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Absence of activating mutations of CXCR4 in pituitary tumours

Yong-ho Lee1, Tae Woong Noh, Mi Kyung Lee

  • 1Endocrinology, Internal Medicine, Institute of Endocrine Research, Yonsei University College of Medicine, Seoul, Korea.

Clinical Endocrinology
|May 29, 2009
PubMed
Abstract

Insights

Activating mutations in CXCR4 are not a common cause of pituitary tumors. Researchers found CXCR4 is highly expressed in GH-producing adenomas and NFPAs, but activating mutations were rare in these pituitary tumors.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Mutations in the gsp oncogene cause 30-40% of GH-producing pituitary adenomas and 10% of nonfunctioning pituitary adenomas (NFPAs).
  • The chemokine receptor CXCR4 and its ligand CXCL12 are implicated in GH production and pituitary adenoma cell proliferation.
  • Constitutive activation of CXCR4, a Gi-coupled receptor, could potentially drive pituitary tumor formation via cAMP-independent pathways.

Purpose of the Study:

  • To investigate if somatic activating mutations of CXCR4 contribute to the tumorigenesis of gsp-negative GH-secreting pituitary adenomas and NFPAs.
  • To determine the role of CXCR4 mutations in pituitary tumor development.

Main Methods:

  • Genomic DNA from 37 gsp-negative GH-producing pituitary tumors and 14 CXCR4-expressing NFPAs was analyzed.
  • Direct sequencing of coding exons of CXCR4 was performed using polymerase chain reaction-amplified products.
  • Immunohistochemistry and double immunofluorescent staining were used to assess CXCR4 expression in pituitary tissues.

Main Results:

  • CXCR4 was highly expressed in both GH-producing pituitary adenomas and NFPAs.
  • Two synonymous mutations in exon 2 of CXCR4 (87 C > T and 414 C > T) were identified in 4 out of 51 pituitary tumors.
  • These mutations were not found to be activating.

Conclusions:

  • Activating mutations of CXCR4 are unlikely to be a common pathogenic mechanism in the development of GH-producing pituitary tumors and NFPAs.
  • Further research may be needed to identify other genetic alterations involved in pituitary tumorigenesis.

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