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Relative expression of the RET9 and RET51 isoforms in human pheochromocytomas

H Le Hir1, N Charlet-Berguerand, A Gimenez-Roqueplo

  • 1Centre de G¿en¿etique Mol¿eculaire, Laboratoire associ¿e ¿a l'Universit¿e Pierre et Marie Curie, Gif-sur-Yvette, France.

Oncology
|June 6, 2000
PubMed

Insights

Activating RET oncogene mutations cause MEN2. The study found higher Ret51 transcript levels in familial MEN2 tumors, suggesting this isoform offers a growth advantage for multiple endocrine neoplasia type 2.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Activating mutations in the RET oncogene are linked to multiple endocrine neoplasia type 2 (MEN2).
  • The RET gene produces multiple mRNA isoforms, including Ret9 and Ret51, with Ret51 exhibiting higher in vitro transforming activity when mutated.
  • Preferential expression of more transforming isoforms may contribute to tumor development.

Purpose of the Study:

  • To investigate if the more transforming Ret51 protein isoform is preferentially expressed in MEN2 tumors compared to normal tissues or sporadic pheochromocytomas.
  • To determine the relative abundance of Ret9 and Ret51 transcripts in different tumor types and normal tissues.

Main Methods:

  • Quantitative RNase protection assays were employed to measure the absolute abundance of 3' RET splice variants.
  • Analysis was performed on pheochromocytomas (familial MEN2 and sporadic) and normal tissues.

Main Results:

  • The proportion of RET51 transcripts showed significant variability across all samples.
  • Familial MEN2 tumors exhibited a significantly higher proportion of RET51 transcripts (48.1%) compared to sporadic tumors (36.75%).

Conclusions:

  • Preferential expression of the Ret51 isoform, although moderate, appears to provide a growth advantage in MEN2 tumors.
  • This finding highlights the potential role of alternative splicing in the pathogenesis of multiple endocrine neoplasia type 2.

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