GTPase
JammingVille
Recently, I wrote (quite a lot) about the development of a new drug that has shown real efficacy against hard-to-treat pancreatic cancers.
The initial findings with 'daraxonrasib', a truly innovative inhibitor against the virulent Ras oncoprotein that drives these tumours were so positive that it has been deemed a breakthrough wonder drug.
Except, as so often happens with new anti-cancer treatments, it is turning out that a significant percentage of the treated tumours rapidly evolve and become resistant to the drug.
As a result, clinicians are have ramped up follow-up studies in which the tumours of treated patients are being longitudinally biopsied/sampled before and during treatment in an effort to identify ways that the tumors can be better treated for more long lasting responses.
So far, preliminary findings, which were presented at a conference of the American Association for Cancer Research last week, suggest two not necessarily mutually exclusive possibilities:
1) The fraction of tumor cells that survive the initial treatment may be more susceptible to classical chemotherapy which suggests that a combinatorial treatment strategy may be effective.
2) The surviving tumor cells also appear to start producing increased amounts of the Ras oncoprotein. This suggests that whacking the cells with multiple Ras inhibitors (there are a bunch more of them in the pipeline) might also be effective.
It's important to reiterate that these findings are still preliminary. They are also correlative and have not been functionally tested yet. Additionally, the work has not yet been rigorously peer-reviewed.
Having said all that, it sure is interesting to see the science being reported,pretty much in real time, given that the initial FDA approval of daraxonrasib was only granted in August of this year in response to the initial breakthrough clinical trial results.
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