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Updated: Sep 20, 2025

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
Published on: February 8, 2020
No Time to Die: How Kidney Cancer Evades Cell Death
Carlo Ganini1,2, Manuela Montanaro1, Manuel Scimeca1
1Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133 Rome, Italy.
Abstract:
The understanding of the pathogenesis of renal cell carcinoma led to the development of targeted therapies, which dramatically changed the overall survival rate. Nonetheless, despite innovative lines of therapy accessible to patients, the prognosis remains severe in most cases. Kidney cancer rarely shows mutations in the genes coding for proteins involved in programmed cell death, including p53. In this paper, we show that the molecular machinery responsible for different forms of cell death, such as apoptosis, ferroptosis, pyroptosis, and necroptosis, which are somehow impaired in kidney cancer to allow cancer cell growth and development, was reactivated by targeted pharmacological intervention. The aim of the present review was to summarize the modality of programmed cell death in the pathogenesis of renal cell carcinoma, showing in vitro and in vivo evidence of their potential role in controlling kidney cancer growth, and highlighting their possible therapeutic value.
Insights
Targeted therapies can reactivate programmed cell death pathways, like apoptosis and ferroptosis, in kidney cancer. This research reviews evidence for their therapeutic potential in renal cell carcinoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Renal cell carcinoma (kidney cancer) pathogenesis understanding led to targeted therapies improving survival.
- Despite advances, prognosis for many kidney cancer patients remains poor.
- Programmed cell death pathways, including p53, are often impaired in kidney cancer.
Purpose of the Study:
- To review programmed cell death modalities in renal cell carcinoma pathogenesis.
- To summarize in vitro and in vivo evidence of cell death's role in controlling kidney cancer growth.
- To highlight the therapeutic potential of targeting cell death pathways in kidney cancer.
Main Methods:
- Literature review of studies on programmed cell death in renal cell carcinoma.
- Analysis of in vitro and in vivo experimental evidence.
- Examination of targeted pharmacological interventions.
Main Results:
- Kidney cancer exhibits impaired apoptosis, ferroptosis, pyroptosis, and necroptosis, facilitating tumor growth.
- Targeted pharmacological interventions demonstrated the ability to reactivate these cell death mechanisms.
- Evidence suggests these pathways can be therapeutically exploited to control kidney cancer.
Conclusions:
- Reactivating programmed cell death pathways presents a promising therapeutic strategy for renal cell carcinoma.
- Further research into targeting apoptosis, ferroptosis, pyroptosis, and necroptosis is warranted for kidney cancer treatment.
- Understanding cell death's role is crucial for developing novel kidney cancer therapies.
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