One of our popular series from conferences is Gems from the Poster Halls, where we take a look at some of the studies or research data that caught our attention and explain how they may have future significance. In the past, posters have lead to phase 2 or 3 trial designs and subsequent approval. Others have sadly missed signals in small studies that could have prevented an expensive phase 3 faiure. Hence, it is often important to pay attention to posters.
The ESMO16 Poster Hall Maze
Posters can also give early warning for what’s developing in pipelines. The BTK inhibitor, ibrutinib, was originally codenamed CRA–032765 (at Celera) and later PCI–32765 (at Pharmacyclics), for example, while the PI3K-delta inhibitor, idelalisib started life as CAL–101 (at Calistoga). We previously followed the progress of these compounds while they were in preclinical and phase 1 and documented progress long before they became active drugs in a race to market in CLL.
My favourite codename is always going to be STI–571 (imatinib). We would start planning ASCO and ASH activities every January and September, so companies should be well in hand in their preparations for ASH and SABCS by now. There’s a tremendous amount of work involved behind the scenes in order to have a great event, and I’m not talking about the fripperies like exhibits and light boxes here.
Last year at ECCO, StemCentRx burst on the scene and were subsequently acquired at a significant premium by AbbVie, taking quite a few people by surprise.
So what can we learn about the data from ESMO this year? What new trends are emerging this time around?
Here, we take a fresh look at FOUR interesting new developments from small and large pharma/biotech companies alike in Part 2 of the Gems series. In the first one [Link], we interviewed an expert and discussed their approach to biomarkers in early small studies to help them better design larger follow-on trials more effectively.
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One of the (many) highlights for me at the recent annual meeting of the American Association for Cancer Research (AACR) was a “Meet the Expert” session presented by Professor George Coukos.
Prof George Coukos AACR 2016
Professor Coukos is Director of Oncology at the University Hospital of Lausanne and Director of the Ludwig Institute for Cancer Research in Switzerland.
Ovarian cancer is becoming a fascinating battleground for cancer immunotherapy, with multiple challenges that must be overcome before we see improvements in outcomes, especially for women advanced disease.
The interview with Prof Coukos is a follow-on to the one we did on advanced ovarian cancer and checkpoint blockade at ECCO 2015 in Vienna with Dr Nora Disis (Link).
If you missed it, you can still listen to highlights in Episode 7 of the Novel Targets Podcast (Link).
After his AACR presentation, Prof Coukos kindly spoke with BSB and in a wide ranging discussion, highlighted some of the innovative clinical trial strategies he is working on to move the cancer immunotherapy field forward in ovarian cancer.
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Spring has arrived in many parts of the world, and with it I am always reminded of William Wordsworth’s classic poem, “I Wandered Lonely as a Cloud:”
I wandered lonely as a cloud
That floats on high o’er vales and hills,
When all at once I saw a crowd,
A host, of golden daffodils;
Beside the lake, beneath the trees,
Fluttering and dancing in the breeze.
So what does the future hold for cancer immunotherapy?
Inspired by Wordsworth, I’ve sat on my cloud and have looked at some of the recent review papers and thought pieces published by experts in the field. Do they offer a Jerry Maguire – like mission statement: “The Things We Think and Do Not Say: The Future of Our Business” or will we have to wait till AACR 2016 in New Orleans to learn more?
This is the latest in our pre-AACR 2016 annual meeting series. Subscribers can login to read more or you can purchase access.
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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