Related Experiment Video

Updated: Jun 11, 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

Temsirolimus in VEGF-refractory metastatic renal cell carcinoma

M J MacKenzie1, B I Rini2, P Elson2

  • 1Department of Medical Oncology, London Regional Cancer Program, London, Ontario, Canada.

Annals of Oncology : Official Journal of the European Society for Medical Oncology
|July 3, 2010
PubMed
Abstract

Insights

Temsirolimus showed manageable toxicity in metastatic renal cell carcinoma (RCC) patients previously treated with VEGF inhibitors. The median time to progression was nearly 4 months in this poor-prognosis group.

Area of Science:

  • Oncology
  • Pharmacology

Background:

  • Temsirolimus is an intravenous mTOR inhibitor used in first-line metastatic renal cell carcinoma (RCC).
  • Its efficacy after prior vascular endothelial growth factor (VEGF) inhibitor failure was previously unknown.

Purpose of the Study:

  • To evaluate the efficacy and toxicity of temsirolimus in metastatic RCC patients who failed prior VEGF inhibitors.

Main Methods:

  • Retrospective review of 87 metastatic RCC patients treated with temsirolimus under a compassionate use program.
  • Data collected included demographics, toxicity, and objective response rates (RECIST criteria).

Main Results:

  • Objective response rate was 5%, with 65% achieving stable disease.
  • Median time to progression (TTP) was 3.9 months; median overall survival was 11.2 months.
  • Common toxicities included hyperglycemia and noninfectious pneumonitis.

Conclusions:

  • Weekly intravenous temsirolimus demonstrates manageable toxicity in pre-treated metastatic RCC patients.
  • The treatment provides a time to progression approaching 4 months in this patient population.

More Related Videos

A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies06:38

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

Published on: April 12, 2017

Utilization of Ultrasound Guided Tissue-directed Cellular Implantation for the Establishment of Biologically Relevant Metastatic Tumor Xenografts07:50

Utilization of Ultrasound Guided Tissue-directed Cellular Implantation for the Establishment of Biologically Relevant Metastatic Tumor Xenografts

Published on: May 25, 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...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...