Highlight: Scientific breakdown of cancer reveals promising results

Sep 09, 2010

The chemical structure of the melanoma-shrinking drug PLX4032 is revealed in a new Nature paper that describes the drug’s discovery, development and functioning.

PLX4032 recently showed promising results in an early clinical trial of patients carrying a mutated version of the BRAF gene. Gideon Bollag and colleagues now explain the science behind the success story.

In particular, they note that sufficiently high levels of the drug, which works by blocking the activity of the oncogenic B-RAF , are needed to yield clinical effects, because the ERK signalling pathway, downstream of B-RAF, needs to be almost completely blocked.

The study demonstrates how the design of early clinical trials based on the biological mechanisms underlying tumour formation can speed the translation of anti-cancer drug from laboratory to clinic. And whilst the long-term effects of PLX4032 remain uncertain, it’s hoped that the small molecule inhibitor prove useful in combination with other targeted agents, immunotherapies or chemotherapies.

Explore further: Gene test aids cancer profile

More information: Paper: DOI: 10.1038/nature09454

add to favorites email to friend print save as pdf

Related Stories

Recommended for you

Gene test aids cancer profile

58 minutes ago

The first round of chemotherapy did little to suppress Ron Bose's leukemia. The second round, with 10 times the dose, knocked the proliferating blast cells down, but only by half.

How a common antacid could lead to cheaper anti-cancer drugs

18 hours ago

A popular indigestion medication can increase survival in colorectal cancer, according to research published in ecancermedicalscience. But in fact, scientists have studied this for years - and a group of cancer advocates want t ...

User comments : 0

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.