One of the most significant obstacles in cancer treatment is drug resistance. Many drugs have immediate positive effects on patients only to lose potency over time. Because cancer cells have a unique ability to adapt, the ways in which they thwart sophisticated medicine can be different for each cancer type. Scientists like former Damon Runyon Scholar Ramesh A. Shivdasani, MD, PhD, are working to identify how cancer cells develop this resistance and designing new methods to overcome these adaptations.
Last month, Ramesh and a team of researchers at the Dana-Farber Cancer Institute discovered how some cancer cells evade Erbitux, a commonly-used treatment for colorectal and head and neck cancers.
Known generically as cetuximab, Erbitux successfully halts cancer cell growth in many patients. Unfortunately, its effectiveness mysteriously diminishes after about one year. Ramesh and his colleagues found that the protein ERBB2 signaled cancer cells to continue growing, essentially overriding the anti-growth signals from Erbitux. “Because ERBB2 isn’t affected by cetuximab, this is an easy way for cancers to become resistant to the drug,” said Pasi Janne, MD, PhD, a lead author of the study.
With up to 40% of colorectal cancers thought to be Erbitux-resistant, the team hopes that future clinical studies will reveal that a combination of Erbitux and ERBB2-blocking therapies can increase the treatment’s long-term potency and, ultimately, save lives.
> Video: Watch Ramesh discuss his work
> See how Erbitux works on YouTube
Quotes adapted from ScienceDaily.com
