Three cases had lymph node metastases that met the extended criteria for EMR/ESD. EMR and/or ESD should be limited to M cancers without ulcer or differentiated-type M cancer with ulcers smaller than 2 cm. When the depth of tumor invasion is deeper than M, then a gastric resection with lymph node dissection is necessary.
Previously, we found that allogeneic rat heart transplantation induced the blood-borne migration of donor DCs to the host spleen and hepatic lymph nodes (LNs) via the liver. 6 These migrated DCs formed clusters with DNA-synthesizing (5-bromo-2Ј-deoxyuridine [BrdU]-positive [BrdU ϩ ]) host T cells (BrdU ϩ cluster) in which the T cell proliferative response begun, representing the sites of direct allosensitization. 4 Furthermore, host interdigitating DCs captured donor MHC antigens and formed BrdU ϩ clusters with host proliferating cells, suggesting an indirect pathway. 4 Therefore, the BrdU ϩ cluster formation by donor or host DCs in situ could be a hallmark indicating that the alloresponse is ongoing there.
We investigated the role of hepatic macrophages in the inflammatory response following reperfusion injury by blocking Kupffer cell phagocytosis with gadolinium chloride (GdCl3). Liver ischemia was induced in rats by occluding the portal vein for 30 minutes. A bolus of GdCl3 (7 mg/kg) was injected intravenously 1 and 2 days before surgery. The serum levels of cytokine-induced neutrophil chemoattractant (CINC) in untreated rats increased following reperfusion, peaked after 6 hours, and then gradually decreased. GdCl3 or heparin alone significantly decreased the serum levels of CINC (P < .05). In addition, pretreatment with GdCl3/heparin further inhibited the rise in the serum levels of CINC following reperfusion compared with those in untreated animals (P < .01). The in vitro production of CINC by Kupffer cells, obtained from animals pretreated with heparin or GdCl3, was significantly lower than that of cells isolated from untreated animals. Pretreatment with GdCl3/heparin further decreased CINC production by Kupffer cells compared with that of cells from animals that were pretreated with heparin or GdCl3 alone. The expression of CINC transcripts in Kupffer cells or in liver tissue peaked 3 hours after reperfusion in untreated animals. Pretreatment with heparin, GdCl3, or both significantly decreased the levels of CINC messenger RNA (mRNA) transcripts. Pretreatment with heparin, GdCl3, or GdCl3/heparin significantly decreased the number of neutrophils that accumulated in the liver 24 hours following reperfusion, compared with those in untreated animals. These results suggest that Kupffer cells release CINC and may play an important role in early neutrophil infiltration into the liver following ischemia/reperfusion.
Although a randomized, controlled trial concerning survival is necessary, according to this study, there is a possibility that limited resection might be accepted for proximal gastric cancer according to the depth of wall invasion.
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