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Updated: Apr 18, 2026

A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies
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A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies

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Oncotargets in different renal cancer subtypes

Holger Moch, Rodolfo Montironi, Antonio Lopez-Beltran

  • 1Institute of Surgical Pathology, University of Zurich, Zurich, Switzerland. holger.moch@usz.ch.

Current Drug Targets
|January 27, 2015
PubMed

Insights

Clear cell renal cell carcinoma (ccRCC) is genetically diverse, with VHL gene alterations common. Understanding these genetic changes and other tumor suppressor genes aids in developing targeted therapies for renal cancer.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Renal cell cancer (RCC) is a heterogeneous disease with clear cell RCC (ccRCC) being the most common subtype in adults.
  • ccRCC is characterized by von Hippel-Lindau (VHL) gene alterations, leading to increased vascular endothelial growth factor (VEGF) production.
  • Recent research has uncovered significant genetic heterogeneity within ccRCC, identifying additional tumor suppressor genes on chromosome 3p.

Purpose of the Study:

  • To review the genetic landscape of renal cell carcinoma, focusing on ccRCC.
  • To explore the role of various genetic alterations in renal tumor carcinogenesis, prognosis, and targeted therapy.
  • To correlate morphologic features with molecular genetics for improved targeted therapy strategies.

Main Methods:

  • Review of current literature on renal cell carcinoma genetics and targeted therapies.
  • Analysis of genetic alterations including VHL, PI3K-mTORC1 pathway, and other tumor suppressor genes (FLCN, TSC1/2, TFE3/B, MITF, FH, SDHB/D, MET, PTEN).
  • Examination of the association between morphologic features and molecular genetics in renal cancer.

Main Results:

  • VHL gene inactivation is a key event in ccRCC, driving VEGF production and promoting angiogenesis.
  • The PI3K-mTORC1 signaling axis is a therapeutic target, with mTOR inhibitors showing promise.
  • Multiple genetic alterations in hereditary cancer syndromes contribute to renal tumor development and influence prognosis.

Conclusions:

  • Targeted therapies, including VEGF inhibitors and mTOR inhibitors, are advancing the treatment of metastatic ccRCC.
  • Understanding the molecular basis of renal cancer, including genetic heterogeneity and specific gene alterations, is crucial for developing effective, personalized treatment strategies.
  • Integrating morphologic and molecular data provides a foundation for precision medicine in renal cancer therapy.

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