To determine whether p53 alterations, which are frequent in human breast cancers, are also common in rat mammary tumors, we examined 40 tumors from 24 rats treated with 7,12-dimethylbenz[a]anthracene (DMBA) and 34 tumors from 14 rats treated with N-nitroso-N-methylurea (NMU) (an N-nitroso compound). DMBA and NMU are known genotoxic mutagens. The entire coding regions of the p53 and Ha-ras genes were examined for mutations by polymerase chain reaction single-strand conformational polymorphism analysis and by direct sequencing. One of the 40 DMBA-induced mammary tumors had a p53 mutation, a single-base substitution (AGC-->GGC) at codon 307, resulting in an amino-acid change from Ser to Gly. No mutations were found in NMU-induced tumors. The incidence of Ha-ras gene mutation was 79% (27 of 34) at codon 12 in the NMU group and 23% (nine of 40) at codon 61 in the DMBA group. Thus, p53 mutation, in contrast to Ha-ras mutation, did not seem to be a prerequisite for carcinogenesis in chemically induced rat mammary tumors.

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Mutations of the APC gene frequently occur in sporadic forms of colorectal adenomas and adenocarcinomas. Phenotypically, the vast majority of these mutations result in the truncation of the APC protein. To demonstrate the defective APC gene product in human colorectal tumors, rabbit region-specific antisera raised against the APC protein of amino acid sequences between 371 and 390 (SPI) and between 1821 and 1840 (SP3) were used to exhibit the truncated APC protein. In all, 86 lesions from 67 cases of sporadic adenoma and adenocarcinoma were examined; abnormal staining patterns were distinguished in 43 lesions (50%); the incidence of abnormalities was not significantly different between adenomas and carcinomas. The majority, 75% exhibited epitopic change with the SPI-positive and SP3-negative phenotype (type P1), and 25% exhibited neither of these phenotypes (type P2). The staining pattern in all lesions was uniform, and studies of carcinomas arising in adenomas showed the same pattern of staining. These findings supported the view that the APC lesion is a very early event in colorectal carcinogenesis. Furthermore, this simple immunohistochemical approach demonstrated that different adenomas from the same patient showed different staining patterns.

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Herewereportacaseofawidespreadcoloninjurybycompressedair.A33-year-oldmanwasadmittedtotheemergencydepartmentofourhospital.Hecomplainedofsevereabdominalpainandhematocheziaimmediatelyafteraccidentalblowingofcompressedairintohisanusathisworkplace.Computed tomography showed no intraperitoneal free air and slight intestinal emphysema at the splenic flexure. Laparoscopic surgery for observation was performed. Widespread colon injury became evident;therefore,thesurgerywasconvertedtolaparotomy.Wenotedmultipleseromuscularlacerationsandsubserosalhemorrhages,butnoperforations.Theinjurywasrepairedandanileostomywasperformed.Early diagnosisandaggressivetreatmentresultedingoodprognosis.

Mucinous cystadenoma of the pancreas is considered as a premalignant lesion, and resection is recommended. The majority of pancreatic cystic lesions are pancreatic pseudocysts, so differentiation between mucinous cystadenoma and pseudocyst is frequently required. We report a rare case of mucinous cystadenoma of the pancreas coexisting with pseudocyst. A 43-year-old woman presented with abdominal pain. Imaging examinations showed a large cystic lesion in the tail of the pancreas, and distal pancreatectomy and splenectomy were performed. Pathological examination revealed that the majority of the cystic wall comprised thick collagen fibrous connective tissue, while part of the cystic wall represented a single layer of columnar, mucin-producing epithelium without atypia. Those findings suggested mucinous cystadenoma with an inflammatory pseudocyst. The mixture of mucinous cystadenoma and pseudocyst within the same cystic lesion appears to be very rare. Complete resection of the cystic lesion seems to allow an excellent prognosis.

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