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Updated: Jul 19, 2026

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers
12:22

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers

Published on: January 22, 2013

Molecular biology of renal cell carcinoma

Begoña Mellado1, Pere Gascón

  • 1Medical Oncology Department, ICMHO, IDIBAPS, Hospital Clinic, Barcelona, Spain. bmellado@clinic.ub.es

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|November 1, 2006
PubMed

Insights

Molecular biology advances clarify renal cell carcinoma (RCC) development, particularly clear-cell type, linked to Von Hippel-Lindau (VHL) gene inactivation. Targeted therapies inhibiting VEGF and mTOR show promise for treating this kidney cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Renal cell carcinoma (RCC) pathogenesis involves complex molecular events.
  • Inactivation of the Von Hippel-Lindau (VHL) tumor suppressor gene is crucial in clear-cell RCC development.
  • VHL loss leads to increased pro-angiogenic factors like VEGF and PDGF.

Purpose of the Study:

  • To review the molecular pathogenesis of inherited and sporadic RCC.
  • To discuss the role of VHL gene inactivation in RCC.
  • To highlight emerging targeted therapies for RCC.

Main Methods:

  • Review of current literature on RCC molecular biology.
  • Elucidation of molecular pathways in oncogenic transformation.
  • Analysis of targeted therapeutic strategies.

Main Results:

  • VHL gene inactivation is a key driver in clear-cell RCC.
  • VEGF and PDGF are significantly upregulated due to VHL loss.
  • Targeted therapies like anti-VEGF agents and mTOR inhibitors demonstrate clinical activity.

Conclusions:

  • Understanding RCC molecular pathways is advancing treatment options.
  • Targeted therapies offer new hope for RCC patients.
  • Further research into RCC pathogenesis can lead to improved therapies.

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