AI Article Synopsis

  • The role of angiogenesis in pituitary tumor development is debated, as these tumors are often less vascularized than normal pituitary tissue, yet invasive prolactinomas show increased vasculature compared to less aggressive forms.
  • Various growth factors, like VEGF and FGF-2, play roles in the development of pituitary tumors, with VEGF being notably higher in dopamine-resistant prolactinomas.
  • Research into angiogenic factors in aggressive prolactinomas could lead to new treatment options, especially as anti-VEGF strategies have shown promise in reducing tumor size.

Article Abstract

The role of angiogenesis in pituitary tumor development has been questioned, as pituitary tumors have been usually found to be less vascularized than the normal pituitary tissue. Nevertheless, a significantly higher degree of vasculature has been shown in invasive or macropituitary prolactinomas when compared to noninvasive and microprolactinomas. Many growth factors and their receptors are involved in pituitary tumor development. For example, VEGF, FGF-2, FGFR1, and PTTG, which give a particular vascular phenotype, are modified in human and experimental pituitary adenomas of different histotypes. In particular, vascular endothelial growth factor, VEGF, the central mediator of angiogenesis in endocrine glands, was encountered in experimental and human pituitary tumors at different levels of expression and, in particular, was higher in dopamine agonist resistant prolactinomas. Furthermore, several anti-VEGF techniques lowered tumor burden in human and experimental pituitary adenomas. Therefore, even though the role of angiogenesis in pituitary adenomas is contentious, VEGF, making permeable pituitary endothelia, might contribute to adequate temporal vascular supply and mechanisms other than endothelial cell proliferation. The study of angiogenic factor expression in aggressive prolactinomas with resistance to dopamine agonists will yield important data in the search of therapeutical alternatives.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4251882PMC
http://dx.doi.org/10.1155/2014/608497DOI Listing

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