxidase (MPO) and glutathione S-transferase pi 1 (GSTP1) are important carcinogen-metabolizing enzymes. The aim of this study was to investigate the association between the common polymorphisms of MPO and GSTP1 genes and lung cancer risk in Chinese Han population. METHODS: A total of 266 subjects with lung cancer and 307 controls without personal history of the disease were recruited in this case control study. The tagSNPs approach was used to assess the common polymorphisms of MOP and GSTP1 genes and lung cancer risk according to the disequilibrium information from the HapMap project. The tagSNP rs7208693 was selected as the polymorphism site for MPO, while the haplotype-tagging SNPs rs1695, rs4891, rs762803 and rs749174 were selected as the polymorphism sites for GSTP1. The gene polymorphisms were confirmed using real-time PCR, cloning and sequencing. RESULTS: The four GSTP1 haplotype-tagging SNPs rs1695, rs4891, rs762803 and rs749174, but not the MPO tagSNP rs7208693, exhibited an association with lung cancer susceptibility in smokers in the overall population and in the studied subgroups. When Phase 2 software was used to reconstruct the haplotype for GSTP1, the haplotype CACA (rs749174+rs1695 + rs762803+rs4891) exhibited an increased risk of lung cancer among smokers (adjust odds ratio 1.53; 95%CI 1.04-2.25, P=0.033). Furthermore, diplotype analyses demonstrated that the significant association between the risk haplotype and lung cancer. The risk haplotypes co-segregated with one or more biologically functional polymorphisms and corresponded to a recessive inheritance model. CONCLUSION: The common polymorphisms of the GSTP1 gene may be the candidates for SNP markers for lung cancer susceptibility in Chinese Han population.

Efficacy and safety of human umbilical cord-derived mesenchymal stem cells in the treatment of refractory immune thrombocytopenia: a prospective, single arm, phase I trial.

Patients with refractory immune thrombocytopenia (ITP) frequently encounter substantial bleeding risks and demonstrate limited responsiveness to existing therapies. Umbilical cord-derived mesenchymal stem cells (UC-MSCs) present a promising alternative, capitalizing on their low immunogenicity and potent immunomodulatory effects for treating diverse autoimmune disorders. This prospective phase I trial enrolled eighteen eligible patients to explore the safety and efficacy of UC-MSCs in treating refractory ITP. The research design included administering UC-MSCs at escalating doses of 0.5 × 106 cells/kg, 1.0 × 106 cells/kg, and 2.0 × 106 cells/kg weekly for four consecutive weeks across three cohorts during the dose-escalation phase, followed by a dose of 2.0 × 106 cells/kg weekly for the dose-expansion phase. Adverse events, platelet counts, and changes in peripheral blood immunity were monitored and recorded throughout the administration and follow-up period. Ultimately, 12 (with an addition of three patients in the 2.0 × 106 cells/kg group due to dose-limiting toxicity) and six patients were enrolled in the dose-escalation and dose-expansion phase, respectively. Thirteen patients (13/18, 72.2%) experienced one or more treatment emergent adverse events. Serious adverse events occurred in four patients (4/18, 22.2%), including gastrointestinal hemorrhage (2/4), profuse menstruation (1/4), and acute myocardial infarction (1/4). The response rates were 41.7% in the dose-escalation phase (5/12, two received 1.0 × 106 cells/kg per week, and three received 2.0 × 106 cells/kg per week) and 50.0% (3/6) in the dose-expansion phase. The overall response rate was 44.4% (8/18) among all enrolled patients. To sum up, UC-MSCs are effective and well tolerated in treating refractory ITP (ClinicalTrials.gov ID: NCT04014166).

Therapeutic and Safety Promise of Mesenchymal Stem Cells for Liver Failure: from Preclinical Experiment to Clinical Application.

Liver failure (LF) is serious liver damage caused by multiple factors, resulting in severe impairment or decompensation of liver synthesis, detoxification, metabolism, and biotransformation. The general prognosis of LF is poor with high mortality in non-transplant patients. The clinical treatments for LF are mainly internal medicine comprehensive care, an artificial liver support system, and liver transplantation. However, none of the above treatment strategies can solve the problems of all liver failure patients and has its own limitations. Mesenchymal stem cells (MSCs) are a kind of stem cells with multidirectional differentiation potential and paracrine function, which play an important role in immune regulation and tissue regeneration. In recent years, MSCs have shown multiple advantages in the treatment of LF in pre-clinical experiments and clinical trials. In this work, we reviewed the biological characteristics of MSCs, the possible molecular mechanisms of MSCs in the treatment of liver failure, animal experiments, and clinical application, and also discussed the existing problems of MSCs in the treatment of liver failure.

