Chicago – the cancer immunotherapy poster session yesterday morning was “mobbed,” that is the only word to describe it. I have never seen such a crowded poster session at any medical meeting before. It speaks to the huge interest in this growing field.
It’s also a reflection that insights into the future direction of the field will be found in posters about preclinical and early work, rather than in oral presentations that reflect strategic decisions made a long time earlier.
We know checkpoint inhibitors work in many cancers, and a few more have been added to the list at this meeting. While that’s interesting, the real question is how do we increase the response rate and also get them to work in non-immunogenic tumors?
Yesterday in the poster session at ASCO, there was a poster that caught our attention on one approach that may achieve this. We briefly wrote about it in the ASCO Day 2 blog.
Also of note yesterday was that the new generic name for the PD-L1 checkpoint inhibitor from Roche/Genentech. MPDL3280A is now atezolizumab. A few presenters stumbled over the pronunciation, it was so new…… and all the z’s add to the trickiness!
As to what Day 3 at ASCO holds, we’ll be updating this blog during the day as our schedule permits.
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Chicago – after an evening of beer and networking at the unofficial ASCO15 Tweetup, the ASCO annual meeting, like a checkpoint inhibitor combination, releases the break and steps on the gas: the main data presentations start today. It’s “super saturday” at ASCO15.
Yesterday, the press had a preview of some of the cancer immunotherapy data to be presented this morning – we’ve shared our preliminary thoughts on this in yesterday’s ASCO15 Day 1 Cancer Immunotherapy post.
So what’s hot at #ASCO15 today?
We’ll be doing a rolling post throughout the day – when the opportunity presents we’ll provide some topline thoughts on sessions we’ve been to.
If you are here at ASCO, one #ImmunOnc presentation to watch out for this morning is the David A Karnofsky memorial award and lecture being given by Suzanne L. Topalian, MD in the main plenary hall (N Hall B1) at 11am.
From the recent presentations we’ve heard from her at AACR and AAI, her lecture entitled, “PD-1 Pathway Blockade – a Common Denominator for Cancer Therapy” should definitely worth listening to!
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Chicago – the 2015 annual meeting of the American Society of Clinical Oncology (ASCO) is underway. It’s the Super Bowl of clinical cancer research with approx 35,000 attendees from all over the world.
Earlier today, in a press briefing focused on cancer immunotherapy, we had a glimpse of some of the data that ASCO thinks is particularly newsworthy at the meeting.
In this post, we’ll offer some top-line thoughts and commentary on the following presentations by:
Dung T. Le “PD-1 Blockade in Tumors with Mismatch Repair Deficiency”
Anthony B. El-Khoueiry “Phase 1/2 Safety and Antitumor Activity of Nivolumab in Patients with Advanced Hepatocellular Carcinoma (HCC): CA209-040
Tanguy Y. Seiwert “Antitumor Activity of the Anti-PD-1 Antibody Pembrolizumab in Biomarker-Unselected Patients with R/M Head and Neck Cancer: preliminary results from the KEYNOTE-012 Expansion cohort.”
Luiz Paz-Ares “Phase III, Randomized Trial Checkmate 057 of Nivolumab (NIVO) versus Docetaxel (DOC) in advanced Non-Squamous (non-SQ) cell Non-small Cell Lung Cancer (NSCLC).
We’ll be writing a daily post from ASCO 2015 with regular updates on sessions we’ve attended, and initial thoughts and reactions. Our usual in-depth coverage will follow after the meeting.
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Yesterday, Juno Therapeutics announced a new deal for a collaboration with Editas Medicine that is:
“Focused on creating chimeric antigen receptor (CAR T) and high-affinity T cell receptor (TCR) therapies to treat cancer. The companies will pursue three research programs together utilizing Editas’ genome editing technologies, including CRISPR/Cas9, with Juno’s CAR and TCR technologies.”
This follows on from their recent deals with Fate Therapeutics and Stage Cell Therapeutics and bluebird bio’s licensing deal with Five Prime for novel antibodies to develop CAR T cell therapy.
One of the most interesting questions in CAR T cell development, is whether you need to incorporate a suicide gene or suicide switch into them that allows you to turn off the response, force the T cells to self-destruct, in the event of severe Cytokine Release Syndrome (CRS) or other serious adverse events.
This review article is another example that straddles data from conferences earlier this month at Immunology 2015 (AAI) and American Society of Gene and Cell Therapy (ASGCT) with the American Society of Clinical Oncology (ASCO) this coming weekend.
At ASGCT we spoke with Dr Carl June and also heard the latest update on what Cellectis are doing from Dr Julianne Smith.
Companies mentioned: Juno Therapeutics, Novartis/U Penn, Cellectis, Bellicum, bluebird bio, Formula, Molmed.
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Have you ever sat in a freezing cold scientific session and been so engrossed in the compelling presentations that followed, you simply forgot to take notes? Not one. That actually happened to me at the American Association for Cancer Research (AACR) in Philadelphia this year in one of the many fringe sessions that I attended.
Reading Terminal Clock, Philadelphia
Granted, the hot topic of the conference was undoubtedly checkpoint inhibition, but I was anxious to escape to the comfort of some meaty and familiar basic and translational science, namely MYC. MYC is largely thought to be a difficult to target, even undruggable protein, and along with RAS and p53, represents a formidable challenge for cancer researchers. These three oncogenic proteins alone are probably responsible for more drug resistance developing and even death from cancer than any other proteins in a patient with advanced disease.
For cancer patients with advanced disease, the clock is ticking on time they have left.
