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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It occurred to me after several such events this year that virtual meetings create a very different pattern for spectators from live events where we all dash from one hall to another trying to optimise the viewing experience and catch as many key talks as we can.
Instead of the annual rugby scrum in the ASCO poster halls, we can imagine ourselves in an entirely different world with social distancing virtually
Many people will no doubt be eager to listen to the various oral presentations of phase 3 data come Friday morning, while the poor posters may well languish until some undetermined time later, so why not take a step back and highlight some of the early work in developmental therapeutics ahead of time?
In the final part of our ASCO Preview series, we offer our independent take and candid commentary on ten abstracts in developmental therapeutics to watch out for.
A word of warning – we don’t take a particular perspective through the lens of rose tinted glasses, so not all the analyses are positive and there are some firm words against some of the selections regarding continued development or the researchers conclusions/recommendations.
Some of these are agents in early development, some are biomarkers or even emerging trends, but all are intriguing in their own unique fashion.
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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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