Resistance of Renal Cell Carcinoma to Sorafenib Is Mediated by Potentially Reversible Gene Expression
2011

Reversible Resistance of Renal Cell Carcinoma to Sorafenib

Sample size: 10 publication 10 minutes Evidence: moderate

Author Information

Author(s): Zhang Liang, Bhasin Manoj, Schor-Bardach Rachel, Wang Xiaoen, Collins Michael P., Panka David, Putheti Prabhakar, Signoretti Sabina, Alsop David C., Libermann Towia, Atkins Michael B., Mier James W., Goldberg S. Nahum, Bhatt Rupal S.

Primary Institution: Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States of America

Hypothesis

Resistance to antiangiogenic therapy in renal cell carcinoma may be reversible due to physiological changes rather than permanent genetic alterations.

Conclusion

Resistance to sorafenib in renal cell carcinoma appears to be reversible, suggesting that treatment breaks may restore sensitivity to therapy.

Supporting Evidence

  • Reimplanted tumors maintained their ability to stabilize on sorafenib despite prior resistance.
  • Gene expression profiles of reimplanted tumors resembled those of untreated tumors.
  • Revascularization and reduced perfusion were observed upon re-exposure to sorafenib.

Takeaway

This study found that some kidney cancer cells can stop resisting a drug called sorafenib if they take a break from it, which means they can be treated again later.

Methodology

Mice with human renal cell carcinoma xenografts were treated with sorafenib, and tumor growth and gene expression were analyzed before and after treatment breaks.

Limitations

The study was conducted in mouse models, which may not fully replicate human responses.

Statistical Information

P-Value

0.0029

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0019144

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication