Annals of Diagnostic Pathology
Volume 12, Issue 4 , Pages 275-282, August 2008

Phosphatase and tensin homologue and pituitary tumor-transforming gene in pituitary adenomas. Clinical-pathologic and immunohistochemical analysis

  • Martha Lilia Tena-Suck, MD

      Affiliations

    • Departamento de Patología Experimental, Instituto Nacional de Neurología y Neurocirugía, Mexico City, cp. 14269 Mexico
    • Corresponding Author InformationCorresponding author. Departamento de Neuropatología, Instituto Nacional de Neurología y Neurocirugía “Manuel Velasco Suárez,” Av Insurgentes Sur 3877 Col. La Fama, Tlalpan CP 14269, Mexico, DF, Mexico. Tel.: +525 56063822x2008.
  • ,
  • Alma Ortiz-Plata, PhD

      Affiliations

    • Departamento de Patología Experimental, Instituto Nacional de Neurología y Neurocirugía, Mexico City, cp. 14269 Mexico
  • ,
  • Horacio Astudillo de la Vega, PhD

      Affiliations

    • Laboratorio de Oncología Molecular, Unidad de Investigación Médica en Enfermedades Oncológicas, Hospital de Oncologia, Centro Medico Nacional Siglo XXI, IMSS, Mexico City, cp. 06720 Mexico

published online 13 June 2008.

Abstract 

Pituitary tumor-transforming gene (PTTG) is also known to induce angiogenesis during pituitary tumorigenesis. It has not been clarified whether PTTG functions as a cytoplasmic or a nuclear protein. Pituitary tumor-transforming gene-1 is usually expressed in most pituitary tumors, and little is known about phosphatase and tensin homologue (PTEN). In our knowledge, it has not been studied in pituitary tumors. The aim of this study was to determine the correlation between proliferating cell nuclear antigen (PCNA) labeling index (LI), PTEN, and PTTG-1 immunoexpression in pituitary adenomas. Forty-five pituitary adenomas were included—46.7% were males and 53.7% were females. The mean age was 43.18 ± 9.42 years (27-70 years). For functional pituitary adenoma (PA), it was 41.92 ± 6.63, and for nonfunctional pituitary adenomas, it was 44.62 ± 11.85 (P = .003). Proliferating cell nuclear antigen LI range was 19.42 ± 5.49; in functional pituitary adenomas, it was 41.92 ± 6.63, and in nonfunctional adenomas, it was 44.62 ± 11.85 (P = .081). The PTEN immunoreaction was positive—weak in 21 (47%), moderate in 19 (42%), and strong in 5 (11%; P = .000). The PTTG-1 gene was positive—weak in 18 (41%), moderate in 19 (41%), and strong in 6 (13%; P = .000). When we correlated PTEN + PCNA, it was P =.004, and PTEN + PTTG-1, it was P = .019. And when we correlated PCNA + PTGG-1, it was P = .262. In our results, we observed higher expression of PCNA-LI and PTTG-1 and loss of expression of PTEN. Nonfunctional hypophysis adenomas presented a higher PCNA, PTTG-1, and PTEN expression than functional ones. There was no difference between single-hormone-producing hypophysis adenomas or multiple-hormone-producing ones. Necrosis and hemorrhage were associated with PTEN expression, whereas atypias and mitosis figures were associated to PTTG-1 expression.

Keywords: Brain tumors, Functional and nonfunctional pituitary tumors, PTEN, PTTG-1 gene, PCNA, Immunohistochemistry

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PII: S1092-9134(08)00020-8

doi:10.1016/j.anndiagpath.2008.02.001

Annals of Diagnostic Pathology
Volume 12, Issue 4 , Pages 275-282, August 2008