Sunday is usually a good day at ESMO congresses and 2017 was no different in that respect.
It does feel weird, however, to be seeing tweets about data from some studies hours before they are presented in that day’s Presidential Symposium, something oncologists attending have started to notice too:
Yesterday we had encouraging readouts from PACIFIC and FLAURA trials to discuss, so what’s in store for today? Are they mostly highights or lowlights?
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Munich – the EORTC-NCI-AACR Molecular Targets and Cancer Therapeutics conference is one of my favourite meetings on the cancer circuit. It’s small enough that you can catch people in the corridor and have a quick chat, while at the same time large enough that it attracts quality data. It’s also the place where you find people who think outside the box.
I want to hear from thought leaders who have the potential to be disrupters.
Talking of another kind of disruption, sadly the travel chaos caused by the Lufthansa pilot’s strike(s) meant some people didn’t make it to the meeting or arrived late. Despite the best efforts of Lufthansa, there was still a good turnout of posters today and several caught my attention!
Those who follow our cancer conference coverage know that the poster hall is often where the gems and insights are to be found, particularly when it comes to early drug development.
If you couldn’t make it to Munich, this post has commentary on four gems from the Wednesday poster session at EORTC-NCI-AACR that caught my attention. I’ve chosen to focus on novel targets and novel combination approaches…
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Over the last couple of years we have heard much about targeting various checkpoints that exert an inhibitory effect on the immune system and the T cells, in particular. The main targets where we have a growing body of evidence to date are CTLA-4, PD-1 and PD-L1, but there are others including LAG-3, TIM-3, ICOS etc.
Earlier this year at AACR, we saw new evidence that combining two checkpoints (anti-CTLA4 and anti-PD1) was superior to monotherapy in metastatic melanoma, albeit with a concomitant increase in toxicities.
What about the other inhibitory signals though? Are they bystanders, much like passenger mutations that have little effect, or do they matter, at least in some tumor types? If so, which ones?
We took a look at some of the emerging data associated with targeting TIM-3 – the results may well surprise some observers.
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