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Updated: Jul 4, 2026

A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies
06:38

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

Published on: April 12, 2017

Chemokines as therapeutic targets in renal cell carcinoma

Karen L Reckamp1, Robert M Strieter, Robert A Figlin

  • 1Divisions of Medical Oncology and Therapeutics Research & Hematology, City of Hope and Beckman Research Institute, 1500 E Duarte Road, MOB 1001, Duarte, CA 91010, USA. kreckamp@coh.org

Expert Review of Anticancer Therapy
|June 7, 2008
PubMed

Insights

Targeting chemokine pathways may improve renal cell carcinoma treatment by inhibiting tumor growth and metastasis. Combining chemokine inhibitors with therapies for angiogenesis and immunity offers potential for better patient outcomes.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Renal cell carcinoma (RCC) progression involves tumor angiogenesis, invasion, and immune evasion.
  • Chemokines play a critical role in promoting RCC growth, metastasis, angiogenesis, and immune evasion.
  • Understanding chemokine-mediated mechanisms is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To explore the role of chemokine signaling in RCC pathogenesis.
  • To identify potential therapeutic targets within chemokine pathways.
  • To investigate the potential of combining chemokine-targeting agents with other therapies.

Main Methods:

  • Review of current literature on chemokine signaling in RCC.
  • Analysis of interactions between chemokine pathways, VEGF, and hypoxia-inducible factor.
  • Evaluation of CXCR3/CXCR3-ligand and CXCR4/CXCL12 axes as therapeutic targets.

Main Results:

  • Chemokine interactions with stromal and neoplastic cells drive RCC progression.
  • Interactions between chemokine signaling, VEGF, and HIF pathways present therapeutic opportunities.
  • Modulation of CXCR3 and CXCR4 axes shows potential for RCC treatment.

Conclusions:

  • Targeting chemokine pathways, such as CXCR3 and CXCR4, offers a promising therapeutic avenue for RCC.
  • Combination therapies involving chemokine inhibitors, anti-angiogenesis agents, and immunotherapies may enhance patient outcomes in RCC.

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