Fall in Boston during the AACR-NCI-EORTC Triple meeting
After recent updates on targeting KRASG12C and HRAS, let’s not forget that there are plenty of other elements of the RAS pathway that can be considered, not least is upstream receptor kinases such as EGFR and sideways to SHP2.
What happens when those worlds collide?
Quite a bit it would seem.
If we want to seriously impact patient outcomes for the better then we need to explore rational combination approaches.
Here’s one way to do it…
Please note that this is an early target with not very many competitors, so there’s plenty that can happen here on multiple fronts!
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Over the last decade we have seen some real progress with some subsets of lung cancer, particularly in EGFR mutated and ALK translocated tumours. Indeed, an incredible amount of translational work has emanated from just a few groups based in Boston, New York and Hong Kong.
Dr Jeff Engelman Source: MGH
At AACR earlier this year, Dr Jeffrey Engelman (MGH, Boston) gave a fantastic talk not just about heterogeneity, resistance mechanisms, but also on how lung cancer can transform. Included in his review was the role of biospies and how he sees those evolving.
I’ve been meaning to write up this important talk since April, but decided to wait until the key publications that were in press at the time were actually published – it was a longer wait than expected!
In general, it is our policy to write up published, rather than unpublished data, out of respect to researchers. It also makes it more useful to readers when the translational and clinical data is publicly available for those interested in reading the in-depth research articles. We also gathered commentary from other though leaders in the lung cancer space for some additional insights.
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