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

Ezzat, Shereen

doi:10.1111/j.1750-3639.2001.tb00405.x

Cited by 54 publications

(22 citation statements)

References 141 publications

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“…All these findings support the evidence that VEGF overexpression could play an important role in early phases of angiogenesis in oestrogen-induced rat pituitary tumour (Ezzat 2001).…”

Section: Introductionsupporting

confidence: 81%

Subcellular localisation of VEGF in different pituitary cells. Changes of its expression in oestrogen induced prolactinomas

et al. 2006

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Vascular endothelial growth factor (VEGF) is an important angiogenic factor in the pituitary gland. The objective of this study was to unveil the VEGF subcellular localisation in different pituitary cell types and to evaluate changes in its expression at different time intervals after oestrogen stimulation. A relevant feature demonstrated was the identification of this cytokine in the nucleus and cytoplasm of lactotrophs, somatotrophs and gonadotrophs, as well as in follicle-stellate cells of male rats. Oestrogen treatment increased the number of VEGF immunopositive cells and its expression detected differentially by western blot in both nucleus and cytoplasm of pituitary cells when compared to the control. At ultrastructural level VEGF appeared associated with nucleolus and euchromatin involving a possible internal autocrine loop. In lactotrophs, the predominant cell of the tumour, VEGF was immunodetected in RER, Golgi complex, and vesicular organelles, supporting further the association with an auto-paracrine effect exerted by VEGF. The nucleus/cytoplasm ratio of VEGF revealed a prevalent accumulation of VEGF in the cytoplasm. The presence of VEGF in the nucleus may probably be associated with a translocation to this cell compartment. This study demonstrated a cytoplasmic and nuclear immunolocalisation of VEGF in normal and tumoural adenohypophyseal cells. In the course of prolactinoma development, the oestrogen stimulated VEGF expression in tumoural cells, promoting a vascular adaptation which contributes to growth and progression of the tumour.

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“…All these findings support the evidence that VEGF overexpression could play an important role in early phases of angiogenesis in oestrogen-induced rat pituitary tumour (Ezzat 2001).…”

Section: Introductionsupporting

confidence: 81%

Subcellular localisation of VEGF in different pituitary cells. Changes of its expression in oestrogen induced prolactinomas

et al. 2006

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“…RTKs are important for normal pituitary function and help to modulate hormone production and cell growth (Ezzat 2001). Aberrant RTK activation possesses the ability to confer proproliferative potential and abnormal hormone production to pituitary cells leading to hyperplastic and/or neoplastic growth.…”

Section: Analysis Of the Rtk/pi3k/akt/mtor Pathways In Pamentioning

confidence: 99%

The PI3K/AKT/mTOR pathway in the pathophysiology and treatment of pituitary adenomas

Monsalves¹,

Juraschka²,

Tateno³

et al. 2014

Endocrine-Related Cancer

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Pituitary adenomas are common intracranial neoplasms. Patients with these tumors exhibit a wide range of clinically challenging problems, stemming either from results of sellar mass effect in pituitary macroadenoma or the diverse effects of aberrant hormone production by adenoma cells. While some patients are cured/controlled by surgical resection and/or medical therapy, a proportion of patients exhibit tumors that are refractory to current modalities. New therapeutic approaches are needed for these patients. Activation of the AKT/phophotidylinositide-3-kinase pathway, including mTOR activation, is common in human neoplasia, and a number of therapeutic approaches are being employed to neutralize activation of this pathway in human cancer. This review examines the role of this pathway in pituitary tumors with respect to tumor biology and its potential role as a therapeutic target.

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“…Here, we show that FGF-2 and EGF blocked the prolactin secretion induced by PrRP. Both growth factors, EGF and specially FGF-2 have been previously involved in the induction of proliferative changes of lactotroph cells and prolactinomas [27][28][29][30]. Moreover, FGF-2 mediates the proliferative response of lactotroph cells to in vivo estrogens treatment in rats, and inducing the expression of the pttg gene [31].…”

Section: Discussionmentioning

confidence: 97%

Prolactin-releasing peptide (PrRP) increases prolactin responses to TRH in vitro and in vivo

Spuch

Diz-Chaves

Pérez-Tilve

et al. 2007

Endocr

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

Cited by 54 publications

References 141 publications

Subcellular localisation of VEGF in different pituitary cells. Changes of its expression in oestrogen induced prolactinomas

Subcellular localisation of VEGF in different pituitary cells. Changes of its expression in oestrogen induced prolactinomas

The PI3K/AKT/mTOR pathway in the pathophysiology and treatment of pituitary adenomas

Prolactin-releasing peptide (PrRP) increases prolactin responses to TRH in vitro and in vivo

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