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ShareFeb. 8, 2013 — Findings from clinical trial patients with metastatic renal cell carcinoma, a common kidney cancer, show they did not have accelerated tumor growth after treatment with sunitinib, in contrast to some study results in animals. Sunitinib is one of several drugs, either on the market or undergoing testing, that target blood vessel growth. There had been debate, based on the animal studies, about whether tumor blood vessel changes induced by these drugs promoted tumor growth and/or caused cancer to spread. In this study, Tito Fojo, M.D., Ph.D., head of the Experimental Therapeutics Section, Medical Oncology Branch and Affiliates, NCI, and his colleagues, found that not to be the case.
Results of their study appeared in Cell Reports, Feb. 7, 2013.
Using a mouse model to assess small, relatively newly developed tumors can be much more challenging than assessment in humans who tend to have more established tumors several centimeters in size. To address whether sunitinib accelerated tumor growth in humans, researchers analyzed data from a randomized phase III trial comparing sunitinib with interferon alfa in patients with kidney cancer. Using a novel methodology for assessing efficacy , they found sunitinib reduced the tumor's growth rate while improving survival, without appearing to negatively alter tumor biology after discontinuation.
Their findings suggest that concerns arising from animal models may not apply to patients receiving sunitinib and most likely will not apply to patients using similar agents, but recognize more studies may need to be done.
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The above story is reprinted from materials provided by National Cancer Institute (NCI) at NIH.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Krastan B. Blagoev, Julia Wilkerson, Wilfred D. Stein, Robert J. Motzer, Susan E. Bates, A. Tito Fojo. Sunitinib Does Not Accelerate Tumor Growth in Patients with Metastatic Renal Cell Carcinoma. Cell Reports, 2013; DOI: 10.1016/j.celrep.2013.01.015
Note: If no author is given, the source is cited instead.
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