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Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
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Published on: April 29, 2014

Epigenetic regulation in RCC: opportunities for therapeutic intervention?

James Larkin1, Xin Yi Goh, Marcus Vetter

  • 1Department of Medicine, The Royal Marsden Hospital, Fulham Road, London SW3 6JJ, UK.

Nature Reviews. Urology
|January 18, 2012
PubMed

Insights

Clear cell renal cell carcinoma (ccRCC) involves genetic changes affecting histone and chromatin regulation. Understanding these changes may reveal new therapeutic targets for kidney cancer.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Renal cell carcinoma (RCC) comprises various histological subtypes originating from kidney parenchyma.
  • Clear cell RCC (ccRCC) is the most common subtype, often linked to von Hippel-Lindau (VHL) gene mutations.
  • Other tumor suppressor genes involved in histone and chromatin regulation, like SETD2, KDM6A, KDM5C, and PBRM1, are also frequently inactivated in ccRCC.

Purpose of the Study:

  • To explore the role of histone and chromatin regulation in ccRCC pathogenesis.
  • To investigate the clinical relevance of PBRM1 loss of function in ccRCC.
  • To identify potential novel therapeutic targets by understanding ccRCC biology and intratumor heterogeneity.

Main Methods:

  • Review of genetic abnormalities in ccRCC, focusing on tumor suppressor genes.
  • Analysis of RNA interference (RNAi) assay data regarding PBRM1 function.
  • Exploration of the link between histone/chromatin regulation and ccRCC progression.

Main Results:

  • Loss of function in VHL is the most common genetic abnormality in ccRCC.
  • Inactivation of genes regulating histone and chromatin (SETD2, KDM6A, KDM5C, PBRM1) is prevalent in ccRCC.
  • RNAi data suggest PBRM1 loss drives ccRCC proliferation, though clinical significance requires further study.

Conclusions:

  • Histone and chromatin regulation plays a critical role in ccRCC development.
  • Restoring function of inactivated tumor suppressor genes may be therapeutically challenging.
  • Further research into ccRCC biology and heterogeneity could uncover new therapeutic strategies.

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