Targeting Cancer
Cancer is not a single disease but is instead caused by the presence of multiple genetic mutations, that are unique in each and every patient. Certain genetic mutations may be shared, but the exact pattern of faulty genes that lead to cancer onset and progression will always be different.
 |
| + Zoom image |
|
|
Cancer drugs are now being developed to the most prevalent mutations, but researchers will also need to target less frequent mutations and develop rational drug combination’s to achieve superior and long lasting effects. Diagnostic screening based upon primary genetic markers and functional SNP signatures will also allow diagnosis, prognosis and the prescription of targeted treatments to be more effective; so it is clear that future medicine will become highly personalised.
A recent breakthrough by the Sanger Institute (Nature 2009) saw the tumour vs. normal genotypes for acute myeloid leukeamia, lung and breast cancer patients mapped. This breakthrough requires a functional annotation of the 20,000 to 30,000 genetic variances identified in order that that a whole new class of diagnostic biomarkers and drug targets can be exploited in the future.
The good news is that 100s of cancer genes have now been characterised for current drug targeting. Recent clinical trials in the colorectal cancer field have begun to identify how composite genetic mutations interact to modify patient responses. Horizon founders have been at centre of determining that (K-Ras, B-Raf & PI3K) mutations impart resistance to marketed cancer drugs; Erbitux and Vectibix.
Even though a direct correlation between patient genotype and drug response is incontrovertible, there remains a key question to be addressed: How can the development of new targeted treatments to specific mutated genes be accelerated so that a toolbox of drugs large enough to rationally mix and match to each patient be assembled?
More information
