Identification of CD133+ Cells in Pituitary Adenomas
Stem-like cells in tumors are capable of self-renewal and pluri-differentiation; they are thought to play important roles in tumor initiation and maintenance. Stem-like cells in malignant glioma express CD133. We examined samples from human pituitary adenoma, a generally benign neoplasm, for CD133 e...
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| Veröffentlicht in: | Neuroendocrinology 2011-01, Vol.94 (4), p.302-312 |
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| creator | Yunoue, Shunji Arita, Kazunori Kawano, Hiroto Uchida, Hiroyuki Tokimura, Hiroshi Hirano, Hirofumi |
| description | Stem-like cells in tumors are capable of self-renewal and pluri-differentiation; they are thought to play important roles in tumor initiation and maintenance. Stem-like cells in malignant glioma express CD133. We examined samples from human pituitary adenoma, a generally benign neoplasm, for CD133 expression using routine immunohistochemical and biochemical methods. Our study of 70 pituitary adenomas (clinically nonfunctioning adenomas and growth hormone-, prolactin-, adrenocorticotropic hormone-, and thyroid-stimulating hormone-producing adenomas) showed that 18 (25.7%) expressed CD133. This rate was higher in clinically nonfunctioning (33.3%) than functioning adenomas (12.0%) (p = 0.085). Real-time PCR assay revealed the expression of CD133 mRNA in samples immunohistochemically positive for CD133. Neither the patient age and gender, nor the tumor size or postoperative recurrence rate correlated with CD133 positivity. CD133+ cells ubiquitously coexpressed CD34, nestin, and VEGFR2 (KDL1). S-100 and GFAP were not coexpressed with CD133. Chromogranin A, Pit-1, SF-1, and NeuroD1 were immune-negative, indicating that CD133+ cells did not have the potential to differentiate into functional endocrine cells. Our data suggest that the expression of CD133 in pituitary adenomas is related to immature endothelial progenitor cells that may play a role in the neovascularization of pituitary adenomas. Further studies are needed to elucidate the significance of CD133+ cells with respect to neovascularization and their sustainable growth in pituitary adenomas. |
| doi_str_mv | 10.1159/000330625 |
| format | Article |
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Stem-like cells in malignant glioma express CD133. We examined samples from human pituitary adenoma, a generally benign neoplasm, for CD133 expression using routine immunohistochemical and biochemical methods. Our study of 70 pituitary adenomas (clinically nonfunctioning adenomas and growth hormone-, prolactin-, adrenocorticotropic hormone-, and thyroid-stimulating hormone-producing adenomas) showed that 18 (25.7%) expressed CD133. This rate was higher in clinically nonfunctioning (33.3%) than functioning adenomas (12.0%) (p = 0.085). Real-time PCR assay revealed the expression of CD133 mRNA in samples immunohistochemically positive for CD133. Neither the patient age and gender, nor the tumor size or postoperative recurrence rate correlated with CD133 positivity. CD133+ cells ubiquitously coexpressed CD34, nestin, and VEGFR2 (KDL1). S-100 and GFAP were not coexpressed with CD133. Chromogranin A, Pit-1, SF-1, and NeuroD1 were immune-negative, indicating that CD133+ cells did not have the potential to differentiate into functional endocrine cells. Our data suggest that the expression of CD133 in pituitary adenomas is related to immature endothelial progenitor cells that may play a role in the neovascularization of pituitary adenomas. Further studies are needed to elucidate the significance of CD133+ cells with respect to neovascularization and their sustainable growth in pituitary adenomas.