Altered Balance between Thyrotropin-Releasing Hormone and Dopamine in Prolactinomas and Other Pituitary Tumors Compared to Normal Pituitaries

Dafniet, M. Le; Blumberg-Tick, J.; Gozlan, H.; Barret, Alain; Bression, D.; Peillon, F

doi:10.1210/jcem-69-2-267

Cited by 13 publications

(4 citation statements)

References 25 publications

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“…These patients exhibit the spectrum of hyperplasia-to-neoplasia (46, 130), suggesting that continuous stimulation by TRH may lead to thyrotroph adenoma (60). TRH has also been shown to be expressed in the pituitary (83,94,110) and by the different types of pituitary adenomas (80)(81)(82)153).…”

Section: Excess Hormonal Stimulation Growth Hormonereleasing Hormonementioning

confidence: 99%

The Role of Hormones, Growth Factors and Their Receptors in Pituitary Tumorigenesis

Ezzat

2001

Brain Pathology

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Numerous factors have been shown to govern adenohypophysial cell proliferation. Human and animal models have documented that the hypothalamic trophic hormone growth hormone‐releasing hormone stimulates cell proliferation, and prolonged stimulation leads to tumor formation. Similarly, lack of dopaminergic inhibition of lactotrophs and lack of feedback suppression by adrenal, gonadal or thyroid hormones are implicated, perhaps through hypothalamic stimulatory mechanisms, in pituitary adenoma formation superimposed on hyperplasia. However, most pituitary tumors are not associated with underlying hyperplasia. Overexpression of growth factors and their receptors, such as EGF, TGFα, EGF‐R and VEGF has been identified in pituitary adenomas, and reduction of follistatin expression has been implicated in gonadotroph adenomas. Aberrant expression of members of the FGF family, an FGF antisense gene and FGF receptors have all been described in pituitary adenomas. The clonal composition of pituitary adenomas attests to the molecular basis of pituitary tumorigenesis, however, the evidence suggests that these various hypophysiotropic hormones and growth factors likely play a role as promoters of tumor cell growth in genetically transformed cells.

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Section: Excess Hormonal Stimulation Growth Hormonereleasing Hormonementioning

confidence: 99%

The Role of Hormones, Growth Factors and Their Receptors in Pituitary Tumorigenesis

Ezzat

2001

Brain Pathology

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“…The presence of the TH transcript in AP cells is not inconsistent with several descriptions of transient or ectopic expression of TH in neurons that are not classically catecholaminergic (Kosaka et al, 1987;Teitelman and Lee, 1987;Verney et al, 1988). Recent studies suggest a neural origin of the AP (Couly and Le Douarin, 1985;Dubois and ElAmraoui, 1995) and others demonstrate that the AP is able to synthesize its own regulatory neurofactors Le Dafniet et al, 1989;Pagesy et al, 1989Pagesy et al, , 1992Levy et al, 1993). In agreement with these reports, the presence of TH mRNA and TH immunoreactivity in this gland should also be considered as an endogenous potential to synthesize DA, the main inhibitory factor involved in the regulation of PRL secretion.…”

Section: Expression Of Th Mrna In the Apmentioning

confidence: 53%

“…However, recent studies Le Dafniet et al, 1989;Pagesy et al, 1989Pagesy et al, , 1992Levy et al, 1993) indicate that several regulatory neurohormones classically associated with the hypothalamus are endogenously synthesized in the AP and might play a paracrine or autocrine role on AP cell functions. Concerning DA, the ability of its de novo synthesis in the AP is still a matter of controversy.…”

Section: Introductionmentioning

confidence: 99%

Multiple tyrosine hydroxylase transcripts and immunoreactive forms in the rat: Differential expression in the anterior pituitary and adrenal gland

Schussler

Boularand

et al. 1995

J of Neuroscience Research

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Several regulatory neurofactors, classically associated with the hypothalamus, may be synthesized in the anterior pituitary (AP). Dopamine (DA) is the main prolactin-inhibiting factor. Its de novo synthesis in the normal AP has not been proved, although the TH transcript has been previously demonstrated by RT/PCR in the AP. We investigated tyrosine hydroxylase (TH) gene expression at both the protein and mRNA levels in the AP of normal random cycling female rats and in a catecholaminergic tissue, the adrenal gland (AG). The Western blot analysis of AP homogenates revealed two immunoreactive forms of TH in the AP, both differing from the TH present in the AG. RT/PCR products from AP and AG mRNA were subcloned and sequenced. In addition to the full-length form, we identified two TH transcripts generated by alternative splicing either involving the use of a new alternate splice-donor site within exon 2 or skipping exon 11. The form lacking exon 11 was not isolated from the AG. In the AP, all three forms were present. Although the AP contained the full-length TH mRNA, the expected size protein was not detected. Thus, there is alternative splicing of the TH primary transcript, and putative additional post-translational regulation may yield TH proteins with no enzymatic activity, at least in non-catecholaminergic tissues.

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“…52 TRH has also been shown to be expressed in the pituitary 72,83,95 and by the different types of pituitary adenomas. [69][70][71]130 TRH signaling appears to be intact in pituitary adenomas as evidenced by intact binding and release of TSH and PRL. 71,130 TRH receptor expression 129 and structure is grossly unaltered even in thyrotroph adenomas.…”

Section: Thyrotropin-releasing Hormone (Trh)/trh Receptormentioning

confidence: 99%

The Pathophysiology of Pituitary Tumors

Ezzat¹,

Sylvia²

2002

Seminars in Neurosurgery

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Numerous factors have been shown to govern pituitary cell proliferation; these various hypophysiotropic hormones and growth factors (GFs) likely play a role as promoters of tumor cell growth in genetically transformed cells. The clonal composition of pituitary adenomas attests to the molecular basis of pituitary tumorigenesis; however, the oncogenes and tumor suppressor genes that are implicated in the transformation events for the vast majority of pituitary tumors remain unknown. Mutations that have been identified in other human malignancies are restricted to a very small subset of pituitary neoplasms implicating novel genetic and/or epigenetic alterations. This review details some of the currently known alterations of GFs and their receptors that have been implicated in pituitary tumorigenesis. Some of the epigenetic changes noted in nuclear components that govern cell cycle control are also reviewed. The emerging knowledge from these studies is shedding new light not only on the pathogenesis of pituitary tumors but on novel mechanisms in the broader context of human neoplasia.Objectives: On completion of this article, the reader should understand the mechanisms involved in the development of pituitary tumors and the differences between experimental models and the primary human pituitary adenomas.

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Altered Balance between Thyrotropin-Releasing Hormone and Dopamine in Prolactinomas and Other Pituitary Tumors Compared to Normal Pituitaries

Cited by 13 publications

References 25 publications

The Role of Hormones, Growth Factors and Their Receptors in Pituitary Tumorigenesis

The Role of Hormones, Growth Factors and Their Receptors in Pituitary Tumorigenesis

Multiple tyrosine hydroxylase transcripts and immunoreactive forms in the rat: Differential expression in the anterior pituitary and adrenal gland

The Pathophysiology of Pituitary Tumors

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