11q13 allelic loss in pituitary tumors in patients with multiple endocrine neoplasia syndrome type 1

Robert J. Weil, Alexander O. Vortmeyer, Steve Huang, Roland Boni, Irina A. Lubensky, Svetlana Pack, Stephen J. Marx, Zhengping Zhuang, Edward H. Oldfield

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Pituitary adenomas may develop sporadically or as part of the multiple endocrine neoplasia type 1 (MEN 1) syndrome. The gene responsible for MEN I syndrome was recently identified and cloned. Low rates of MEN I gene mutations and deletions have been reported in sporadic pituitary adenomas. To elucidate the role of the MEN 1 gene in the pathogenesis of MEN 1-associated pituitary tumors, we examined pituitary adenomas from 11 MEN 1 patients for the presence of 11q13 allelic loss. Ten of the 11 pituitary tumors were informative by PCR-based loss of heterozygosity analysis. Using a combination of family pedigree analysis and restriction analysis directed at the mutated allele in 8 of the 10 informative cases, it was demonstrated in all 8 cases that it is the wild-type allele that undergoes deletion. All 11 tumors, 4 of which were growth hormone secreting, were additionally analyzed for mutation in the Gs α subunit (gsp) gene. None of the tumors (0 of 11 tumors) revealed a gsp gene mutation. Therefore, genetic alterations of the MEN I gene seem to play a dominant role in MEN 1-associated pituitary tumorigenesis, whereas gsp gene mutations do not seem to be a frequent event in either growth hormone- secreting or other types of MEN 1-associated pituitary tumors. These results suggest that MEN 1-associated pituitary tumors develop via genetic pathways that differ from those of most sporadic pituitary tumors.

Original languageEnglish (US)
Pages (from-to)1673-1678
Number of pages6
JournalClinical Cancer Research
Issue number7
StatePublished - Jul 1 1998
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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