Colorectal adenocarcinoma with rhabdoid phenotype is extremely rare, and only 1 case of adenocarcinoma showing rhabdoid dedifferentiation has been reported. The authors present another case of cecal adenocarcinoma with prominent rhabdoid feature in a 66-year-old man. The 13-cm sized tumor consisted mainly of rhabdoid cells and partly of adenocarcinoma, and transition from adenocarcinoma to rhabdoid areas was noted. Ultrastructural analysis revealed intracytoplasmic aggregates of intermediate filaments in the rhabdoid cells. Adenocarcinoma cells were diffusely immunoreactive to cytokeratin 7 and AE1/3, but occasionally positive for vimentin. The rhabdoid cells were negative for cytokeratin 7, weakly/focally immunoreactive to AE1/3, and diffusely positive for vimentin. These results suggested that the rhabdoid cells were dedifferentiated adenocarcinoma. Analysis of the rhabdoid cells with molecular techniques is also presented.

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Regenerating gene family members 1 (REG Ia) and 4 (REG IV) are overexpressed in a subset of gastric cancers. However, comparative characterization of the expression of these family proteins has remained unclear. Therefore, we aimed to elucidate not only the association between REG protein expression and mucin phenotype but also their significance as a prognostic marker for patients with gastric cancer. The expression of REG Ia, REG IV, CDX2, MUC2, and MUC5AC in gastric cancer tissues was examined by immunohistochemistry. The relationship between REG protein expression and clinicopathological parameters or mucin phenotype was then analyzed. REG Ia and REG IV expression was positive in 33 (52%) and 31 (49%) of 63 gastric cancers examined, respectively. REG Ia expression was significantly related to venous invasion and tumor stage, whereas REG IV expression showed no relationship to clinicopathological features. With regard to mucin phenotype, REG IV expression was significantly correlated with MUC2 and CDX2 expression, suggesting an association with the intestinal mucin phenotype of gastric cancer. On the other hand, REG Ia expression had no correlation with MUC2, CDX2, or MUC5AC in gastric cancer tissues. Expression of REG Ia but not REG IV was an independent predictor of poor outcome in patients with gastric cancer. In addition, patients with gastric cancer negative for both REG Ia and REG IV expression had a significantly better outcome than patients positive for either REG Ia or REG IV. Profiling of REG protein expression is useful to for prognostication of patients with gastric cancer. Modern Pathology ( The regenerating gene (Reg) was originally isolated from regenerating rat pancreatic islets, 1 and its gene product was shown to have a trophic effect on not only islet but also gastric epithelial cells. 2,3 Recently, many Reg-related genes have been isolated and shown to constitute a multigene family. 4 Among human REG family proteins, REG Ia and REG IV are reportedly overexpressed in a subset of gastric cancer. 5-9 Moreover, several microarray analyses have recently isolated REG Ia and REG IV as novel genes that are overexpressed in gastric cancer tissues, 10,11 suggesting that both genes have important functions in gastric carcinogenesis. Indeed, we have previously clarified that REG Ia acts as a trophic and/or anti-apoptotic factor in the development of gastric cancer, 12 and others have reported that REG IV protein confers cell resistance to chemotherapeutic agents, 9 suggesting that these proteins are both associated with tumor progression. It is noteworthy that in non-neoplastic tissues REG Ia and REG IV are commonly expressed not only in endocrine cells but also in metaplastic cells that frequently accompany gastric cancer lesions, 5,8,12,13 implying a possible link between REG protein expression and mucin phenotype of gastric lesions. In addition, there is increasing speculation as to whether REG Ia and REG IV protein expression may

Stimulation of the CD155/poliovirus receptor, which localizes in the cell-matrix and at cell-cell junctions, inhibits cell adhesion and enhances cell migration. Necl-5, a mouse homolog of CD155, is implicated in the formation of adherence junctions. Recently, Necl-5 has also been found to enhance cell proliferation via the stimulation of serum and platelet-derived growth factor through the Ras-Raf-MEK-ERK signaling pathway. In our present study, we find that CD155 significantly enhances the serum-induced cell proliferation of NIH3T3 cells which have been transformed by an oncogenic Ras (V12Ras-NIH3T3), but not the parental cells. CD155 expression in V12Ras-NIH3T3 cells is also found to upregulate cyclin D2, downregulate p27 Kip1 and shorten the G 0 /G 1 phase of the cell cycle. An inhibitor of focal adhesion kinase does not reduce this CD155-mediated enhancement of V12Ras-NIH3T3 cell proliferation. The expression of CD155DCP, which lacks the cytoplasmic region including the immunoreceptor tyrosine-based inhibitory motif (ITIM), has a reduced ability to enhance the serum responsiveness of V12Ras-NIH3T3 cells, suggesting that the ITIM might be required for this effect of CD155. In addition, the overexpression of exogenous CD155 enhances the serum responsiveness of HT1080 cells, which harbor a mutant N-ras gene. On the other hand, siRNA-induced knockdown of endogenous CD155 and/or CD155DCP expression significantly repress the serum responsiveness of DLD-1 cells, which express endogenous CD155 and harbor a mutant K-ras gene, suggesting that this mutant may function in a dominant negative manner. Taken together, our present data suggest that CD155, at least in part, enhances the proliferation of ras-mutated cells. ' 2007 Wiley-Liss, Inc.Key words: CD155; Necl-5; ras; proliferation CD155 is an immunoglobulin-like molecule containing a domain structure that comprises 1 extracellular region with 3 immunoglobulin-like loops, 1 single transmembrane region and 1 short cytoplasmic region. 1 CD155 is ubiquitously expressed in many human tissues, including the brain, kidney, ileum, liver, lung, placenta and leukocytes, 1,2 and was originally identified as the receptor for the human poliovirus, which causes the characteristic flaccid paralysis of poliomyelitis. 1-3 CD155 has 4 spliced variants, 2 a and d membrane-bound forms, which serve as the poliovirus receptor, and the b and g forms which are secreted versions of this protein. 2 The transmembrane isoform CD155a, however, is the principle variant, and comprises 65-70% of the gene transcripts. 4 In our present study, the term ''CD155'' denotes the a variant unless otherwise stated.CD155 has been reported to be involved in cell-cell adhesion via a heterophilic trans-interaction with nectin-3 and stimulation of this receptor has been shown to inhibit cell adhesion and enhance cell migration. 5,6 CD155 is also overexpressed in many human cancer cells, 4,6,7 but the significance of this has remained elusive.Mouse nectin-like molecule-5 (Necl-5)/tumor-associated glycoprotein E4 i...