IBYME   02675
INSTITUTO DE BIOLOGIA Y MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
capítulos de libros
Título:
Prolactinomas: Role of VEGF, FGF-2 and CD-31
Autor/es:
PEREZ-MILLÁN, MI; CRISTINA,C.; BERNER, S.I.; BECU-VILLALOBOS, D.
Libro:
Tumors of the Central Nervous System. Editor Hayat,MA.,
Editorial:
Springer Publishers,
Referencias:
Lugar: Union, NJ, USA; Año: 2009;
Resumen:
Pituitary tumors rarely produce metastasis, but cause considerable morbidity and
mortality. Each pituitary tumor of clonal origin, represents the multifactorial
result of failure of different regulatory events where growth and angiogenic
factors may play critical roles in hormone secretion and cell proliferation.
Prolactinomas, pituitary tumors which secrete prolactin, are generally treated
successfully with dopamine agonists, even though a 10-15 % are resistant to
this pharmacological therapy.
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 pituitary prolactinomas when compared to non
invasive prolactinomas. Furthermore it has also been described that
macroprolactinomas are more vascular than microprolactinomas.
Many growth
factors and their receptors were found to be involved in pituitary tumor
development. For example, VEGF, FGF-2, FGFR1 and PTTG, which give a particular
vascular phenotype, are modified in pituitary adenomas. Inhibitors of
angiogenesis, Thrombospondin-1 and FGF-2 endogenous antisense were detected as
well. 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, in dopamine resistant prolactinomas. 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.