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AACR 2026 Chairs Identify Themes and Highlights from the Conference

The American Association for Cancer Research (AACR) Annual Meeting kicks off this weekend in San Diego. A whirlwind of sessions, keynotes, fireside chats, posters, and exhibitors, the meeting is THE annual event for the cancer community.

Before the conference, GEN spoke with AACR program chairs Paul S. Mischel, MD, Professor and Vice Chair for Research for the Department of Pathology at Stanford Medicine of Stanford University and Alice T. Shaw, MD, PhD, Chair of the Department of Medical Oncology and the Chief of Strategic Partnerships at Dana-Farber. In this interview, they share their perspectives on the event, what attendees should be looking out for, and what they, personally, are most looking forward to.

This interview has been edited for length and clarity.

 

GEN: What did you feel were some of the most important themes to include in the conference program?

Shaw: First of all, it’s been such an honor for me to work with Paul as well as our president, Lillian Siu, MD. We had an expert program committee and incredible staff at AACR who all helped shape the program.

This year’s annual meeting feels more meaningful than ever, because of everything going on in the world, including funding challenges, challenging geopolitics, and everything else. It has felt even more important that we have this time to bring together our global community of cancer researchers and investigators.

When Paul and I met last summer, we felt strongly that this meeting was not just about designing an incredibly strong scientific program to showcase the science and all of the innovation, but we wanted to make a point to demonstrate to the audience, and the world, the tangible benefits of scientific research to patients with cancer, and to highlight how all the research we do is done with an eye toward improving the lives of patients with cancer.

We intentionally planned a scientific program with patients and patient impact front and center and have tried to incorporate the patient perspective and even patient voices in some sessions—to emphasize that science drives impact for patients.

Mischel: When we started about a year ago, our conviction—that there probably has never been a more important year for an AACR meeting—grew over the year. This organization is a beacon of light at a time in which there’s been extraordinary progress in cancer, and [there is] the potential to really make a difference in patients’ lives at the face of some very major headwinds. What we’re seeing is a level of enthusiasm and engagement in coming together in the community that’s saying: we won’t be stopped in making a difference for patients with cancer. And there were a number of themes that were central to this meeting.

For example, precision—that you can use information about patients to identify what’s gone wrong and how to develop therapies based upon deep molecular knowledge. Partnership—The growing recognition of how we work together to make a difference for patients. It’s not a winner-take-all strategy. It’s not a race to the top for individuals. It’s a race to the top for people with cancer. And we do it effectively by joining hands to make a difference for patients. And global work—another major theme that we’re really talking about this year, because together we can make a real difference for people with cancer.

We work together with people that span an enormous range of disciplines and expertise. A number of themes came front and center during the year. The technologies to interrogate what’s happening in human beings, whether it’s in their tissue, their blood, or their images—it’s nothing short of breathtaking. The ability to either forestall cancer by detecting if it’s going to happen, or catch it early, or monitor our most effective treatments is really changing the game. New modalities for developing treatments. We’ve heard a lot about harnessing the immune system and about the development of small molecules. There’s all kinds of new chemistry, molecular glues and degraders that are leading the way. And they’re tied to deep investigations into the fundamental biology.

AI is changing the game as well. We are very excited that we’ve brought together perhaps the most interesting AI sessions that you can imagine, that talk about all of the ways that AI can be used—not like an oracle but actually in partnership with helping make a difference for patients, whether it be in the diagnostics or the development of therapeutics. AI is only beginning to be tapped to help us think about how to integrate knowledge across all of these domains. And it goes beyond that because it’s not only about the molecular composition of a person’s tumor, it’s about a human being, what they eat, where they live, what they do, and various other social determinants of health that might increase risks of cancer. A lot of attention is paid in the meeting to that aspect of it as well. So, I think we’re in for an incredibly interesting meeting.

Shaw: One of the themes that came right out from everyone on the program committee was how important it was to highlight AI; I think everyone believes that AI is going to be transformative and it’s going to impact all aspects of cancer research and clinical care in the coming years. We had a number of AI experts on our program committee. They really helped embed AI topics throughout the scientific and also the educational program.

In fact, when Paul and I were planning the opening plenary session, we really wanted one of the opening plenary speakers to be able to speak on AI. So, we have Regina Barzilay, PhD, from MIT, who’s going to speak on her work in the AI space, both in terms of drug discovery and all the way out to clinical applications. We also have an AI-focused plenary session all unto itself as well, to drive home the importance of AI tools and technologies. It is incredible how AI is already being used in terms of foundational discovery and in terms of real-world, clinical data mining and implementation. And Paul already mentioned genomics, precision medicine, biomarker discovery, histopathology, radiology, all of which are already being impacted by AI.

Mischel: One of the things that is perhaps most stunning is this idea that you might be able to prevent cancer. We already see real world examples of that with things like HPV vaccines. The work is advancing so quickly that it might be possible to build vaccines against [something] that might prevent people who are at high risk of developing cancer from getting those cancers. Our colleague and AACR President Lillian Siu, MD, has a presidential symposium focused on that. What I hope that we’re getting across is the real scale and power of the work that’s being presented and the way that it crosses so many disciplines at this meeting.

Shaw: We are going to have a large focus, as we usually do, on molecularly targeted therapies. We have several sessions on the basic research side, but also in the clinical trial sessions around targeting RAS. RAS, of course, is the most commonly mutated oncogene in human cancer and has been undruggable for decades.

In the last five to 10 years, we now finally have small molecule therapies that can target different RAS mutations. In fact, you may have just heard the news about a new RAS inhibitor, daraxonrasib from Revolution Medicines, and pivotal Phase III trial data in previously treated pancreatic cancer. This was an incredibly positive study, doubling overall survival. Not even knowing those results, though, we already had planned quite a lot around RAS.

