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The relationship between specific RET proto-oncogene mutations and disease phenotype in multiple endocrine neoplasia

C Eng1, D Clayton, I Schuffenecker

  • 1Division of Cancer Epidemiology and Control, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115-6084, USA. charis_eng@macmailgw.dfci.harvard.edu

JAMA
|November 20, 1996
PubMed
Abstract

Insights

Specific RET proto-oncogene mutations correlate with Multiple Endocrine Neoplasia type 2 (MEN 2) subtypes, aiding in clinical management. Understanding these genotype-phenotype correlations helps predict disease features and guide patient care.

Area of Science:

  • Endocrinology
  • Genetics
  • Oncology

Background:

  • Multiple Endocrine Neoplasia type 2 (MEN 2) is an autosomal dominant disorder with three subtypes: MEN 2A, MEN 2B, and familial medullary thyroid carcinoma (FMTC).
  • MEN 2 subtypes are characterized by medullary thyroid carcinoma (MTC), pheochromocytoma (pheo), hyperparathyroidism (HPT), and specific stigmata.
  • The RET proto-oncogene is implicated in MEN 2 pathogenesis.

Purpose of the Study:

  • To establish genotype-phenotype correlations between specific RET proto-oncogene mutations and the clinical features of MEN 2.
  • To determine if specific mutation locations and types are associated with particular MEN 2 subtypes or associated conditions.
  • To provide data that could aid in clinical decision-making for MEN 2 patients.

Main Methods:

  • A correlative survey study involving 477 independent MEN 2 families.
  • Data collected from eighteen tertiary referral centers worldwide.
  • Analysis focused on the association between germline mutations in the RET proto-oncogene and the presence of MTC, pheo, HPT, and other features.

Main Results:

  • Mutations at codon 634 of the RET proto-oncogene are significantly associated with pheochromocytoma and hyperparathyroidism.
  • Specific mutations, such as CGC at codon 634, have not been linked to FMTC.
  • Mutations at codons 768 and 804 are associated exclusively with FMTC, while codon 918 mutations are specific to MEN 2B.
  • Rare families with MEN 2 and Hirschsprung disease harbored MEN 2-specific codon mutations, suggesting a need for monitoring these patients for MEN 2 tumors.

Conclusions:

  • Genotype-phenotype correlations in MEN 2 are evident and can be reliably established.
  • These correlations can inform clinical management strategies, including screening, surveillance, and prophylaxis.
  • Understanding specific mutation effects provides insight into the genetic mechanisms underlying MEN 2.

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