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Oncogene-induced senescence in pituitary adenomas and carcinomas.

AbstractOBJECTIVE:
The model of "oncogene-induced senescence" (OIS), resulting in cell-proliferation arrest, has recently been suggested as a possible explanation for the non-progression of pituitary tumours to malignancy. The aim of the study was to compare the expression of β-galactosidase as a molecular marker of OIS, and p21/p16 as additional markers involved in mediating OIS, in pituitary adenomas, carcinomas and normal pituitary tissue.
DESIGN:
We performed: a) semi-quantitative immunohistochemistry (β-galactosidase, p16, p21) in 41 pituitary adenomas [(11 GH-secreting, 9 PRL-secreting, 10 ACTH-secreting, 11 non-functioning (NFPAs)], 6 carcinomas (3 multihormonal: PRL/ACTH/GH, PRL/ACTH, PRL/GH/FSH; 1 non-functioning; 2 ACTH-secreting) and 7 normal pituitary tissues; b) quantitative PCR of mRNA (p16 and p21) in 6 GH-secreting, 6 NFPAs and 6 normal pituitary tissues.
RESULTS:
β-galactosidase was significantly increased in GH-secreting tumours (P=0.002), NFPAs (P=0.04), macroadenomas (P=0.03) and carcinomas (P=0.02), as compared to normal pituitary tissue. We found that p16 expression was significantly lower in all tumours (both adenomas and carcinomas) probably secondary to reduced transcription, at least for NFPAs; p21 showed a different biological behaviour, implying that p21 and p16 may play different roles in the senescence of each individual type of adenoma.
CONCLUSIONS:
β-galactosidase was significantly over-expressed in GH-secreting and NFPAs, and unexpectedly also in carcinomas. We speculate that the senescence pathway, which may explain the rarity of malignant progression to carcinomas in GH-secreting and NFPAs, might not be universal but cell-type specific.
AuthorsKrystallenia I Alexandraki, Mohammed Munayem Khan, Harvinder S Chahal, Nadezhda S Dalantaeva, Giampaolo Trivellin, Dan M Berney, Philippe Caron, Vera Popovic, Marija Pfeifer, Suzanne Jordan, Márta Korbonits, Ashley B Grossman
JournalHormones (Athens, Greece) (Hormones (Athens)) 2012 Jul-Sep Vol. 11 Issue 3 Pg. 297-307 ISSN: 2520-8721 [Electronic] Switzerland
PMID22908062 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • Adrenocorticotropic Hormone
  • Growth Hormone
  • beta-Galactosidase
Topics
  • Adenoma (metabolism, physiopathology)
  • Adrenocorticotropic Hormone (metabolism)
  • Aging
  • Cyclin-Dependent Kinase Inhibitor p16 (biosynthesis)
  • Cyclin-Dependent Kinase Inhibitor p21 (biosynthesis)
  • Growth Hormone (metabolism)
  • Humans
  • Immunohistochemistry
  • Pituitary Gland (metabolism)
  • Pituitary Neoplasms (metabolism, physiopathology)
  • Prolactinoma (metabolism)
  • beta-Galactosidase (biosynthesis)

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