{"title":"垂体腺瘤的认识进展。","authors":"Vera Popović-Brkić","doi":"10.1159/000192441","DOIUrl":null,"url":null,"abstract":"signalling pathways have been identified as important factors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of current research. This is because current treatment modalities fail to completely control this disorder and prevent the associated morbidity and mortality. Pituitary microadenomas, which have a diameter of less than 1 cm, are exceedingly common at autopsy and on pituitary imaging, with a prevalence of 25%. Most microadenomas remain clinically occult and stable in size without an increase in tumour cells and without local mass effects. Recent studies try to explain this cessation of growth in a neoplasm, which would not be expected to occur. It was thought that apoptosis may play a role in curtailing outgrowth, but this did not explain the maintenance of a stable size for years. Lack of induction of vascular stroma was thought to be relevant, but again was an insufficient explanation. Proliferative activity of microadenomas is very low, indicating that the tumour cells are growth arrested, and in his presentation at the 10th KIGS/ KIMS Expert Meeting, Wolter Mooi introduced the currently most likely factor for growth arrest. The hypothesis is that cells after a certain number of cell divisions display a change in cell phenotype (i.e. they enter into a senescence-like state). Thus, growth arrest in pituitary microadenomas may be due to oncogene-induced cellular senescence. The demonstration that the majority of","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 2 ","pages":"75-7"},"PeriodicalIF":0.0000,"publicationDate":"2009-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000192441","citationCount":"1","resultStr":"{\"title\":\"Advances in understanding pituitary adenomas.\",\"authors\":\"Vera Popović-Brkić\",\"doi\":\"10.1159/000192441\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"signalling pathways have been identified as important factors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of current research. This is because current treatment modalities fail to completely control this disorder and prevent the associated morbidity and mortality. Pituitary microadenomas, which have a diameter of less than 1 cm, are exceedingly common at autopsy and on pituitary imaging, with a prevalence of 25%. Most microadenomas remain clinically occult and stable in size without an increase in tumour cells and without local mass effects. Recent studies try to explain this cessation of growth in a neoplasm, which would not be expected to occur. It was thought that apoptosis may play a role in curtailing outgrowth, but this did not explain the maintenance of a stable size for years. Lack of induction of vascular stroma was thought to be relevant, but again was an insufficient explanation. Proliferative activity of microadenomas is very low, indicating that the tumour cells are growth arrested, and in his presentation at the 10th KIGS/ KIMS Expert Meeting, Wolter Mooi introduced the currently most likely factor for growth arrest. The hypothesis is that cells after a certain number of cell divisions display a change in cell phenotype (i.e. they enter into a senescence-like state). Thus, growth arrest in pituitary microadenomas may be due to oncogene-induced cellular senescence. The demonstration that the majority of\",\"PeriodicalId\":13225,\"journal\":{\"name\":\"Hormone research\",\"volume\":\"71 Suppl 2 \",\"pages\":\"75-7\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000192441\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Hormone research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000192441\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2009/4/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hormone research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000192441","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2009/4/29 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
signalling pathways have been identified as important factors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of current research. This is because current treatment modalities fail to completely control this disorder and prevent the associated morbidity and mortality. Pituitary microadenomas, which have a diameter of less than 1 cm, are exceedingly common at autopsy and on pituitary imaging, with a prevalence of 25%. Most microadenomas remain clinically occult and stable in size without an increase in tumour cells and without local mass effects. Recent studies try to explain this cessation of growth in a neoplasm, which would not be expected to occur. It was thought that apoptosis may play a role in curtailing outgrowth, but this did not explain the maintenance of a stable size for years. Lack of induction of vascular stroma was thought to be relevant, but again was an insufficient explanation. Proliferative activity of microadenomas is very low, indicating that the tumour cells are growth arrested, and in his presentation at the 10th KIGS/ KIMS Expert Meeting, Wolter Mooi introduced the currently most likely factor for growth arrest. The hypothesis is that cells after a certain number of cell divisions display a change in cell phenotype (i.e. they enter into a senescence-like state). Thus, growth arrest in pituitary microadenomas may be due to oncogene-induced cellular senescence. The demonstration that the majority of