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Pathology, pathogenesis and therapy of growth hormone (GH)-producing pituitary adenomas: technical advances in histochemistry and their contribution.

Osamura RY, Egashira N, Kajiya H, Takei M, Tobita M, Miyakoshi T, Inomoto C, Takekoshi S, Teramoto A - Acta Histochem Cytochem (2009)

Bottom Line: Experimentally, GHomas have been induced in GH-releasing hormone (GHRH) or Prop-1 transgenic animals.Immunohistochemical detection of somatostatin receptor (SSTR2a) has recently emphasized their role in the response of GHomas to somatostatin analogue therapy.In this review, the advances in technology and their contribution to cell biology and medical practice are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Tokai University School of Medicine, 143 Shimokasuya, Isehara-city, Kanagawa 259-1193, Japan. osamura@is.icc.u-tokai.ac.jp

ABSTRACT
Growth hormone (GH)-producing adenomas (GHomas) are one of the most frequently-occurring pituitary adenomas. Differentiation of hormone-producing cells in the pituitary gland is regulated by transcription factors and co-factors. The transcription factors include Pit-1, Prop-1, NeuroD1, Tpit, GATA-2, SF-1. Aberrant expression of transcription factors such as Pit-1 results in translineage expression of GH in adrenocorticotropic hormone-producing adenomas (ACTHomas). This situation has been substantiated by GFP-Pit-1 transfection expression in the AtT20 cell line. Experimentally, GHomas have been induced in GH-releasing hormone (GHRH) or Prop-1 transgenic animals. Immunohistochemical detection of somatostatin receptor (SSTR2a) has recently emphasized their role in the response of GHomas to somatostatin analogue therapy. In this review, the advances in technology and their contribution to cell biology and medical practice are discussed.

No MeSH data available.


Related in: MedlinePlus

Experimental model for GH-producing pituitary adenoma induced in the hGHRH transgenic mice. The pituitary tumor cells in hGHRH transgenic mice are immunohistochemically positive for GH, PRL and TSH. They are also positive for GHRH and Pit-1 [23].
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Figure 7: Experimental model for GH-producing pituitary adenoma induced in the hGHRH transgenic mice. The pituitary tumor cells in hGHRH transgenic mice are immunohistochemically positive for GH, PRL and TSH. They are also positive for GHRH and Pit-1 [23].

Mentions: In human GHRH transgenic mice, the pituitaries were enlarged and histologically exhibited GH-producing adenomas and diffusely increased hyperplastic GH cells in the pituitary glands [23]. In particular, the tumors contained nodules which express only GH and PRL and not ACTH or FSH/LH (Fig. 7). Using a sensitive IHC method, Matsuno et al. have reported that 15 of 25 GHomas were positive for GHRH [12]. These findings indicate that at least some proportion of GHomas could overexpress GHRH, resulting in tumor formation.


Pathology, pathogenesis and therapy of growth hormone (GH)-producing pituitary adenomas: technical advances in histochemistry and their contribution.

Osamura RY, Egashira N, Kajiya H, Takei M, Tobita M, Miyakoshi T, Inomoto C, Takekoshi S, Teramoto A - Acta Histochem Cytochem (2009)

Experimental model for GH-producing pituitary adenoma induced in the hGHRH transgenic mice. The pituitary tumor cells in hGHRH transgenic mice are immunohistochemically positive for GH, PRL and TSH. They are also positive for GHRH and Pit-1 [23].
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2742723&req=5

Figure 7: Experimental model for GH-producing pituitary adenoma induced in the hGHRH transgenic mice. The pituitary tumor cells in hGHRH transgenic mice are immunohistochemically positive for GH, PRL and TSH. They are also positive for GHRH and Pit-1 [23].
Mentions: In human GHRH transgenic mice, the pituitaries were enlarged and histologically exhibited GH-producing adenomas and diffusely increased hyperplastic GH cells in the pituitary glands [23]. In particular, the tumors contained nodules which express only GH and PRL and not ACTH or FSH/LH (Fig. 7). Using a sensitive IHC method, Matsuno et al. have reported that 15 of 25 GHomas were positive for GHRH [12]. These findings indicate that at least some proportion of GHomas could overexpress GHRH, resulting in tumor formation.

Bottom Line: Experimentally, GHomas have been induced in GH-releasing hormone (GHRH) or Prop-1 transgenic animals.Immunohistochemical detection of somatostatin receptor (SSTR2a) has recently emphasized their role in the response of GHomas to somatostatin analogue therapy.In this review, the advances in technology and their contribution to cell biology and medical practice are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Tokai University School of Medicine, 143 Shimokasuya, Isehara-city, Kanagawa 259-1193, Japan. osamura@is.icc.u-tokai.ac.jp

ABSTRACT
Growth hormone (GH)-producing adenomas (GHomas) are one of the most frequently-occurring pituitary adenomas. Differentiation of hormone-producing cells in the pituitary gland is regulated by transcription factors and co-factors. The transcription factors include Pit-1, Prop-1, NeuroD1, Tpit, GATA-2, SF-1. Aberrant expression of transcription factors such as Pit-1 results in translineage expression of GH in adrenocorticotropic hormone-producing adenomas (ACTHomas). This situation has been substantiated by GFP-Pit-1 transfection expression in the AtT20 cell line. Experimentally, GHomas have been induced in GH-releasing hormone (GHRH) or Prop-1 transgenic animals. Immunohistochemical detection of somatostatin receptor (SSTR2a) has recently emphasized their role in the response of GHomas to somatostatin analogue therapy. In this review, the advances in technology and their contribution to cell biology and medical practice are discussed.

No MeSH data available.


Related in: MedlinePlus