The Promise of Mesenchymal Stem Cells Therapy for Acute Respiratory Distress Syndrome Caused by COVID-19.

The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) since Dec 2019, known as COVID-19 or 19-nCoV, has led to a major concern of the potential for not only an epidemic but a pandemic in China and now it seems to be a public health problem all over the world. The general mortality rate of the COVID-19 was about 3%. However, the mortality risk seems to be a significant increase in elderly and cases with chronic disease, who are more likely to develop into acute respiratory distress syndrome (ARDS). There still lacks effective methods for ARDS of COVID-19 patients and the prognosis was poor. Mesenchymal Stem Cells (MSCs) based treatment has the advantage of targeting numerous pathophysiological components of ARDS by secreting a series of cell factors, exerting anti-inflammatory, antioxidative, immunomodulatory, antiapoptotic, and proangiogenic effects, resulting in significant structural and functional recovery following ARDS in various preclinical models. Recently, pilot clinical studies indicated MSCs based therapy was promise in treatment of ARDS caused by SARS-CoV-2. However, little is known about MSCs therapy for ARDS caused by COVID-19.

[A meta analysis on the relationship between myeloperoxidase G-463A genetic polymorphisms and lung cancer susceptibility].

BACKGROUND AND OBJECTIVE: The relationship between myeloperoxidase G-463A genetic polymorphisms and lung cancer susceptibility has been studied extensively. However, the outcomes are not consistent. The aim of this study is to evaluate the relationship between myeloperoxidase genetic polymorphisms and lung cancer susceptibility by meta analysis. METHODS: Documents published were retrieved through databases associated with the study. Taking into account the possibilities of heterogeneity of the studies, a statistical test for heterngeneity was performed. The odds ratio and 95% CI were used to evaluate the risks. The meta analysis was applied with RevMan software 4.2, and the forest plot and funnel plot of meta analysis were worked out. RESULTS: A total of 5 381 cases and 5 827 controls from studies for Caucasian and a total of 1 558 cases and 1 755 controls from studies for East Asians were included. For Caucasian the pooled OR was 0.91 (95% CI: 0.81-1.02); For East Asians, the pooled OR is 0.83 (95% CI: 0.63-1.09). Publication bias exits in the study for Caucasian, but not for East Asians. CONCLUSION: The results of this study indicated that the polymorphism of myeloperoxidase G-463A was not significantly associated with the lung cancer risk for Caucasian or East Asians. However, further studies for the East Asians is needed for the few subjects.

[Systematic review of the relationship between family history of lung cancer and lung cancer risk].

BACKGROUND AND OBJECTIVE: Fourty years ago, Tokuhata and Lilienfeld provided the first epidemiologic evidence of familial aggregation of lung cancer. Familial aggregation and increased familial risk for lung cancer have been reported in several studies, subsequently. But the results are not consistent with each other. The aim of this study is to further explore the relationship between family history of lung cancer and lung cancer risk. METHODS: By searching PubMed, CENTRAL, CBM, CNKI and VIP, we collected both domestic and overseas published documents before November, 2009 on family history of lung cancer and lung cancer risk. RevMan version 4.2 was used to perform meta-analysis on the case-control study results, the combined odds ratio (OR) and the 95% confidence interval (CI) were calculated as well. RESULTS: Twenty-eight publications were included into the combined analysis, which indicated that the lung cancer risk of the probands' first-degree relatives was 1.88 times higher than that of their controls' (P < 0.001). In the sub-study, compared with the controls' father mother and siblings, the OR of the probands' father mother and siblings was 1.62 (P < 0.001), 1.96 (P < 0.001) and 1.92 (P < 0.001), respectively. For smoking status, lung cancer risk in first-degree relatives of smoking probands was 1.73 (P < 0.001) times higher than that of their corresponding controls'. And for non-smoking subjects the lung cancer risk was 1.42 (P = 0.02) times higher in proboands' first-degree relatives. For gender categories, lung cancer risk in first-degree relatives of female probands was 1.89 (P < 0.001) times higher than that of their corresponding controls'. And for male subjects, the lung cancer risk was 1.99 (P < 0.001) times higher in proboands' first-degree relatives. CONCLUSION: Lung cancer risk was increased in probands' first-degree relatives, and obvious familial aggregation of lung cancer was observed in this study.

