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Pituitary

, Volume 10, Issue 1, pp 47–52 | Cite as

Gene expression profiling in human null cell pituitary adenoma tissue

  • Ji Hu
  • Huaidong Song
  • Xuanchun Wang
  • Ye Shen
  • Fengling Chen
  • Yu Liu
  • Shiqi Li
  • Yongfei Wang
  • Xuefei Shou
  • Yulin Zhang
  • Renming Hu
Article

Abstract

It is estimated that up to one in five individuals develops pituitary gland tumors, despite the common occurrence of these tumors, the pathogenetic mechanisms underlying their development mainly remain unknown. We studied the gene expression in null cell adenomas compared with normal pituitary by expressed sequence tags (EST) sequencing and cDNA microarray on large scale. Both approaches of EST sequencing and microarray analysis showed that 17 genes were differentially expressed in human null cell pituitary adenoma tissues, among which 14 genes were overexpressed and three genes were underpressed. Five of the genes with potential oncogenic significance by RT-real time quantitative PCR. Synaptotagmin (SYT) are integral membrane proteins of synaptic vesicles considered to serve as Ca2+ sensors in the process of vesicular trafficking and exocytosis. Calcium binding to participates in triggering neurotransmitter release at the synapse. In view of our finding that SYT is overexpressed in null cell adenomas, these tumors may be capable of secreting some unknown hormones or peptides. ATP5B and MDH1 were involved in the energy metabolism, whose overexpression in null cell adenomas provide us with a new perspective of exploring the oncogenesis of these tumors. All of these data may contribute to the understanding of null cell adenoma formation and development.

Keywords

Pituitary adenoma Null cell Gene expression profiling 

Notes

Acknowledgements

The study was funded by grants to RenMing Hu from the Key Project of National Natural Science Foundation of China (30230380), the National Natural Science Foundation of China (39900072), the Chinese High Tech Program (2002BA711A05 and 2001AA221201), the National Key Basic Research and Development Program (2002CB713703) and the Shanghai Commission for Science and Technology (01JC14026). The work was also funded by a grant to Xuanchun Wang from the National Natural Science Foundation of China (30300162).

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Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • Ji Hu
    • 1
    • 3
  • Huaidong Song
    • 1
  • Xuanchun Wang
    • 1
  • Ye Shen
    • 1
  • Fengling Chen
    • 1
  • Yu Liu
    • 1
  • Shiqi Li
    • 2
  • Yongfei Wang
    • 2
  • Xuefei Shou
    • 2
  • Yulin Zhang
    • 2
  • Renming Hu
    • 1
  1. 1.State Key Laboratory of Genetics Engineering, Institute of Endocrinology and Diabetology, Department of Endocrinology, Huashan HospitalFuDan UniversityShanghaiP.R. China
  2. 2.State Key Laboratory of Genetics Engineering, Institute of Endocrinology and Diabetology, Department of Neurosurgery, Huashan HospitalFuDan UniversityShanghaiP.R. China
  3. 3.Department of Endocrinology, 2nd HospitalSoochow UniversitySuzhouP.R. China

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