Núñez VJM, Ramos-Zúñiga R

Language: Spanish
References: 12
Page: 22-28
PDF size: 141.50 Kb.

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 anadenoma 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 understoodonly 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.

REFERENCES

1. Alexander JM. Tumor suppressor loss in pituitary tumors. Brain Pathol 2001; 11:342-55.

2. Asa SL, Ezzat S. The pathogenesis of pituitary tumors. Nature Neurosci 2002; 2:836-49.

3. Ezzat S. The role of hormones, growth factors and their receptors in pituitary tumorigenesis. Brain Pathol 2001;11:356-70.

4. Clayton RN, Farrel WE. Clonality of pituitary tumors: more complicated than initially envisaged? Brain Pathol 2001;11:313-27.

5. William’s textbook of endocrinology, 10th edition, 2003. Editorial Elsevier. Consultado en MD consult: http://home.mdconsult.com/das/book/42351865-2/view/1091 el 11/8/04.

6. Levy A. Is monoclonality in pituitary adenomas synonymous with neoplasia?. Clin Endocrinol 2000; 52: 393-7.

7. Shimon I, Melmed S. Genetic basis of endocrine disease: pituitary tumor pathogenesis. J Clin Endocrinol Metab 1997;82:1675-81.

8. Yu R, Melmed S. Oncogene activation in pituitary tumors. Brain Pathol 2001; 11: 328-41.

9. Saez C, Japón MA, Ramos-Morales F, Romero F, Segura D, Tortolero M, et al. hpttg is overexpressed in pituitary adenomasand other primary epithelial neoplasias. Oncogene 1999; 18:5473-6.

10. Kirschner LS, Sandrini F, Monbo J, Lin PJ, Carney JA, Stratakis CA. Geneteic heterogenicity and spectrum of mutations od the PRKAR1A gene in patients cith Carney complex. Hum Mol Gen2000; 9: 3037-46.

11. Reubi JC, Waser B, Vale W, Rivier J. Expression of CRF1 and CRF2 receptors in human cancers. J Clin Endocrinol Metab2003; 88:3312-20.

12. Assa SL. Transgenic and knouckout mice models clarify pituitary development, function and disease. Brain Pathol 2001; 11:370-83.