[Meta-analysis of the relationship between passive smoking population in China and lung cancer].

BACKGROUND AND OBJECTIVE: Studies of passive smoking exposure in China however are of particular interest, because of the high lung cancer rate in people who are mostly non-smokers. The aim of this study is to explore the relationship between passive smoking and lung cancer among non-smoking Chinese. METHODS: By searching Medline, PubMed, CENTRAL (the Cochrane central register of controlled trials), CBM, CNKI and VIP, et al, we collected both domestic and overseas published documents between 1987 and 2007 on passive smoking and lung cancer among non-smoking Chinese. Random or fixed effect models were applied to conduct meta-analysis on the case control study results, and the combined odds ratio (OR) and the 95% confidence interval (CI) were calculated as well. RESULTS: Sixteen documents were included into the combined analysis, which indicated that there was statistical significance between passive smoking and lung cancer (OR = 1.13, 95% CI: 1.05-1.21, P = 0.001). It was significant of lung cancer among non-smoking subjects associated with amount of tobacco passively smoked more than 20 cigarettes daily, with life period in adulthood passive smoking exposure, with gender female, and with exposure to workplace. The P value, OR and 95% CI were P = 0.0003, OR = 1.78, 95% CI: 1.30-2.43; P = 0.0001, OR = 1.50, 95% CI: 1.23-1.83; P = 0.000 7, OR = 1.50, 95% CI: 1.19-1.90; P < 0.0001, OR = 1.41, 95% CI: 1.19-1.66; respectively. And there was no significant difference between passive smoking and lung cancer with amount of tobacco passively smoked within 20 cigarettes daily, with life period in childhood passive smoking exposure, with gender male and with exposure to spouse and parents. CONCLUSION: Passive smoking is an important risk factor of lung cancer among non-smoking Chinese, and for non-smoking women who expose to environment tobacco smoke in a long period of time have a close relationship with lung cancer risk.

Bioinformatics analysis of LINC00426 expression in lung cancer and its correlation with patients' prognosis.

BACKGROUND: To investigate the expression of long noncoding RNA (lncRNA) LINC00426 (long intergenic nonprotein coding RNA 426) in non-small cell lung cancer (NSCLC) patients and its correlation with their prognosis. METHODS: The expression of long noncoding RNA LINC00426 of non-small cell lung cancer (NSCLC) in The Cancer Genome Atlas (TCGA) database was screened. According to the expression level of LINC00426 in tumor tissue of NSCLC patients, the patients were divided into high and low LINC00426 expression groups. The correlation between LINC00426 expression group and the prognosis of the patient was analyzed by log-rank test. A total of 72 NSCLC patients who had undergone surgery were retrospectively included in this study. LINC00426 relative expression of tumor and normal lung tissue of the included 72 NSCLC patients were examined by real-time quantitative PCR assay. The correlation between LINC00426 expression and the patients' clinical characteristics were also evaluated. RESULTS: LINC00426 relative expression was not statistically different between cancer and normal tissue (P > 0.05) of NSCLC patients in the TCGA database. The amplification and deep deletion mutation of LINC00426 gene was found in 0.5% of NSCLC patients. The overall survival (OS) of the LINC00426 high expression group was significantly higher than that of the low expression group (HR = 0.81, P = 0.044), while there was no significant difference between the high and low expression group (HR = 0.97, P = 0.82) for disease-free survival (DFS). LINC0042646 expression level was elevated in 46 cases in normal lung tissue compared to the tumor tissue of the 72 NSCLC patients. LINC0042646 expression level was significantly correlated with the clinical stage (P < 0.05). CONCLUSION: Long noncoding RNA LINC00426 was downregulated in the tumor tissue of NSCLC patients and correlated with poor prognosis.

Review of aerobic glycolysis and its key enzymes - new targets for lung cancer therapy.

Most tumor cells show different metabolic pathways than normal cells. Even under the conditions of sufficient oxygen, they produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol, which is known as aerobic glycolysis or the Warburg effect. Lung cancer is a malignant tumor with one of the highest incidence and mortality rates in the world at present. However, the exact mechanisms underlying lung cancer development remain unclear. The three key enzymes of glycolysis are hexokinase, phosphofructokinase, and pyruvate kinase. Lactate dehydrogenase catalyzes the transfer of pyruvate to lactate. All four enzymes have been reported to be overexpressed in tumors, including lung cancer, and can be regulated by many oncoproteins to promote tumor proliferation, migration, and metastasis with dependence or independence of glycolysis. The discovery of aerobic glycolysis in the 1920s has provided new means and potential therapeutic targets for lung cancer.

