Today, I’m going to summarise some of my notes on what we learned about lung cancer and immunotherapy at AACR. The burgeoning immuno-oncology topic is way too big to do justice in one single post, so over the next couple of days, you’ll find a mini series evolving here on BSB to cover many of the points relating to checkpoint inhibitors from AACR. It was the first time in 15 years I’ve seen immunotherapy dominate a basic scientific meeting and it was good to see it happen. It is definitely very much the focus – and excitement – of many major cancer centres in the US.
Sometimes you get lucky before a conference and catch an interview with a thought leader ahead of time when it’s more relaxed and less fraught with all the demands of meetings etc while there.
This weekend, a controversy erupted at the American Association for Cancer Research (AACR) relating to Juno’s chimeric antigen receptor (CAR) T cell therapy following a series of tweets by Jonah Lomu, a keen biotech investor:
In the past, I’ve sometimes been accused of being a bit of an immunotherapy bear for my dislike of cancer vaccines as a single agent therapy in advanced disease where the tumour burden is very high. That particular field has undoubtedly been a huge graveyard for many companies, much in the same way that metastatic melanoma was, until novel therapeutics and immunotherapeutics emerged to push through the envelope.
“You may say I’m a dreamer
But I’m not the only one.”
John Lennon, Imagine
For the third part of the series on the AACR Previews, I wanted to switch directions and take a broad look at five completely different approaches in cancer research that we haven’t discussed on Biotech Strategy before and look at how they are doing and which ones might be promising going forward. Some of these scientific developments could potentially impact existing compounds in development.
Following on from yesterday’s post on the potential for small basket trials in ER+ breast cancer with the ESR1 mutation, I wanted to highlight another area where these type of highly focused and rational studies appear to be not only useful but also potentially produce stunning responses.
Today brings the launch of our series on the AACR annual meeting Previews. A variety of different topics will be covered over the next two weeks, not just by tumour type and pathway, but also to highlight some novel research that is emerging on various driver mutations that not only can cause resistance to occur, but may also be viable targets for therapeutic intervention.
Every year at AACR meetings there seems to be a new update on how researchers are doing with their work on overcoming resistance in metastatic melanoma. We’ve seen some stunning photos where targeting the BRAF V600E mutation with a specific kinase inhibitor such as vemurafenib (Zelboraf) or dabrafenib (Tafinlar) results in dramatic reduction, and sometimes even complete disappearance of the lesions, only for resistance to set in and the melanoma sadly comes back with a vengeance. Adding a MEK inhibitor such as trametinib (Mekinist) was originally thought to be a rather promising strategy, until it became clear that this only gave a few extra months with exactly the same result.