J Clin Oncol 2009, 27:1746–1752 PubMedCrossRef 24 Sakaki M, Maki

J Clin Oncol 2009, 27:1746–1752.PubMedCrossRef 24. Sakaki M, Makino R, Hiroishi K, Ueda K, Eguchi J, Hiraide A,

Doi H, Omori R, Imawari M: Cyclooxygenase-2 gene promoter polymorphisms affect susceptibility to hepatitis C virus infection and disease progression. Hepatol Res 2010, 40:1219–1226.PubMedCrossRef Competing interests The authors declared that they have no competing interest. Authors’ contributions YHC, HHZ and HSC contributed SAHA HDAC nmr to the conception and design of the study. YHC and HHZ performed the statistical analysis and drafted and revised the manuscript. JXZ and WJL collected blood samples. GXH and RF performed the technical experiments. XWX interpreted the molecular analyses. LLQ collected blood samples and clinical information. LW participated in the design of the study and collected the clinical information. All authors read and approved the final version of the manuscript.”
“Background Pleural effusion is a common disease that is caused by pulmonary carcinomas and other malignant tumors, such as breast cancer and ovarian cancer, and even some nonmalignant diseases including tuberculosis and pneumonia [1, 2]. Malignant pleural effusion (MPE) is usually associated with cancer-related selleck chemical mortality and morbidity. Thus,

it is important to diagnose MPEs and to treat and evaluate prognosis. Cytology detection is the conventional method used to distinguish tumor cells in pleural effusions, Ixazomib manufacturer as described in the International Union Against Cancer/American Joint Committee on Cancer’s tumor-node metastasis (TNM) classification system [3]. However, cytology detection is imperfect in diagnosing MPEs. Moreover, when pleural effusion cytology cannot establish a patient’s diagnosis, additional invasive procedures must be performed to sample pleura for histological examination to enhance the diagnostic rate [2]. However, there are high risks associated with these procedures, and many hospitals do not have these

technologies, which limits their clinical application. Therefore, the diagnosis of MPE presents challenges to clinicians, and it is urgent to search for an effective diagnostic biomarker for this disease. Lung cancer markers, including carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), squamous cell carcinoma (SCC) antigen, and cytokeratin 19 (CK19), have been generally utilized to identify malignant and nonmalignant pleural effusions [4–7]. However, the diagnostic utility of these markers is unsatisfactory. Lung-specific X protein (Lunx), which was isolated by Yoshiyuki and colleagues through differential-display mRNA analysis, is a 206 bp cDNA fragment specifically amplified in the lung [8]. The Lunx gene consists of 1,015 nucleotides, including an open reading frame of 768 nucleotides that encodes 256 amino acids [8].

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