Gems from the poster halls yielded some fascinating novel approaches and new twists on old targets
In this latest post ASH review, we explore some intriguing early developments from several small and large companies alike, explain why they matter and why we should be interested in them.
Sometimes the wisdom of the crowds isn’t always the best indicator of what’s coming down the pike in terms of oncology pipelines.
Part of our cunning plan this year involved going to ‘off Broadway’ sessions where we thought others would skip in favour of a more obviously popular session (the ones in the big halls) and merrily tweet them so you could easily follow along in parallel while the smaller rooms rapidly filled up and quietly closed to those desperately trying to get in late.
Our selections here include several gems from the poster halls (imagine trying to just pick a few highlights out of 4,000 poster options?!), as well as a couple of oral presentations that were missed by many – not surprising given how jam-packed the schedule was with double and even triple choices of selections in parallel to choose from!
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Time for some reflection
Before we get to the World Congress in Lung Cancer (WCLC) taking place this weekend, I want to take a moment to reflect on some of the things we have learn over the last few weeks.
It’s time for a reader mailbag as we answer reader questions on the recent MYC mini-series, as well as covering bromodomain inhibitors (what’s going on there?) and discuss a new PROTAC compound in early development that looks quite interesting.
We also explain why that is the case…
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Philadelphia – Day 3 of the AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics meeting continues to deliver on high quality talks with excellent data to discuss and parse.
Dr Jay Bradner (NIBR) at #Targets17
The session on epigenetics and transcription factors is always one of my favourites and this year didn’t disappoint.
There were also sessions on imaging, non-mutated genes, the tumour microenvironment and of course, a long poster session to browse. Thankfully the poster halls weren’t as mobbed as they were at ASCO earlier in the year, but they were still pretty busy and well attended.
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Have you ever sat in a freezing cold scientific session and been so engrossed in the compelling presentations that followed, you simply forgot to take notes? Not one. That actually happened to me at the American Association for Cancer Research (AACR) in Philadelphia this year in one of the many fringe sessions that I attended.
Reading Terminal Clock, Philadelphia
Granted, the hot topic of the conference was undoubtedly checkpoint inhibition, but I was anxious to escape to the comfort of some meaty and familiar basic and translational science, namely MYC. MYC is largely thought to be a difficult to target, even undruggable protein, and along with RAS and p53, represents a formidable challenge for cancer researchers. These three oncogenic proteins alone are probably responsible for more drug resistance developing and even death from cancer than any other proteins in a patient with advanced disease.
For cancer patients with advanced disease, the clock is ticking on time they have left.
Solve these three problems (MYC, RAS and p53) and we may have a shot at dramatically improving outcomes. As Dr Gerard Evan (Cambridge) noted:
“I think it’s fair to say that we don’t really know why interruption of any oncogenic signal actually kills cancer cells, but one of the reasons that we’re interested in MYC is because it seems to be a common downstream effector of many, maybe all cancers.”
Sure, the road to success is paved with an enormous graveyard of failures, just as metastatic melanoma was before checkpoint blockade came along, ironically. What I heard at AACR both inspired and filled me with greater confidence… we’re finally getting somewhere.
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