Solve these three problems (MYC, RAS and p53) and we may have a shot at dramatically improving outcomes. As Dr Gerard Evans (Cambridge) noted:
“I think it’s fair to say that we don’t really know why interruption of any oncogenic signal actually kills cancer cells, but one of the reasons that we’re interested in MYC is because it seems to be a common downstream effector of many, maybe all cancers.”
Sure, the road to success is paved with an enormous graveyard of failures, just as metastatic melanoma was before checkpoint blockade came along, ironically. What I heard at AACR both inspired and filled me with greater confidence… we’re finally getting somewhere.
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Multiple myeloma (MM) has been very much in the news this week after the American Society of Clinical Oncology (ASCO) abstracts were released to much anticipation.
Myeloma is largely thought to be an incurable disease despite the option of an autologous stem cell transplant for newly diagnosed patients. That said, I have actually met some people who have had two or 3 transplants over several decades, a testament to their strength and fortitude in enduring such a challenging procedure.
This year, the news media have focused on elotuzumab (BMS/AbbVie), a CS1/SLAMF7 inhibitor that has previously shown clinical activity in earlier trials, after it was showcased in the ASCO Presscast last week. This why you see many articles on the data reported from this particular abstract.
It’s not the most exciting new data in this disease for me though, that honour goes to two other therapeutics of an entirely different kind. They come completely out of left field and what we saw over the last two months really caught our attention and may surprise you too.
Indeed, we saw hints of some of this data at the American Society for Gene and Cell Therapy (ASGCT) meeting last week in New Orleans.
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New Orleans – in today’s plenary session at the 2015 annual meeting of the American Urological Association (Twitter: #AUA15), Dr Celestia Higano (Seattle), presented the results of the STRIVE trial (NCT01664923) – a multicenter phase 2 study of enzalutamide (Xtandi) versus bicalutamide in men with nonmetastatic (M0) or metastatic castration-resistant prostate cancer (M1). These were men who were asymptomatic or mildly symptomatic.
Dr Higano noted that this was a very late breaking abstract; topline results were only announced a little over a month ago on April 2.
The TERRAIN trial also compared the efficacy of enzalutamide head-to-head against bicalutamide. We’ve updated our EAU 2015 TERRAIN post with the additional data presented here at AUA 2015 in New Orleans.
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The annual meeting of the 2015 American Urological Assoication (AUA) is being held in New Orleans… Yes, we’re on the third and final leg of our Louisiana trip encompassing AAI, ASGCT and now the triumvirate of AUA-SBUR-SUO.
This morning, I attended the Urologic Oncology Research Symposium, “High impact science in urologic oncology and progress in biomedical imaging.” In particular, I was keen to hear about the latest research in urothelial bladder cancer (UBC) with regards to checkpoint blockade with anti-PDL1 and PD-1 therapies.
In the past, any session on bladder cancer guaranteed the lucky (or hapless) presenters with an audience of a dozen or so people. Not any more – the room was packed with standing room only very quickly – a nice change for a disease that has seen no new therapies for 30 years.
Part of this renewed enthusiasm is due to the excitement for the checkpoint therapies making a huge impact in this disease, at least in clinical trials to date. While waiting for the session to start, one urologist I spoke to told me he bought the ASCO Virtual Meeting last year just to hear Dr Tom Powles talk on anti-PDL1 therapy with MPDL3280A in advanced urothelial cancer. What did you think of it, I asked?
“Wow, just wow!”
Later this month an update on the more mature data from that phase I trial is due at the American Society of Clinical Oncology (ASCO) from Dr Daniel Petrylak (Yale)… who just happened to be one of the presenters at AUA this morning.
He discussed the checkpoint data with MPDL3280A in urothelial bladder cancer, as well as the pembrolizumab data from ESMO last fall and what’s happening with nivolumab. These drugs are quite different in many ways, not just in terms of the efficacy, but also in terms of the biomarker data, as we discovered today.
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Whew, after posting the interview with Dr Tom Gajewski this morning from the American Association of Immunologists (AAI), we headed across town to the American Society for Gene and Cell Therapy (ASGCT) morning session and then dashed back to complete the first of the American Society of Clinical Oncology (ASCO) Previews for 2015!
What a busy week it’s been, never mind the hurly burly of today.
The ASCO 2015 abstracts went live at 5pm ET, with the exception of the late breaking abstracts, which are usually embargoed to the day of the actual presentation.
There are a number of topics well worth highlighting this year, so today kicks off the first of our annual Preview series on BSB. There will be much more to come – we wrote nearly 30 articles before, during and after the conference last year – this year will probably be similar with so much data to review and discuss.
New Orleans – one of the presentations of note at Immunology 2015 (the annual meeting of the American Association of Immunologists) was by Thomas J. Gajewski MD, PhD from the University of Chicago. His presentation on “Innate immune sensing of cancer via the STING pathway” was well worth the trip to New Orleans.
Readers may recall the post we wrote in March on “What is STING and why does it matter in cancer immunotherapy?” It followed the news that Novartis were collaborating with Aduro Biotech (NASDAQ: ADRO) on agonists that activate the STING (Stimulator of Interferon Genes) signaling pathway in immune cells.
I had the privilege to talk with Dr Gajewski (pictured below) after his presentation at AAI.
Excerpts from the interview will feature on Episode 2 of the Novel Targets podcast (@TargetsPodcast). (Do sign up for the Novel Targets Newsletter if you want to be among the first to know when this will air). Subscribers can read more from the interview below.
You should read and/or buy access to this post if you don’t know the answers to the following:
- What role does the tumor microenvironment play in response to cancer immunotherapy?
- How could the tumor microenvironment be a biomarker of response to checkpoint inhibitors?
- Why target the STING pathway?
- Reasons Novartis are collaborating with Aduro Biotech?
- How may a STING agonist be brought to the clinic?
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