The value of serum Cyfra21-1 as a biomarker in the diagnosis of patients with non-small cell lung cancer: a meta-analysis.

OBJECTIVE: The serum level of Cyfra21-1 was always elevated in patients with nonsmall cell lung carcinoma. The aim of this meta-analysis was to evaluate the serum Cyfra21-1 as a biomarker in the diagnosis of nonsmall cell lung cancer (NSCLC). METHODS: All the articles associated with serum Cyfra21-1 in the diagnosis of NSCLC were searched in the PubMed, Medline, and CNKI databases. The number of patients for true positive, false positive, false negative and true negative were extracted from each individual study. The pooled sensitivity, specificity, positive likely hood ratio (+lr), negative likely hood ratio (-lr), diagnosis odds ratio (dor) and summary receiver operating characteristic (sroc) curve were calculated by MetaDiSc 1.4 software. RESULTS: After searching the databases, 17 studies with 4221 subjects were met the inclusion criteria and finally included in this meta-analysis. The pooled diagnosis sensitivity, specificity, +lr, -lr and dor were 0.72 (95% confidence interval [CI]: 0.70-0.73), 0.94 (95%CI: 0.93-0.95), 8.81 (95%CI: 6.36-12.22), 0.42 (95%CI: 0.32-0.55) and 22.57 (95%CI: 13.89-36.68) respectively. The area under the sroc curve was 0.95. And significant publication bias was found in this meta-analysis (P = 0.049). CONCLUSION: With published data, the serum Cyfra21-1 was a useful biomarker for diagnosis of NSCLC. OBJECTIVE: The serum level of Cyfra21-1 was always elevated in patients with nonsmall cell lung carcinoma. The aim of this meta-analysis was to evaluate the serum Cyfra21-1 as a biomarker in the diagnosis of nonsmall cell lung cancer (NSCLC). METHODS: All the articles associated with serum Cyfra21-1 in the diagnosis of NSCLC were searched in the PubMed, Medline, and CNKI databases. The number of patients for true positive, false positive, false negative and true negative were extracted from each individual study. The pooled sensitivity, specificity, positive likely hood ratio (+lr), negative likely hood ratio (-lr), diagnosis odds ratio (dor) and summary receiver operating characteristic (sroc) curve were calculated by MetaDiSc 1.4 software. RESULTS: After searching the databases, 17 studies with 4221 subjects were met the inclusion criteria and finally included in this meta-analysis. The pooled diagnosis sensitivity, specificity, +lr, -lr and dor were 0.72 (95% confidence interval [CI]: 0.70-0.73), 0.94 (95%CI: 0.93-0.95), 8.81 (95%CI: 6.36-12.22), 0.42 (95%CI: 0.32-0.55) and 22.57 (95%CI: 13.89-36.68) respectively. The area under the sroc curve was 0.95. And significant publication bias was found in this meta-analysis (P = 0.049). CONCLUSION: With published data, the serum Cyfra21-1 was a useful biomarker for diagnosis of NSCLC.

[A meta-analysis of Association between MGMT gene promoter methylation and non-small cell lung cancer].

BACKGROUND: DNA promoter methylation of the tumor suppressor genes was one of the key mechanism for gene silence. The aim of this study is to investigate the difference of MGMT gene promoter methylation rate in tumor tissue and autologous controls (serum, normal lung tissue and bronchial lavage fluid) in patients with non-small cell lung cancer (NSCLC). METHODS: The databases of Medline, EMBSE, CNKI and Wanfang were searched for selection of published articles of MGMT gene promoter methylation and non-small cell lung carcinoma risk. The pooled odds ratio (OR) and percentage of MGMT for lung cancer tissue of NSCLC patients compared with normal lung tissue, plasma and the bronchial lavage fluid were pooled. RESULTS: 15 articles of association between MGMT gene promoter methylation and non small cell lung carcinoma risk were included in this meta-analysis. The combined results demonstrated the methylation rate of MGMT in NSCLC cancer tissue was 38% (95%CI: 23%-53%). For normal lung tissue, plasma and the bronchial lavage fluid were 16% (95%CI: 5%-27%), 23% (95%CI: 10%-34%) and 39% (95%CI: 23%-55%) respectively. The OR in cancer tissue was much higher than that in normal lung tissue and plasma odds ratio (OR) 3.98 (95%CI: 2.71-5.84, P<0.05) and OR 1.88 (95%CI: 1.16-3.05, P<0.05), but not in bronchial lavage fluid OR 2.05 (95%CI: 0.88-4.78, P>0.05). CONCLUSIONS: Mehtylation rate in MGMT gene promoter of cancer tissue in NSCLC patients was much higher than that in normal lung tissue and plasma, which showed a close association between NSCLC cancer and MGMT gene promoter methylation.

