The entity of serrated adenoma of the colorectum was first proposed in 1990, and it was characterized as epithelial neoplasia combining the architectural features of a hyperplastic polyp with the cytological features ...The entity of serrated adenoma of the colorectum was first proposed in 1990, and it was characterized as epithelial neoplasia combining the architectural features of a hyperplastic polyp with the cytological features of an adenoma. Over the past few years, various clinicopathological studies on serrated adenoma have been reported, but its histogenesis remains unclear. Recently the existence of a “ serrated neoplasia pathway" leading to malignancy, which is different from the so- called adenoma- carcinoma sequence, has been discussed. Yao et al. reported that hyperplastic polyps and serrated adenomas share a common cell lineage with gastric differentiation. To clarify the existence of the serrated neoplasia pathway, we performed immunohistochemical staining of cytokeratin 7 (CK7) and cytokeratin 20 (CK20), which are commonly used to determine the primary site of a metastatic lesion, and we examined the pattern of CK7/CK20 expression in various colorectal lesions including 44 serrated adenomas, 25 hyperplastic polyps, 20 traditional adenomas, and 48 carcinomas. An obvious difference existed in the pattern of CK7/CK20 expression between the serrated lesions (hyperplastic poly- ps and serrated adenomas) and others. The majority of serrated adenomas and hyperplastic polyps presented a CK7+ /CK20+ pattern, whereas most conventional adenomas and adenocarcinomas expressed CK7- /CK20+ . Adenocarcinoma developing in serrated adenoma also presented a CK7+ /CK20+ pattern. There are several reports that CK7 is a possible marker of transient dedifferentiation in the gastric carcinogenesis process. Taken together with the present results, a distinct pathway of colorectal carcinogenesis must exist, which is different from the adenoma- carcinoma sequence. CK7 is a possiblemarker for the serrated neoplasia pathway of colorectal carcinogenesis.展开更多
Microwave coagulation therapy (MCT) has recently been applied to treat hepatic tumors. However, the histological changes in the liver following MCT have not been fully elucidated. A type of cell death known as microwa...Microwave coagulation therapy (MCT) has recently been applied to treat hepatic tumors. However, the histological changes in the liver following MCT have not been fully elucidated. A type of cell death known as microwave fixation has been reported in areas adjacent to the microwave irradiator electrodes, and these areas are without acid phosphatase (AcP) activity. Diagnosis of microwave- fixed tissue by hematoxylin and eosin (HE) staining is very difficult because morphology is well maintained for months. In an effort to clarify the histological changes and the mechanisms of microwave fixation, we performed HE staining, enzyme histochemistry for AcP, and electron microscopy in both rat and human liver samples after MCT. Although the microwave- fixed tissues maintained their structure on HE staining, membranes of microwave- fixed cells were seriously damaged and there were no apparent organelle structures in these cells on electron microscopy. Erythrocytes were also damaged in these tissues on both light and electron microscopy. The cause of microwave fixation is thought to be injury of the membrane, which is similar to coagulative necrosis. In conclusion, microwave fixation can be considered a type of coagulative necrosis without enzyme digestion. Disruption of erythrocytes on HE staining is an interesting and important diagnostic clue in distinguishing nonviable fixed tissues from viable tissues following MCT.展开更多
文摘The entity of serrated adenoma of the colorectum was first proposed in 1990, and it was characterized as epithelial neoplasia combining the architectural features of a hyperplastic polyp with the cytological features of an adenoma. Over the past few years, various clinicopathological studies on serrated adenoma have been reported, but its histogenesis remains unclear. Recently the existence of a “ serrated neoplasia pathway" leading to malignancy, which is different from the so- called adenoma- carcinoma sequence, has been discussed. Yao et al. reported that hyperplastic polyps and serrated adenomas share a common cell lineage with gastric differentiation. To clarify the existence of the serrated neoplasia pathway, we performed immunohistochemical staining of cytokeratin 7 (CK7) and cytokeratin 20 (CK20), which are commonly used to determine the primary site of a metastatic lesion, and we examined the pattern of CK7/CK20 expression in various colorectal lesions including 44 serrated adenomas, 25 hyperplastic polyps, 20 traditional adenomas, and 48 carcinomas. An obvious difference existed in the pattern of CK7/CK20 expression between the serrated lesions (hyperplastic poly- ps and serrated adenomas) and others. The majority of serrated adenomas and hyperplastic polyps presented a CK7+ /CK20+ pattern, whereas most conventional adenomas and adenocarcinomas expressed CK7- /CK20+ . Adenocarcinoma developing in serrated adenoma also presented a CK7+ /CK20+ pattern. There are several reports that CK7 is a possible marker of transient dedifferentiation in the gastric carcinogenesis process. Taken together with the present results, a distinct pathway of colorectal carcinogenesis must exist, which is different from the adenoma- carcinoma sequence. CK7 is a possiblemarker for the serrated neoplasia pathway of colorectal carcinogenesis.
文摘Microwave coagulation therapy (MCT) has recently been applied to treat hepatic tumors. However, the histological changes in the liver following MCT have not been fully elucidated. A type of cell death known as microwave fixation has been reported in areas adjacent to the microwave irradiator electrodes, and these areas are without acid phosphatase (AcP) activity. Diagnosis of microwave- fixed tissue by hematoxylin and eosin (HE) staining is very difficult because morphology is well maintained for months. In an effort to clarify the histological changes and the mechanisms of microwave fixation, we performed HE staining, enzyme histochemistry for AcP, and electron microscopy in both rat and human liver samples after MCT. Although the microwave- fixed tissues maintained their structure on HE staining, membranes of microwave- fixed cells were seriously damaged and there were no apparent organelle structures in these cells on electron microscopy. Erythrocytes were also damaged in these tissues on both light and electron microscopy. The cause of microwave fixation is thought to be injury of the membrane, which is similar to coagulative necrosis. In conclusion, microwave fixation can be considered a type of coagulative necrosis without enzyme digestion. Disruption of erythrocytes on HE staining is an interesting and important diagnostic clue in distinguishing nonviable fixed tissues from viable tissues following MCT.
