A recent Institute of Cancer Research study published in the New England Journal of Medicine describes a novel way of treating BRCA-gene based cancers. Mutations in the BRCA-1 and BRCA-2 genes are routinely linked with higher incidence of breast and ovarian cancers in women; however, in healthy cells, the aforementioned genes are involved in a repair mechanism.The new drug, Olaparib, works by inhibiting an enzyme (PARP) involved in a different repair mechanism. Since healthy cells have the BRCA-based pathway as well as the PARP pathway, they can always repair themselves using the former method if the latter is inhibited. On the other hand, BRCA-based cancers do not have the BRCA pathway as an option, so inhibiting the PARP pathway destroys their only repair pathway. Quite a mouthful, but simple to understand. ๐
Eliminating two methods of cellular repair sure does pose a threat to the propagation of cancer cells. ๐ Studies have shown that healthy cells remain relatively unscathed (since they have several options for self-repair), but cancer cells die. I surmise that future studies will encompass cancers not directly related to a mutation in the BRCA1 and BRCA2 genes.
This is one fork of the future of personalized medicine – using an individual’s own molecular weaknesses for positive results.
I love how fundamental concepts can be used in such radical ways. In this case, analyzing the difference between healthy cells and cancer cells, and exploiting any variations to damage the latter while preserving the former. Medicine really is a grand application of simple ideas. ๐



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