Cancer is a very complicated process, characterized by the uncontrolled, unbalanced overgrowth of malignant cells. The complexity of oncogenic processes and cancer progressions has demanded the discovery of biomarkers with a high sensitivity and specificity for diagnosis, prognosis, diseases monitoring, and therapeutic response prediction. Unfortunately, a discrete biomarker for colon cancer has yet to be discovered, although nearly 800,000 new colorectal cancer cases are thought to globally occur each year, which account for ϳ10% of all incident cancers, and the mortality from colorectal cancer is estimated at nearly 450,000 per year (1). MLI1 and MSH genes are associated with hereditary non-polyposis colon cancer (2), and the APC gene is associated with familial adenomatous polyposis (3), but those factors fail to account for an occurrence of wide range of colon cancer. Moreover, colon cancer is one of the epithelium-derived cancers in which the circumstantial factors govern over hereditary genetic factors. These require a clear marker that serves as tracer molecule for the efficacious treatment of colon cancer.Recent proteomics have focused on a dynamic alteration of post-translational modification of proteins, and many lines of evidence indicate that changes in post-translational modification of proteins are closely associated with the pathogenic processes of cells. An aberrant glycosylation induced by Nacetylglucosaminyltransferase V (GnT-V), 1 is a representative example of such protein modification as is implicated in tumor progression. An increase in ␤1,6-branching on N-linked glycans is associated with metastatic potential of cancer cells (4). Several target molecules for GnT-V were proposed to be involved in cancer progressions, including matriptase (5), ␤ 1 integrin (6), and N-cadherin (7). However, those proteins are membrane-bound proteins and were not demonstrated to be aberrantly glycosylated in sera or tissues of cancer patients. Recent work stresses the discrete roles of the microenviron-

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Pulmonary tuberculosis (TB) is a known risk factor for lung cancer. However, a detailed analysis of lung cancer type, age, sex, smoking, and TB burden associated with geographic and socioeconomic status has not been performed previously. We systematically appraised relevant observational studies reporting an association between pulmonary TB and lung cancer. All studies were included in the primary analysis, and studies that used robust TB diagnostic methods, such as validated medical diagnostic codes, were included in the secondary analysis. Thirty-two articles were included. The association between the history of pulmonary TB and diagnosis of lung cancer was statistically significant (OR 2.09, 95% CI: 1.62–2.69, p < 0.001). There was a high heterogeneity (I2 = 95%), without any publication bias. The analysis indicated a high association in advanced articles describing stringent pulmonary TB diagnosis (OR 2.26, 95% CI: 1.29–3.94, p = 0.004). The subgroup analyses suggested a significant association in countries with medium or high TB burdens, from East Asia and the Pacific region, and upper-middle income countries. Heterogeneity within the subgroups remained high in a majority of the subgroup analyses. A meta-regression analysis revealed that younger patients showed a significantly higher association between TB and lung cancer (regression coefficient = 0.949, p < 0.001). The history of pulmonary TB is an independent risk factor for lung cancer, especially in younger patients diagnosed with pulmonary TB. Clinicians should be aware of this association while treating young patients with a history of pulmonary TB.

To understand better the mechanism underlying gastric cancer and search for potential markers for gastric cancer prognosis, the proteomic analysis of gastric cancer tissues was conducted using two-dimensional gel electrophoresis and lectin blot, followed by electrospray ionization-mass spectrometry. These approaches permitted identification of glyco- or putative glycosylated proteins which may be associated with tumorigenesis. The proteins identified include molecules involved in sugar metabolism, signal transduction, proteolysis, and stress, as well as several unknown proteins, which were aberrantly glycosylated as evidenced by the L-phytohemagglutinin blot.

It is known that the etiology and clinical outcomes of autoimmune diseases are associated with a combination of genetic and environmental factors. In the case of the genetic factor, the SNPs of the PTPN22 gene have shown strong associations with several diseases. The recent exploding numbers of genetic studies have made it possible to find these associations rapidly, and a variety of autoimmune diseases were found to be associated with PTPN22 polymorphisms. Proteins encoded by PTPN22 play a key role in the adaptative and immune systems by regulating both T and B cells. Gene variants, particularly SNPs, have been shown to significantly disrupt several immune functions. In this review, we summarize the mechanism of how PTPN22 and its genetic variants are involved in the pathophysiology of autoimmune diseases. In addition, we sum up the findings of studies reporting the genetic association of PTPN22 with different types of diseases, including type 1 diabetes mellitus, systemic lupus erythematosus, juvenile idiopathic arthritis, and several other diseases. By understanding these findings comprehensively, we can explain the complex etiology of autoimmunity and help to determine the criteria of disease diagnosis and prognosis, as well as medication developments.