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Somatostatin receptor subtypes sst 1 , sst 2 , sst 3 and sst 5 expression in human pituitary, gastroentero‐pancreatic and mammary tumors
Author(s) -
Schaer JeanClaude,
Waser Beatrice,
Mengod Guadalupe,
Reubi Jean Claude
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970304)70:5<530::aid-ijc7>3.0.co;2-z
Subject(s) - somatostatin receptor , somatostatin , endocrinology , medicine , biology , neuroendocrine tumors , octreotide , somatostatin receptor 2 , pituitary tumors , mammary gland , pancreas , receptor , cancer research , breast cancer , cancer
Using in situ hybridization techniques with selective oligoprobes, the gene expression of sst 1 , sst 2 , sst 3 and sst 5 was studied in a series of 32 human pituitary adenomas, 28 breast tumors and 21 endocrine gastroentero‐pancreatic tumors, shown to express somatostatin receptors to variable extents. In most of these tumors the sst 2 receptor subtype was abundantly expressed, even though a significant number of pituitary adenomas, breast and gastroentero‐pancreatic tumors expressed sst 1 and/or sst 3 as well. A very high incidence of the sst 5 subtype was found in growth hormone‐producing pituitary adenomas and, to a lesser extent, in inactive pituitary adenomas, whereas breast tumors seldom expressed sst 5 ; gastroentero‐pancreatic tumors showed all possible combinations of sst expression, with, however, a predominance of sst 2 and sst 1 . Overall, the presence of sst 2 mRNA and/or sst 5 mRNA generally correlated with the presence of octreotide binding sites. A lack of octreotide binding sites corresponded with a lack of sst 2 mRNA. Several tumors exhibiting a low number of octreotide binding sites had no measurable sst 2 mRNA, despite abundance of β‐actin mRNA, suggesting in these cases a very low abundance of sst mRNAs or a too low sensitivity of the in situ hybridization methodology. In all other cases, the method allowed precise localization of the respective mRNAs on the tumor tissue, notably in breast tumors with non‐homogeneous receptor distribution. Tumors without measurable amounts of somatostatin receptors had no detectable sst mRNA. Our results indicate a highly variable abundance of the various sst mRNAs in individual somatostatin receptor‐containing tumors. Int. J. Cancer 70:530–537. © 1997 Wiley‐Liss Inc.