Can we break through the barriers of a hostile tumour microenvironment?
Who would have thought that after 30 years of no new therapies that urothelial carcinomas would suddenly be almost constantly in the spotlight with enticing words like cancer immunotherapy, biomarkers, tumour microenvironment, translational immunology etc?
And yet it has happened – with a lot more to come in this highly competitive niche too.
Prior to AACR in Chicago, we highlighted TGFβ in our Preview series as an important emerging target that is gathering attention and may be relevant in tumour types, such as urothelial carcinoma and ovarian cancer.
After the meeting, Dr Paul Rennert (CSO, Aleta Biotherapeutics) noted:
I don’t disagree with either of these sentiments – there was a reason we interviewed a lot of NK cell enthusiasts recently and we have since been rolling out our thought leader mini-series focused on TGFβ. Yesterday, we kicked off with perspectives from an academic researcher active in this field and tomorrow will showcase some practical clinical perspectives.
On deck today, we have a interview with a research scientist who has conducted both basic and translational work for a discussion about how he sees the learnings that have arisen from bench to bedside and back again.
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2018 is likely to be the year of various immunotherapy combinations as we go beyond monotherapy approaches to see which doublets or triplets will yield improved outcomes. Originally, we had expected to see key data last year, but moving overall survival to a co-primary endpoint with PFS in many studies delayed the readouts by 12 or more months.
SGO 2018 – Who dat?
What’s happening now is that we have started to see some of the early data trickle out and there’s much more to come in the next few months as we head into ASCO and ESMO.
The last two months have seen much attention on lung cancer, but what about a less hyper-mutated tumour types such as ovarian or endometrial cancers? What’s happening in these women’s cancers?
Going beyond monotherapy with PARP inhibitors or checkpoint blockade is important if we truly want to start pushing the survival curves upwards and to the right.
It’s time for a new update on this hypercompetitive niche…
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A short, but quite important, post today highlighting an early target we are keen to follow in terms of combination trials in both GI and GU cancers, as well as others.
There’s been a lot of focus this year on the so-called inflamed (hot) and non-inflamed (cold) tumours, but what about the intermediate ones that many refer to as the immune excluded phenotype?
View of Geneva from Cathedral St Pierre, Switzerland
Clearly it makes sense to consider different combination approaches in each category, but what would be appropriate? Before we can set about doing that, we first have to uncover the mechanisms causing the inhibition on the tumour microenvironment and then figure out how best to identify those patients most likely to benefit.
Over the last couple of years, we’ve seen and written a lot about various potential candidates (not all will be useful), including myeloid derived suppressor cells (MDSCs), regulatory T cells (Tregs), tumour associated macrophages (TAMs), chemokines, cytokines, adenosine fog and many others.
There is one target that has started gathering a little bit steam over the last year that we have mentioned a couple of times on BSB and now there is something new to discuss here, at least from a big picture perspective.
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