</description><identifier>ISSN: 0028-3835</identifier><identifier>EISSN: 1423-0194</identifier><identifier>DOI: 10.1159/000330625</identifier><identifier>PMID: 21912092</identifier><identifier>CODEN: NUNDAJ</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>AC133 Antigen ; Adenoma - genetics ; Adenoma - metabolism ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Antigens, CD34 - metabolism ; Biological and medical sciences ; Endocrinopathies ; Endothelial Cells - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; Glycoproteins - genetics ; Glycoproteins - metabolism ; Humans ; Hypothalamus. Hypophysis. Epiphysis (diseases) ; Intermediate Filament Proteins - metabolism ; Male ; Medical sciences ; Middle Aged ; Nerve Tissue Proteins - metabolism ; Nestin ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Original Paper ; Peptides - genetics ; Peptides - metabolism ; Pituitary Neoplasms - genetics ; Pituitary Neoplasms - metabolism ; Real-Time Polymerase Chain Reaction ; S100 Proteins - metabolism ; Stem Cells - metabolism ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; Vertebrates: endocrinology</subject><ispartof>Neuroendocrinology, 2011-01, Vol.94 (4), p.302-312</ispartof><rights>2011 S. Karger AG, Basel</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 S. Karger AG, Basel.</rights><rights>Copyright (c) 2011 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-5460997839e664f86852e6ff816047de8b9e7b73d6b760a5faee553c60ae3eb33</citedby><cites>FETCH-LOGICAL-c460t-5460997839e664f86852e6ff816047de8b9e7b73d6b760a5faee553c60ae3eb33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25331800$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21912092$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yunoue, Shunji</creatorcontrib><creatorcontrib>Arita, Kazunori</creatorcontrib><creatorcontrib>Kawano, Hiroto</creatorcontrib><creatorcontrib>Uchida, Hiroyuki</creatorcontrib><creatorcontrib>Tokimura, Hiroshi</creatorcontrib><creatorcontrib>Hirano, Hirofumi</creatorcontrib><title>Identification of CD133+ Cells in Pituitary Adenomas</title><title>Neuroendocrinology</title><addtitle>Neuroendocrinology</addtitle><description>Stem-like cells in tumors are capable of self-renewal and pluri-differentiation; they are thought to play important roles in tumor initiation and maintenance. Stem-like cells in malignant glioma express CD133. We examined samples from human pituitary adenoma, a generally benign neoplasm, for CD133 expression using routine immunohistochemical and biochemical methods. Our study of 70 pituitary adenomas (clinically nonfunctioning adenomas and growth hormone-, prolactin-, adrenocorticotropic hormone-, and thyroid-stimulating hormone-producing adenomas) showed that 18 (25.7%) expressed CD133. This rate was higher in clinically nonfunctioning (33.3%) than functioning adenomas (12.0%) (p = 0.085). Real-time PCR assay revealed the expression of CD133 mRNA in samples immunohistochemically positive for CD133. Neither the patient age and gender, nor the tumor size or postoperative recurrence rate correlated with CD133 positivity. CD133+ cells ubiquitously coexpressed CD34, nestin, and VEGFR2 (KDL1). S-100 and GFAP were not coexpressed with CD133. Chromogranin A, Pit-1, SF-1, and NeuroD1 were immune-negative, indicating that CD133+ cells did not have the potential to differentiate into functional endocrine cells. Our data suggest that the expression of CD133 in pituitary adenomas is related to immature endothelial progenitor cells that may play a role in the neovascularization of pituitary adenomas. Further studies are needed to elucidate the significance of CD133+ cells with respect to neovascularization and their sustainable growth in pituitary adenomas.</description><subject>AC133 Antigen</subject><subject>Adenoma - genetics</subject><subject>Adenoma - metabolism</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, CD34 - metabolism</subject><subject>Biological and medical sciences</subject><subject>Endocrinopathies</subject><subject>Endothelial Cells - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - metabolism</subject><subject>Humans</subject><subject>Hypothalamus. Hypophysis. Epiphysis (diseases)</subject><subject>Intermediate Filament Proteins - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nestin</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Original Paper</subject><subject>Peptides - genetics</subject><subject>Peptides - metabolism</subject><subject>Pituitary