Detection of Extrinsic Text Plagiarism using Natural Language Processing and Intelligent Computing Techniques

Abstract

Gallbladder cancer (GBC) is a prevalent cancer of the biliary tract and is the fifth common cancer of the gastrointestinal tract worldwide in term of incidence. It often manifests at an advanced and unresectable stage. The detection of GBC is incidental with complete surgical resection being the only potential curative option. The prognosis is dismal with a one year survival rate of 10% for advanced stages. Various markers including carbohydrate antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) have been explored in the diagnosis of GBC. However, they lack sensitivity and specificity in the diagnosis of GBC. The response to chemotherapy and radiotherapy is extremely limited without significant improvement in the disease prognosis and quality of life. Targeted therapy for GBC is limited with bevacizumab, which is a vascular endothelial growth factor (VEGF) inhibitor. Apart from bevacizumab, other targeted therapies such as estrogen receptor, hedgehog signaling and mTOR inhibitors are pending clinical validation. This calls for an immediate need to identify novel therapeutic targets to improve treatment options and disease outcome. A better understanding of the molecular mechanisms involved in the pathogenesis of the disease will aid in developing novel targeted therapies for patients with GBC. In this study, a proteomic analysis of GBC cell lines was carried out using an isobaric tags for relative and absolute quantitation (iTRAQ) labeling-based quantitative proteomic approach. Four GBC cell lines were chosen for this study based on their invasive ability (non-invasive to highly invasive). The quantitative proteomic experiment led to the identification of 3,653 proteins, of which 654 were found to be overexpressed and 387 to be downregulated in the invasive GBC cell lines (OCUG-1, NOZ and GB-d1) compared to the non-invasive GBC cell line, TGBC24TKB. Among the overexpressed proteins, macrophage migration inhibitory factor (MIF) was found to be overexpressed in two of the invasive cell lines.