Today we continue the second of a two part interview with a global thought leader who is also a scientist-clinician and well versed in cancer research as well as clinical trials.
Old Town Hall, Munchen
We explore how we can do clinical trials better in order to learn via a more rigorous process what works, what doesn’t, and why. After all, we we don’t know why certain approaches didn’t work or what the mechanisms of resistance are, how can we possibly improve?
Randomness is not necessarily a good thing in clinical research, especially if you don’t know what target you’re actually trying to hit!
If you missed the first part of this latest KOL interview and want to catch up then you can find it here (Link).
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Two of the most intriguing developments in cancer research over the last 5 years have been checkpoint blockade and CAR T cell therapies. There’s no doubt that they work – in some patients – or that toxicities can be challenging to manage at times, but what has been very interesting to me has been physician reactions to the rise of immunotherapies.
There has been much noise about biomarkers, including whether they work or not in this niche, as well as how do we go about selecting patients for therapies and combinations?
Ultimately, immunotherapies will be no different from targeted therapies in that we need to better understand the underlying biology in order to move forward beyond the low hanging fruit and figure out how we can best select appropriate therapy for each individual based on their particular characteristics.
The worry that many researchers have is that we could end up making the same mistakes with immunotherapies as targeted therapies, i.e. treat them in a broad fashion akin to throwing mud at the wall. Indeed, some companies are already doing this, much to the consternation of the research community.
So how do we go about doing things better and thinking more strategically about what needs to be done?
Up next is the first in a two-part interview series with a global thought leader who is a scientist-clinician with expertise in both immunology and oncogenic pathways. What does he have to say about where we are now and importantly, what does the future hold?
This is the penultimate article in our coverage from the Triple meeting in Munich, held in November 2016.
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We’re continuing our series of posts from the 2016 San Antonio Breast Cancer Symposium (SABCS) with an expert interview on how circulating tumor DNA could change breast cancer treatment.
There has been a noticeable increase in attention and focus on the application of liquid tests – especially from blood – over the last five years, culminating in a spinoff company called Grail from the deep sequencing giant, Illumina, announcing a massive funding round earlier this month.
At the time of the BSB expert interview in San Antonio, we had no idea that the Grail news was going to hit just a couple of weeks later!
While much of the media attention surrounding Grail has focused on the early detection of cancer in apparently healthy individuals, there’s actually a much more useful application where it could be more immediately applied to great effect.
Circulating tumor DNA (ctDNA) or cell free DNA (cfDNA) has the potential to revolutionise and improve monitoring over time for people with cancer who are receiving therapy.
This is the third in our series of expert interviews from the 2016 San Antonio Breast Cancer Symposium (#SABCS16).
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BioTwitter is all a-flutter today with the announcement from BMS that the CheckMate–026 trial in first line non-small cell lung cancer (NSCLC) comparing nivolumab (Opdivo) to chemotherapy did NOT meet its primary endpoint of progression-free survival (PFS).
The news was not entirely a surprise to us at BSB, here’s why…
Figurative statute representing Science on Holborn Viaduct in City of London.
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Biomarkers are a hotly debated topic at the moment within the cancer immunotherapy field.
At the recent Society for Immunotherapy of Cancer annual meeting (SITC 2015), there was even a debate with industry representatives arguing the “pros” and “cons.” Daniel Chen, MD PhD from Genentech (pictured right) argued “pro” and Steven Averbuch MD (pictured left) from BMS argued “con.”
The challenging question for anyone at the moment is if your Parent, Spouse or Best Friend were PD-L1 negative, would you still want them to receive a PD-1/PD-L1 checkpoint inhibitor (presuming it was indicated for the disease) and have a chance of a response, even if their PD-L1 negativity would suggest only a slim chance of responding?
AT SITC 2015 we spoke with an industry expert who offered insights into a leading company’s biomarker strategy and what the future may look like in 5-7 years time.
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Several groups have banded together to produce the first CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference (Twitter #cicon15) which focuses on the science underlying the immune system as it relates to cancer. You can view the program agenda here.
These groups include the American Association for Cancer Research (AACR), Cancer Research Institute (CRI), Association for Cancer Immunotherapy (CIMT), the European Academy of Tumor Immunology (EATI).
We’ll hopefully be covering key abstracts at this event over the next few days and reporting on not only what the data is, but also the broader significance of the findings.
It’s time for the August mailbag where we answer questions about cancer research and R&D from subscribers.
After the recent queries about immuno-oncology, it’s time to focus a little on targeted therapies again. Neither chemotherapies nor targeted therapies are going to go away – they are still the bedrock of many treatment approaches in the clinic today. Sadly though, much of the new data for the latter trials were easily swamped by the sheer tsunami of immunotherapy data in Philadelphia (AACR) and Chicago (ASCO).
One important area that we have been discussing on both blogs for some time is the value of well designed basket trials. It’s time to revisit this concept in the light of new data relating to the BRAF V600 mutation outside of metastatic melanoma.
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Anyone who has been regularly to the American Society of Clinical Oncology (ASCO) over the last decade or two will have have sat through quite a lot of trials with doublets and triplets in numerous advanced solid tumours and seen an impressive graveyard of failed cytotoxics and targeted therapies build up… Too toxic, lack of efficacy, futile even. This is especially true for some of the more difficult to treat cancers such as pancreatic, small cell lung cancer, melanoma, glioblastoma and soft tissue sarcomas.
There is hope though, after all, things have changed quite dramatically in the metastatic melanoma landscape over the last five years that it is now quite unrecognisable compared to a decade or even five years ago. This is very good news indeed.
What about the other tumour types in that list, though? How are we making progress with those?
In the latest series here on BSB, we’re going to focus on the new developments happening on the fringes of cancer research out of the main spotlight and look in more depth at what’s looking promising in some of these areas. Today, we’re going to start with small cell lung cancer (SCLC), a truly devastating disease with a horribly dismal prognosis.
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It’s now time to turn our attention to genitourinary oncology and, in particular, prostate, renal and urothelial bladder cancers. This week brings this ASCO GU meeting (#GU15), which is being held in Orlando this year and began this morning.
There are quite a few interesting topics being covered here, particularly in the poster sessions over the next three days. Hopefully, 2015 will also bring more good news in this space as 2014 was a rather dismal one on several fronts!
We decided to highlight some of the most interesting abstracts on castrate resistant prostate cancer and urothelial bladder cancer in our latest conference preview.
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After the intensity of gastrointestinal cancer, we now turn our attention to genitourinary (GU) cancers with the upcoming ASCO GU meeting later this week in Orlando.
Two of the big topics here will be prostate and renal cell (RCC) cancers.
Unfortunately, the long awaited data in adjuvant RCC demonstrated that early treatment with sorafenib or sunitinib did not improve outcomes in locally advanced kidney cancer after resection. According to the ASCO press release, the trial conducted by Dr Haas and colleagues at U Penn discovered that:
“The average period to disease recurrence was similar between those who received sorafenib or sunitinib after surgery (5.6 years) and those treated with placebo (5.7 years).”
We will therefore turn our attention to castration resistant prostate cancer (CRPC).
One of the recent and ongoing controversies is splice variants, especially AR-V7, which is thought by some research groups to confer resistance to the hormonal therapies, enzalutamide and abiraterone. The big question though, is does it, and how useful is an assay in helping to determine appropriate therapy? Are there other factors at play?
We looked at the latest data and put the findings in context with what we know from other published research.
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