Related Experiment Video

Updated: Jun 22, 2026

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy

Published on: April 29, 2014

Inhibition of mTOR in kidney cancer

A Kapoor

    Current Oncology (Toronto, Ont.)
    |May 30, 2009
    PubMed

    Insights

    Targeting the mammalian target of rapamycin (mTOR) pathway shows significant promise in treating advanced renal cell carcinoma (RCC). mTOR inhibitors like temsirolimus and everolimus improve survival outcomes for RCC patients.

    Area of Science:

    • Oncology
    • Pharmacology

    Background:

    • The mammalian target of rapamycin (mTOR) pathway is a critical mechanism in cancer development and progression.
    • Renal cell carcinoma (RCC) is a complex malignancy where targeted therapies are increasingly important.

    Purpose of the Study:

    • To evaluate the efficacy of mTOR inhibitors in the treatment of advanced renal cell carcinoma (RCC).
    • To review the clinical evidence supporting mTOR-targeted therapy in RCC management.

    Main Methods:

    • Review of clinical trial data for mTOR inhibitors (temsirolimus, everolimus) in RCC treatment.
    • Comparison of mTOR inhibitors against standard treatments (interferon alfa) and placebo.

    Main Results:

    • Temsirolimus demonstrated improved overall and progression-free survival compared to interferon alfa in first-line RCC treatment for poor-prognosis patients.
    • Everolimus showed improved progression-free survival in patients with advanced RCC progressing after VEGFR tyrosine kinase inhibitor therapy.

    Conclusions:

    • Targeting the mTOR pathway is a clinically validated and effective strategy for managing advanced renal cell carcinoma.
    • mTOR inhibitors represent a significant advancement in the treatment landscape of RCC.
    Keywords:
    Temsirolimuseverolimuskidney cancermtor inhibitorsrenal cell carcinomasirolimus

    More Related Videos

    Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

    Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

    Published on: July 21, 2018

    Related Concept Videos

    mTOR Signaling and Cancer Progression03:03

    mTOR Signaling and Cancer Progression

    The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
    The mTOR pathway or the...
    mTOR Signaling and Cancer Progression03:03

    mTOR Signaling and Cancer Progression

    The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
    The mTOR pathway or the...
    PI3K/mTOR/AKT Signaling Pathway01:22

    PI3K/mTOR/AKT Signaling Pathway

    The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
    Inhibition of Cdk Activity02:34

    Inhibition of Cdk Activity

    The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
    Inhibition of CDK Activity02:34

    Inhibition of CDK Activity

    The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...