September 1st… as the hot summer floats away from London town and cooler autumn days draw in, it’s time to think about the upcoming fall cancer conference season – it’s quite a busy one this year!
In the coming weeks, I will be rolling out our series on the ESMO 2016 Previews (Twitter #ESMO16) and taking a more in-depth look at various topics of interest. The Copenhagen meeting is later than usual and also more compressed, with numerous sessions now held simultaneously. It used to be that you could take a break between key sessions, but not any more – there’s a lot going on this year.
One of the things that jumped out to me from a preliminary review of this year’s hectic ESMO program is an interesting novel target that had some early preclinical data at AACR, but that sadly got lost in the tsunami of data there.
It is good to have that reminder and be able to return to it in the context of broader data because overcoming barriers to drug resistance with targeted therapies is still an important issue that is worth researching.
You likely won’t see it in many analyst reports or previews, however, although it’s a hidden gem of great interest and well worth exploring in terms of what we know so far. This means that readers will be both prepared and intrigued – don’t be surprised to hear about some BD&L deals in this niche in the future.
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Continuing our series on the ASCO GI meeting, today marks the end of the conference coverage with an interesting look at overcoming resistance to EGFR therapies such as Erbitux and Vectibix.
One of the hallmarks of EGFR monotherapy in colorectal cancer is stable disease with eventual relapse, but few dramatic responses. This suggests that other factors may play a role in driving oncogenic activity.
Dr Tejpar, Leuven
Recently, patient derived xenografts (PDX) have begun to play an increasingly important role in helping to understand the biology of the disease and facilitate improved trial design.
Earlier this week, we discussed the molecular characterisation of the disease based on the keynote talk by Dr Sabine Tejpar. Her group in Belgium as well as others in Italy and Spain have been very active in European translational work in this area to identify and map the pathways influencing EGFR therapy in GI cancers.
What can we learn from the latest findings in this space?
The answer may well surprise you.
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After the recent raft of posts on immunotherapy, it’s time to turn our attention back to oncogenic addiction. A couple of key topics have dominated colorectal cancer over the years, namely what causes EGFR resistance and why don’t patients with the BRAF V600 mutation do as well with RAF monotherapy compared to melanoma patients?
In today’s post, we take a more detailed look at BRAF mutant colon cancer in terms of what we’ve learned so far and what the potential therapeutic solutions are, which could influence patient outcomes in a positive way.
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The ASCO 2014 season kicks off with the release of the embargo on main abstracts (other than the late breakers and plenary sessions) yesterday evening. Over the next week, I’m planning to cover some of the highlights (positive and negative) that I found interesting or worthwhile discussing. While there was nothing particularly earth shattering or new in the press briefing at lunch time yesterday, that’s not to say there aren’t some important data this year buried amongst the 5000+ abstracts.
Today I’m driving to Orlando and on Friday will be at the American Urological Association (AUA) meeting, so a lighter post will appear here on BSB regarding my initial topline highlights and lowlights tomorrow.
I decided to kick off the ASCO Previews first and focus on an altogether different topic, one that we’ve covered longitudinally on either PSB and BSB – originally with some scientific and translational data – and now with some initial clinical trials that look pretty encouraging thus far. The bench-to-bedside transition is often fraught with many challenges, but occasionally, they actually turn out quite well in practice.
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“You may say I’m a dreamer
But I’m not the only one.”
John Lennon, Imagine
As part of our ongoing series on the AACR Previews, today I want to take a closer look at some interesting scientific and clinical data in triple negative breast cancer (TNBC). One reason for this is that we need to remember that the disease, as currently defined, is essentially what’s left after taking out the ER+, HER2+ and inflammatory breast cancer subsets. In other words, it’s a very heterogeneous catch-all population, making clinical trials rather challenging at best. It also means that the chances of success in general all-comer trials is rather low.
It is my hope that as we learn more about the biology of this disease, we may see further subsets be defined by molecular peculiarities, much in the same way that gastrointestinal stromal tumours (GIST) were defined by KIT expression and CD117. Once we have more homogenous subsets, it will be easier to conduct trials just looking at those specific patients, thereby improving the chances of clinical success with therapeutic intervention.
There’s been a lot of work focused on this area over the last few years, so it seems a good point to find out where the progress has got to.
Without much further ado, what can we learn about the biology of TNBC from AACR this year and which potential new targets might emerge?
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