It’s February 2nd, which means Groundhog Day in America. I was idly wondering how accurate the rodent Punxsutawney Phil was, after all, he’s got a 50:50 shot of being right or wrong. Who knew someone had analysed the predictions already and what’s more – published them?!
Meanwhile we don’t need no predictions for today’s post, where we look at the evidence gleaned from several clinical studies in lung cancer and come to some important strategic conclusions about the findings.
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A look at upregulated targets outside of the BCR signalling pathway and what small molecules are looking promising
In our final preview of ASH 2020 exploring key abstracts and what to watch out for this weekend, we offer the second half of our discussion around small molecules in early stage development.
There’s always a roller coaster ride in any early stage drug development and small molecule inhibitors are no different from antibodies, bispecifics, or even immunotherapies in this respect.
There are certainly some unexpected and surprising overlaps discussed and uncovered here plus also some novel combination approaches either being considered or which may potentially need to be considered in the future.
So what’s in store this time around?
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Rodin’s The Thinker sculpture Source: Wikimedia Commons
Recently, I have been pondering a raft of clinical and translational data we have seen emerge across multiple virtual conferences from several different categories of therapies such as checkpoint blockade, targeted therapies, PARP inhibition, epigenetics, and even mathematics.
Many people tend to look at these disparate categories and see them as quite different therapeutic options, but lately I have began to wonder if they are in fact much more inextricably linked than seems obvious at first glance?
This turned into a broader strategic post about advanced solid tumours and how we might think a little differently about underlying concepts and conceptual frameworks…
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It’s the dog days of summer and time for some meaty controversy to read!
For the longest time there have been several cancer types which have been incredibly difficult to treat therapeutically.
Metastatic melanoma and non-small cell lung cancer (NSCLC) both used to be in this category, as did glioblastoma and advanced pancreatic ductal adenocarcinoma (PDAC).
We have made great strides in changing the face (and more importantly outcomes!) for people with both metastatic melanoma and lung cancer, so what’s happening on the pancreatic cancer front?
The last two years gave certainly thrown up a series of disappointing clinical trial readouts such as RESOLVE, HALO–301, CanStemIIIP, and SEQUIOA, for example, where in each and every case the findings favoured the control arm of gemcitabine plus nab-paclitaxel over the experimental arm in terms of improving survival. Not one of them was able to raise the bar and show a significant improvement over standard therapy, which is pretty disappointing.
So what can be done to change the face of PDAC?
If we want to improve further then we need to go back to basics and enhance not only our understanding of the funadamental biological mechansisms and processes, but also the models we use to interrogate the systems involved.
In this post, we look at six key new areas of research in PDAC and explain what we’ve learned and why they matter if we are to see new therapeutic developments arise from the ashes of the past…
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The Francis Crick Institute in London has an admirable program of engagement with the public and external researchers.
Attending a Crick Lecture recently presented by Cancer Research UK (CRUK) Chief Scientific Officer, Prof Karen Vousden CBE FRS, reminded me of my days as a PhD student at nearby King’s College London.
Regular BSB readers will recall that Prof Charles Swanton FRS is the Chief Clinician of CRUK.
In her Crick lecture, Prof Vousden elegantly explained to the audience why p53 mattered and how it might be targeted by small molecules.
What is the potential of this research for translational drug development? In this post, we take a look at new developments in the basic understanding of what p53 does, the current state of targeting p53 and Prof Vousden’s latest approaches.
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