Pathogenesis of pituitary adenomas [Patog�nesis de los adenomas hipofisiarios]

Abstract

Pituitary adenomas make up to 10-15% of all intracranial tumors. Pos-mortem exams have found them in up to 20% of the general population. They represent 25% of all intracranial tumors operated on. After seeing a patient with evidence of recent growth of a pituitary adenoma we set up to investigate how long does it take for an adenoma to grow and to summarize the most important concepts in pituitary adenoma pathogenesis. Discussion: a brief description is made of the clinical case that motivated the review. Following is described how, in spite of the demonstrated monoclonality of pituitary adenomas, up to 30% of them could be polyclonal and how 60% of recurrent tumors are of different clonality to the original tumor. The most notably involved oncogenes are gsp, gip2, D-type Cyclins and PTTG while the most frequently tumor suppressor genes found to be inactivated are MEN-1, CNC, IFS, VHL (which cause familiar syndromes associated with pituitary adenomas) Rb and CDK-1 (in isolated tumores). The roll of hypothalamic, pituitary and target organ hormones in pituitary oncogenesis is also reviewed. Conclusion: pituitary adenomas are the most frequent intracranial tumor but their pathogenesis is understood only partially. It is difficult to know the time it takes for a pituitary adenoma to grow. We present a case with evidence of recent growth and review the current knowledge in pituitary pathogenesis. �INNN, 2006.