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Immature myeloid cells, also known as myeloid-derived suppressor cells (MDSCs), include neutrophilic and monocytic myeloid cells, and are found in inflammatory loci and secondary lymphoid organs in mice with intestinal inflammation, inflammatory bowel disease (IBD) patients, and tumor tissues. However, the roles of MDSCs in IBD are not yet well understood, and there are controversies regarding their immunosuppressive functions in IBD. In addition, recent studies have suggested that endoplasmic reticulum (ER) stress in intestinal epithelial cells, especially in Paneth cells, is closely associated with the induction of IBD. However, the ER stress in MDSCs accumulated in the inflamed tissues of IBD patients is not yet fully understood. In the current review, we discuss the presence of accumulated MDSCs in the intestines of IBD patients, and further speculate on their physiological roles in the inflammatory condition with interleukin 17-producing cells, including Th17 cells. In particular, we will discuss the divergent functions of MDSCs in ER stressed intestinal environments, including their pro-inflammatory or immunosuppressive roles, based on the consideration of unfolded protein responses initiated in intestinal epithelial cells by ER stress.

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Overwhelming evidences supports the idea that inflammatory bowel disease (IBD) is caused by a complex interplay between genetic alterations of multiple genes and an aberrant interaction with environmental factors. There is growing evidence that epigenetic factors can play a significant part in the pathogenesis of IBD. Significant effort has been invested in uncovering genetic and epigenetic factors, which may increase the risk of IBD, but progress has been slow, and few IBD-specific factors have been detected so far. It has been known for decades that DNA methylation is the most well studied epigenetic modification, and analysis of DNA methylation is leading to a new generation of cancer biomarkers. Therefore, in this review, we summarize the role of DNA methylation alteration in IBD pathogenesis, and discuss specific genes or genetic loci using recent molecular technology advances. Here, we suggest that DNA methylation should be studied in depth to understand the molecular pathways of IBD pathogenesis, and discuss epigenetic studies of IBD that may have a significant impact on the field of IBD research.

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Behçet's disease (BD) is a systemic vasculitis, while myelodysplastic syndrome (MDS) is a heterogeneous group of clonal hematologic disorders characterized by ineffective hematopoiesis. Some studies suggest a relationship between MDS and BD, especially intestinal BD, and trisomy 8 seems to play an important role in both diseases. There are several reports on patients with BD comorbid with MDS involving trisomy 8 that frequently have intestinal lesions refractory to conventional medical therapies. Tumor necrosis factor (TNF)-α is strongly involved in the pathophysiology of several autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease, and BD. In addition, TNF-α plays an important role in the pathophysiology of MDS by inhibiting normal hematopoiesis and inducing the programmed cell death of normal total bone marrow cells and normal CD34+ cells. Recent clinical reports demonstrate the favorable effect of TNF-α antagonists in patients with refractory intestinal BD and in those with MDS. We present the case of a patient with intestinal BD and MDS involving trisomy 8 who was successfully treated with adalimumab.

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Anorectal melanoma is a rare neoplasm that accounts for less than 1-4% of anorectal malignant tumors. The main therapeutic modality for anorectal melanoma is surgical treatment, with abdominoperineal resection or wide local excision being the most common approaches. A 77-year-old male with a history of cerebral infarction and hypertension presented with anal bleeding. Here, we report a case of anorectal melanoma treated by endoscopic mucosal resection with adjuvant interferon therapy rather than surgical resection. The patient has been disease-free for 5 years after endoscopic treatment.

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Lymph node metastasis is rare in small (i.e., <10 mm) rectal neuroendocrine tumors (NETs). In addition to tumor size, pathological features such as the mitotic or Ki-67 proliferation index are associated with lymph node metastasis in rectal NETs. We recently treated a patient who underwent endoscopic treatment of a small, grade 1 rectal NET that recurred in the form of perirectal lymph node metastasis 7 years later. A 7-mm-sized perirectal lymph node was noted at the time of the initial endoscopic treatment. The same lymph node was found to be slightly enlarged on follow-up and finally confirmed as a metastatic NET. Therefore, the perirectal lymph node metastasis might have been present at the time of the initial diagnosis. However, the growth rate of the lymph node was extremely low, and it took 7 years to increase in size from 7 to 10 mm. NETs with low Ki-67 proliferation index and without mitotic activity may grow extremely slowly even if they are metastatic.

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