Adenoma malignum of the uterine cervix (mucinous type of minimal deviation adenocarcinoma, mucinous MDA), is a unique neoplasm that is difficult to diagnose owing to the deceptively benign appearance of the tumour cells. The present study was undertaken to explore the phenotypic expression of this tumour compared with those of non-neoplastic cervical tissues and of cervical carcinomas of various types. Ten cases of mucinous MDA, 50 cases with non-neoplastic cervical tissues, 13 of cervical adenocarcinoma including the mucinous (endocervical or intestinal type) and endometrioid types, and 2 of mucoepidermoid carcinoma were examined by various histochemical staining methods, including those for gastric mucins, pepsinogen, lysozyme, chromogranin A and carcinoembryonic antigen. The results revealed that mucinous MDA characteristically exhibited gastric phenotypes. The presence of gastric metaplasia was also demonstrated in 9 cases of mucinous MDA and in 5 of the other cases examined. The 7 endocervical-type adenocarcinomas also included 4 that expressed gastric phenotypes, and 2 of the 3 intestinal-type adenocarcinomas showed the same properties focally. These results indicate the presence of a group of lesions expressing gastric phenotypes in the uterine cervix and suggest a close relationship between these lesions. Cervical adenocarcinomas expressing gastric phenotypes are probably derived from MDA.
Purposes: Fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) has been widely used for the diagnosis of pancreatic cancer. Because autoimmune pancreatitis is easily misdiagnosed as pancreatic cancer and can be tested for by FDG-PET analysis based on the presence of suspected pancreatic cancer, we attempted to clarify the differences in FDG-PET findings between the two conditions. Methods: We compared the FDG-PET findings between 15 patients with autoimmune pancreatitis and 26 patients with pancreatic cancer. The findings were evaluated visually or semiquantitatively using the maximum standardized uptake value and the accumulation pattern of FDG. Results: FDG uptake was found in all 15 patients with autoimmune pancreatitis, whereas it was found in 19 of 26 patients (73.1%) with pancreatic cancer. The accumulation pattern of nodular shape was frequently seen in pancreatic cancer with significance, whereas a longitudinal shape indicated the existence of autoimmune pancreatitis. Heterogeneous accumulation was found in almost all cases of autoimmune pancreatitis, whereas homogeneous accumulation was found in pancreatic cancer. Most cases of pancreatic cancer showed solitary localization with significant difference, whereas multiple localizations in the pancreas favored the existence of autoimmune pancreatitis. FDG uptakes in the hilar lymph node were more frequently seen in autoimmune pancreatitis than in pancreatic cancer with significance, and those in the lachrymal gland, salivary gland, biliary duct, retroperitoneal space, and prostate were only seen in autoimmune pancreatitis. Conclusions: FDG-PET provides a useful tool for differentiating autoimmune pancreatitis from suspected pancreatic cancer, if its accumulation pattern and extra-pancreatic involvements are considered. IgG4 measurement and other current image tests will confirm further diagnosis.
Cancer chemotherapy targeted to angiogenic vessels is expected to cause indirect tumor regression through the damage of the neovasculature without the induction of drug resistance. To develop a tool for neovasculaturespeci®c drug delivery, we isolated novel peptides homing to angiogenic vessels formed by a dorsal air sac method from a phage-displayed peptide library. Three distinct phage clones that markedly accumulated in murine tumor xenografts presented PRPGAPLAGSWPGTS-, DRWRPALPVVLFPLH-or ASSSYPLIHWRPWARpeptide respectively. After the determination of the epitope sequences of these peptides, we modi®ed liposomes with epitope penta-peptides. Liposome modi®ed with APRPG-peptide showed high accumulation in murine tumor xenografts, and APRPG-modi®ed liposome encapsulating adriamycin eectively suppressed experimental tumor growth. Finally, speci®c binding of APRPG-modi®ed liposome to human umbilical endothelial cells, and that of PRP-containing peptide to angiogenic vessels in human tumors, i.e., islet cell tumor and glioblastoma, were demonstrated. The present study indicates the usefulness of APRPG-peptide as a tool for anti-neovascular therapy, a novel modality of cancer treatment.
The protective ability of gastric mucins may depend largely on their oligosaccharide chains. We evaluated the effects of H. pylori infection on the glycosylation of gastric mucins. Gastric biopsy specimens from 20 H. pylori-infected patients before and after cure of the H. pylori infection and 8 normal uninfected volunteers were examined by immunostaining for simple mucin-type glycoproteins and blood-group-related antigens bearing type 1 chain backbone. The immunoreactivity in different gastric compartments was evaluated. Simple mucin-type glycoproteins and blood-group-related antigens were expressed in surface mucous cells. Simple mucin-type glycoproteins showed antrum-predominant expression in normal volunteers and were found in significantly fewer surface mucous cells in infected patients than in normal volunteers; their expression was restored after eradication of H. pylori. Sialyl Lewis(a) and Lewis(b) were expressed in fewer surface mucous cells after than before eradication. The patterns of glycosylation of gastric mucins vary in different gastric compartments and are reversibly altered by H. pylori infection. These alterations may affect the protective functions of gastric mucins.
Hilar and pancreatic accumulation of gallium-67 is a characteristic feature of autoimmune pancreatitis during the active stage of the disease, when IgG4 serum levels are high.
ADP was expressed in a small proportion of lung ADCs. ADP-positive lung ADC was significantly associated with apocrine-like features, wild-type EGFR, and poor prognosis, suggesting that ADP-positive lung ADC could be a distinct subtype of lung adenocarcinoma, induced by up-regulation of the lipogenic pathway.
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