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Overweight is believed to be associated with colorectal cancer risk. Adipose tissue is loose connective tissue composed of adipocytes. It is now recognized as a major endocrine organ, secreting humoral factors collectively called adipokines. Aberrant hormonal systems consisting of modulated adipokines and their receptors are thought to play a role in colorectal carcinogenesis and cancer progression in obese conditions. However, it is still unclear whether and how each adipokine relates to colorectal carcinogenesis. Notably, a couple of molecules that were initially proposed to be obesity-related adipokines were disqualified by subsequent studies. The adipokines, adiponectin, and intelectin-1 (also known as omentin-1), whose levels are decreased in obesity, act as tumor suppressor factors in various cancers. Numerous studies have demonstrated a link between the insufficient expression and function of adiponectin and its receptor, T-cadherin, in colorectal carcinogenesis. Moreover, our recent study indicated that loss of TMEM207, which is critical for the proper processing of intelectin-1 in the colon mucosa, leads to insufficient intelectin-1 production, thus participating in colorectal carcinogenesis. Here, we discuss the recent understanding of the role of adipokines in colorectal carcinogenesis and subsequently describe the potent tumor suppressor roles of intelectin-1 and TMEM207 in colorectal cancer. [ABSTRACT FROM AUTHOR]

“Amphicrine” (in Greek, amphi-means “both” or “double”) refers to cells that synchronously exhibit the endocrine and exocrine phenotypes. Gastric amphicrine carcinoma is very rare, and only a few case reports are found in the English literature; thus, its pathobiological features remain unclear. Here, we report a case of amphicrine gastric carcinoma. A woman in her sixth decade of life presented with anemia and underwent upper endoscopy, followed by histopathological examination of biopsy specimens. She appeared to have gastric cancer with a tumor measuring 5.0 cm × 4.0 cm in size. Subsequently, the patient underwent total gastrectomy with lymph node dissection. Histopathological examination revealed a poorly cohesive carcinoma that sparsely coexisted with signet-ring cell carcinoma cells with regional lymph node metastasis. Interestingly, synaptophysin immunoreactivity with the coexistence of Alcian blue was found in individual signet-ring cell carcinoma cells. Furthermore, the present amphicrine carcinoma cells immunohistochemically expressed CD44 variant 9, a functional cancer stem cell marker. We believe that the present case findings may support the idea of multipotent stem cells being an origin of amphicrine gastric cancers. [ABSTRACT FROM AUTHOR]

Background: Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive and associated with poor prognosis. Basic research to develop new treatment regimens is critically needed. Methods: The effects of imatinib mesylate on MPNSTs were examined in six human MPNST cell lines and in a xenograft mouse model. Results: The results showed expression of platelet-derived growth factor receptor-β and suppression of its phosphorylation by imatinib mesylate in all six cell lines. Imatinib mesylate effectively suppressed MPNST cell growth in vitro at concentrations similar to those used clinically (1.46 - 4.6 μM) in three of six cell lines. Knockdown of PDGFR-β by transfection with a specific siRNA also caused significant reduction in cell proliferation in the sensitive cell lines, but not in the resistant cell lines. Furthermore, imatinib mesylate also significantly suppressed colony formation within soft agar and tumor growth in xenograft models using two of the three sensitive MPNST cell lines. There was excellent agreement between in vitro and in vivo sensitivity to imatinib mesylate, suggesting possible selection of imatinib-sensitive tumors by in vitro analysis. Conclusions: The results suggest that imatinib mesylate may be useful in the treatment of MPNST patients and in vitro studies may help select cells that are sensitive to imatinib mesylate in vivo. [ABSTRACT FROM AUTHOR]