Bromocriptine Resistant Prolactinomas and Non-Functioning Pituitary Tumors: Somatic Mutational Analyses of the Dopamine Type 2 Receptor and the MEN1 Gene

Michal Mark, Orit Jakobovitz-Picard, Eitan Friedman, Anna Maria Morelli, Maria Luisa Brandi, Eric F. Adams, Michael Buchfelder, Robert M.W. Hofstra, Inge M. Mulder, Luiz DeMarco, Eitan Friedman

Research output: Contribution to journalArticlepeer-review

Abstract

The molecular mechanisms underlying pituitary tumor development are largely unknown, but presumably involve inactivation of the MEN1 gene, and in prolactinomas, uncoupling of the dopamine receptor (DRD2) from intracellular effectors. To test this notion, 50 sporadic pituitary tumors (28 non-functioning, 22 prolactinomas) were analyzed for somatic MEN1 mutations, and 14 prolactinomas for DRD2 mutations. PCR amplification of all coding exons of the DRD2 and the MEN1 genes was followed by denaturing gradient gel electrophoresis (DGGE) analysis and DNA sequencing. No abnormal sequences were detected in the prolactinomas within the DRD2 gene. Two tumors displayed novel missense mutations in the MEN1 gene: C⊒T alteration at g4795, altering proline 245 to leucine in a prolactinoma, and C⊒A change at position g2677, altering arginine 130 to serine in a non-functioning tumor. There is no evidence of inactivating mutations at the DRD2 gene level in prolactinomas, and somatic mutations of the MEN1 gene in pituitary tumors are infrequent.

Original languageEnglish
Pages (from-to)149-158
Number of pages10
JournalInternational Journal on Disability and Human Development
Volume1
Issue number3
DOIs
StatePublished - 2000
Externally publishedYes

Keywords

  • DGGE
  • allelic loss
  • dopamine receptor
  • pituitary tumors
  • somatic mutations

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