A meta-analysis of the relationship between RARß gene promoter methylation and non-small cell lung cancer.

BACKGROUND: Hypermethylation of CpG islands in tumor suppressor gene plays an important role in carcinogenesis. Many studies have demonstrated that hypermethylation in promoter region of RARß gene could be found with high prevalence in tumor tissue and autologous controls such as corresponding non-tumor lung tissue, sputum and plasma of the NSCLC patients. But with the small number subjects included in the individual studie, the statistical power is limited. Accordingly, we performed this meta-analysis to further asses the relationship of methylation prevalence between the cancer tissue and atuologous controls (corresponding non-tumor lung tissue, sputum and plasma). METHODS: The published articles about RARß gene promoter hypermethyltion were identified using a systematic search strategy in PubMed, EMBASE and CNKI databases. The pooled odds ratio (OR) of RARß promoter methylation in lung cancer tissue versus autologous controls were calculated. RESULTS: Finally, eleven articles, including 1347 tumor tissue samples and 1137 autologous controls were included in this meta-analysis. The pooled odds ratio of RARß promoter methylation in cancer tissue was 3.60 (95%CI: 2.46-5.27) compared to autologous controls with random-effect model. Strong and significant correlation between tumor tissue and autologous controls of RARß gene promoter hypermethylation prevalence across studies (Correlation coefficient 0.53) was found. CONCLUSION: RARß promoter methylation may play an important role in carcinogenesis of the NSCLC. With significant methylation prevalence correlation between tumor tissue and autologous of this gene, methylation detection may be a potential method for searching biomarker for NSCLC.

Effect of amifostine in head and neck cancer patients treated with radiotherapy: a systematic review and meta-analysis based on randomized controlled trials.

BACKGROUND: Amifostine is the most clinical used chemical radioprotector, but its effect in patients treated with radiation is not consistent. METHODS: By searching Medline, CENTRAL, EMBASE, ASCO, ESMO, and CNKI databases, the published randomized controlled trials (RCTs) about the efficacy of amifostine in HNSCC patients treated with radiotherapy were collected. The pooled efficacy and side effects of this drug were calculated by RevMan software. RESULTS: Seventeen trials including a total of 1167 patients (604 and 563 each arm) were analyzed in the meta-analysis. The pooled data showed that the use of amifostine significantly reduce the risk of developing Grade 3-4 mucositis (relative risk [RR],0.72; 95% confidence interval [CI],0.54-0.95; p<0.00001), Grade 2-4 acute xerostomia (RR,0.70; 95%CI,0.52-0.96; p = 0.02), or late xerostomia (RR,0.60; 95%CI,0.49-0.74; p<0.00001) and Grade 3-4 dysphagia (RR,0.39; 95%CI,0.17-0.92; p = 0.03). However, subgroup analysis demonstrated that no statistically significant reduction of Grade 3-4 mucositis (RR,0.97; 95% CI,0.74-1.26; p = 0.80), Grade 2-4 acute xerostomia (RR,0.35; 95%CI,0.02-5.44; p = 0.45), or late xerostomia (RR,0.40; 95%CI,0.13-1.24; p = 0.11) and Grade 3-4 dysphagia (RR,0.23; 95%CI,0.01-4.78; p = 0.35) was observed in patients treated with concomitant chemoradiotherapy. Compared with placebo or observation, amifostine does not show tumor protective effect in complete response (RR,1.02; 95%CI,0.89-1.17; p = 0.76) and partial response (RR,0.90; 95%CI, 0.56-1.44; p = 0.66). For the hematologic side effect, no statistical difference of Grade 3-4 leucopenia (RR,0.60; 95%CI,0.35-1.05; p = 0.07), anemia (RR,0.80; 95%CI, 0.42-1.53; p = 0.50) and thrombocytopenia (RR,0.43; 95%CI,0.16-1.15; p = 0.09) were found between amifostine and control groups. The most common amifostine related side effects were nausea, emesis, hypotension and allergic with an average incidence rate (Grade 3-4) of 5%, 6%, 4% and 4% respectively. CONCLUSION: This systematic review showed that amifostine significantly reduce the serious mucositis, acute/late xerastomia and dysphagia without protection of the tumor in HNSCC patients treated with radiotherapy. And the toxicities of amifostine were generally acceptable.