Neoplasms - genetics</subject><subject>Pituitary Neoplasms - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>S100 Proteins - metabolism</subject><subject>Stem Cells - metabolism</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>Vertebrates: endocrinology</subject><issn>0028-3835</issn><issn>1423-0194</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqN0M1LwzAYBvAgipvTg3eRIoiIVJO8TZocR_0aDPSg55K2iWT2Yybtwf_eyOoET16SHH4875sHoWOCrwlh8gZjDIA5ZTtoShIKMSYy2UVTjKmIQQCboAPvV4FRCXQfTSiRhGJJpyhZVLrtrbGl6m3XRp2JslsCcBVluq59ZNvo2faD7ZX7jObBdo3yh2jPqNrro_Geodf7u5fsMV4-PSyy-TIuE477mIVTylSA1JwnRnDBqObGCMJxklZaFFKnRQoVL1KOFTNKa8agDG8NugCYoYtN7tp1H4P2fd5YX4a9VKu7weeSsERQQdJ_SCKBScqCPPsjV93g2vCNXNJUYgIiCehyg0rXee-0ydfONqGCnOD8u_J8W3mwp2PgUDS62sqfjgM4H4HypaqNU21p_a9jAESEuBk62bh35d6024JxzhdPLozB</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Yunoue, Shunji</creator><creator>Arita, Kazunori</creator><creator>Kawano, Hiroto</creator><creator>Uchida, Hiroyuki</creator><creator>Tokimura, Hiroshi</creator><creator>Hirano, Hirofumi</creator><general>Karger</general><general>S. 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Psychology</topic><topic>Glycoproteins - genetics</topic><topic>Glycoproteins - metabolism</topic><topic>Humans</topic><topic>Hypothalamus. Hypophysis. Epiphysis (diseases)</topic><topic>Intermediate Filament Proteins - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nestin</topic><topic>Non tumoral diseases. Target tissue resistance. 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Stem-like cells in malignant glioma express CD133. We examined samples from human pituitary adenoma, a generally benign neoplasm, for CD133 expression using routine immunohistochemical and biochemical methods. Our study of 70 pituitary adenomas (clinically nonfunctioning adenomas and growth hormone-, prolactin-, adrenocorticotropic hormone-, and thyroid-stimulating hormone-producing adenomas) showed that 18 (25.7%) expressed CD133. This rate was higher in clinically nonfunctioning (33.3%) than functioning adenomas (12.0%) (p = 0.085). Real-time PCR assay revealed the expression of CD133 mRNA in samples immunohistochemically positive for CD133. Neither the patient age and gender, nor the tumor size or postoperative recurrence rate correlated with CD133 positivity. CD133+ cells ubiquitously coexpressed CD34, nestin, and VEGFR2 (KDL1). S-100 and GFAP were not coexpressed with CD133. Chromogranin A, Pit-1, SF-1, and NeuroD1 were immune-negative, indicating that CD133+ cells did not have the potential to differentiate into functional endocrine cells. Our data suggest that the expression of CD133 in pituitary adenomas is related to immature endothelial progenitor cells that may play a role in the neovascularization of pituitary adenomas. Further studies are needed to elucidate the significance of CD133+ cells with respect to neovascularization and their sustainable growth in pituitary adenomas.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>21912092</pmid><doi>10.1159/000330625</doi><tpages>11</tpages></addata></record> |
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| subjects | AC133 Antigen Adenoma - genetics Adenoma - metabolism Antigens, CD - genetics Antigens, CD - metabolism Antigens, CD34 - metabolism Biological and medical sciences Endocrinopathies Endothelial Cells - metabolism Female Fundamental and applied biological sciences. Psychology Glycoproteins - genetics Glycoproteins - metabolism Humans Hypothalamus. Hypophysis. Epiphysis (diseases) Intermediate Filament Proteins - metabolism Male Medical sciences Middle Aged Nerve Tissue Proteins - metabolism Nestin Non tumoral diseases. Target tissue resistance. Benign neoplasms Original Paper Peptides - genetics Peptides - metabolism Pituitary Neoplasms - genetics Pituitary Neoplasms - metabolism Real-Time Polymerase Chain Reaction S100 Proteins - metabolism Stem Cells - metabolism Vascular Endothelial Growth Factor Receptor-2 - metabolism Vertebrates: endocrinology |
| title | Identification of CD133+ Cells in Pituitary Adenomas |
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