Concomitant EGFR inhibitors combined with radiation for treatment of non-small cell lung carcinoma.

Epidermal growth factor receptor (EGFR) is considered to be one of the key driver genes in non-small cell lung cancer (NSCLC). Several clinical trials have shown great promise of EGFR tyrosine kinase inhibitors (TKIs) in the first-line treatment of NSCLC. Many advances have been made in the understanding of EGFR signal transduction network and the interaction between EGFR and tumor microenvironment in mediating cancer survival and development. The concomitant targeted therapy and radiation is a new strategy in the treatment of NSCLC. A number of preclinical studies have demonstrated synergistic anti-tumor activity in the combination of EGFR inhibitors and radiotherapy in vitro and in vivo. In the present review, we discuss the rationale of the combination of EGFR inhibitors and radiotherapy in the treatment of NSCLC.

Extrathoracic malignant peripheral nerve sheath tumor of the lateral chest wall locally recurred and metastasized to peritoneum: Report of a case.

Malignant peripheral nerve sheath tumors (MPNSTs) are rare, with an expected incidence of 0.0001% per year in the general population and 4.6% in patients with von Recklinghausen's disease. They are defined as any malignant tumors arising or differentiating from cells of the peripheral nerve sheath. MPNSTs can develop in various sites including the trunk and head/neck region. However, its onset on the chest wall is very rare. Here we report a case of MPNST growing outside the thorax on the chest wall. The patient developed a local recurrence twice, which caused multiple metastases to the lung and peritoneum.

Association between P(16INK4a) promoter methylation and non-small cell lung cancer: a meta-analysis.

BACKGROUND: Aberrant methylation of CpG islands acquired in tumor cells in promoter regions plays an important role in carcinogenesis. Accumulated evidence demonstrates P(16INK4a) gene promoter hypermethylation is involved in non-small cell lung carcinoma (NSCLC), indicating it may be a potential biomarker for this disease. The aim of this study is to evaluate the frequency of P(16INK4a) gene promoter methylation between cancer tissue and autologous controls by summarizing published studies. METHODS: By searching Medline, EMBSE and CNKI databases, the open published studies about P(16INK4a) gene promoter methylation and NSCLC were identified using a systematic search strategy. The pooled odds of P(16INK4A) promoter methylation in lung cancer tissue versus autologous controls were calculated by meta-analysis method. RESULTS: Thirty-four studies, including 2 652 NSCLC patients with 5 175 samples were included in this meta-analysis. Generally, the frequency of P(16INK4A) promoter methylation ranged from 17% to 80% (median 44%) in the lung cancer tissue and 0 to 80% (median 15%) in the autologous controls, which indicated the methylation frequency in cancer tissue was much higher than that in autologous samples. We also find a strong and significant correlation between tumor tissue and autologous controls of P(16INK4A) promoter methylation frequency across studies (Correlation coefficient 0.71, 95% CI:0.51-0.83, P<0.0001). And the pooled odds ratio of P(16INK4A) promoter methylation in cancer tissue was 3.45 (95% CI: 2.63-4.54) compared to controls under random-effect model. CONCLUSION: Frequency of P(16INK4a) promoter methylation in cancer tissue was much higher than that in autologous controls, indicating promoter methylation plays an important role in carcinogenesis of the NSCLC. Strong and significant correlation between tumor tissue and autologous samples of P(16INK4A) promoter methylation demonstrated a promising biomarker for NSCLC.

Esophageal cancer associated with right aortic arch and thyroid adenoma.

A 55-year-old Chinese woman with thoracic esophageal cancer associated with right aortic arch and thyroid adenoma was admitted to our hospital. Computed tomography revealed a right aortic arch with mirror-image branching and a mass in the esophagus. The following barium-coated esophagograms and esophagoscopy showed an ulcerative and infiltrative tumor in the upper thoracic esophagus. The patient also had an almost 10-year history of thyroid adenoma.