In that context of precision therapies, I also want to mention that I’m excited about one of our discovery science plenaries on Saturday that is going to focus on minimal residual disease (MRD) in solid tumors. Here the question is, if we have such incredibly effective targeted therapies for oncogene-driven cancers like RAS, EGFR, and ALK, why aren’t we curing more patients who have these types of cancers? We believe that a lot of the reason is because we can’t eliminate every cancer cell. And if we could just understand what allows those residual cells to survive, perhaps we could eradicate those and then be on the road to curing patients who have advanced disease. So, this whole plenary will focus on the science around MRD and how that then leads to clinical applications as well.

Mischel: Fundamental science is deeply central to this process. We frame a lot of things in terms of what it means for patients’ lives. I think an important part of this meeting is also integrating how those discoveries really flow from the work in fundamental science. For example, in the opening plenary, we’re going to be hearing about how tumors change their stripes effectively to become resistant to treatments, the lineage plasticity, this idea that they adopt new states to become resistant. And then what can you do about it?

When people used to be diagnosed with terminal cancer, it meant that they were going to die soon, and now people can be diagnosed with terminal cancer and live for years. That’s stunning. And that is happening because of cancer research and the integration of cancer research all the way from the most mechanistic to the most applied. One of the deepest themes of this meeting comes into this concept of partnership, that we highlight the critical nature of each component and the integration of those components, all the way from fundamental discovery to translation to patients.

 

GEN: What are some of the biggest scientific challenges you’re seeing right now in cancer biology that you think people will be discussing at the meeting?

Mischel: Cancer is hard because it is evolution on steroids. The mechanism that I study—extrachromosomal DNA, the ability of cancer cells and tumors to change quickly to resist treatment—is all about that. And it comes from us; it’s our cells that have gone bad. We have to find ways to show how they’re different and target those differences. We’re getting better at it through our understanding of science.

Shaw:  I am someone who sits between basic research and the clinic, so I do a lot of translational research. What the AACR meeting does well is gets at this key challenge around how we translate basic discoveries into the clinic. We all just want better cancer therapies for our patients. There are many aspects that really make the translation of discoveries difficult, and these will come out in various forms at the meeting. We’ve been talking about how hard it is to understand the biology, and to identify and validate new targets for drug discovery, for cancer treatments in the future.

I have spent some time on the industry side, so I also recognize how challenging it is, even when you have what you think is a perfect target, to drug that target. At the annual meeting, we’re going to talk a lot about different modalities, ways of thinking about going after what we believe are important targets, be it a small molecule or maybe it’s a new degrader or maybe it’s some other very complicated biologic.

I want to emphasize that to use or to identify the optimal modality requires that we understand the biology and the science behind it. The other challenge that I’ve seen in the translational space is around identifying which patients are going to benefit from a new therapy. A good example of where we’ve seen struggles is immunotherapy and identifying novel immunotherapy combinations and which ones have robust activity. But we can’t tell exactly which patients are deriving that benefit. Oftentimes with no biomarker to guide us, we can’t move forward with what could be a promising combination. At the annual meeting, we try to highlight a lot of these correlative or translational biomarker studies from early phase clinical trials.

The last thing I’ll mention is around how we use preclinical models most effectively to predict what’s going to be a promising new therapy. Often, these models are just models; they’re simpler than human cancers. They can’t recapitulate the complexity of human biology, and they can lead us the wrong way. For example, to overestimate how effective a therapy may be. Fine-tuning our models and making them as predictive as possible is a key challenge.

Mischel: Data seems to suggest that very often you might need to combine agents to make differences for patients. And that of course makes enormous sense from a biological standpoint, but it’s much harder to do when you start thinking about how you design the trials to do that. It’s a slow process. And so, there is increasing recognition of the need to figure out how to combine agents and hopefully ways to figure out how practically to begin to test them more effectively and in a more cost-effective fashion.

 

GEN: What have been some of the biggest advances since the last meeting?

Mischel: I just keep coming back to RAS because it’s such a big deal. An undruggable target that we’re now seeing a huge change in. It’s a huge deal.

Shaw: I would agree with that. And it’s not simply the RAS inhibitor itself. Many of us believe that that is just the start of how we most effectively treat RAS-driven cancers. We need the best RAS inhibitor to serve as an anchor and then we will build these combinations around that which will hopefully be even more effective and allow us to maximally cytoreduce or debulk cancers and then allow us to take in other even higher order combinations.

We have sessions this year all around RAS-mutant cancers. We have a designated session just focused on pancreatic cancer biology, because understanding that biology well is going to be critical to developing these types of combination approaches.

The other thing that’s exciting—and this space is always evolving—is a plenary session on innovative new therapeutic modalities. This session will focus on a couple key modalities that are already transforming the space. Antibody-drug conjugates (ADC), for example. They are basically entering every therapeutic space that we have in cancer [and] understanding of the biology around how you’re targeting certain tumor-selective antigens.

Also, the design of the ADC itself can be very, very sophisticated and can be tweaked to further enhance activity. We’ll have some great talks around the next generation of ADCs that are going to be even more effective and even safer than what we currently have.

And in that same session around innovative modalities, we’ll also have talks around immune cell engagers; also, new data and next generation immune cell engagers that have built upon the early data with the first-generation immune cell engagers. The other very innovative new therapy that we will highlight, even in more detail than last year, is around radioligand therapies—a way to selectively target tumor cells with radiation. Unlike ADCs where the payload is chemotherapy, here the payload is radiation therapy. We’ve already seen really that these radioligand therapies are incredibly important for patients; they are coming out in all different therapeutic spaces. We thought it was important to highlight the latest advances in radioligand therapies, and we also have some education sessions so that physicians and scientists understand the basics around this innovative and exciting modality.

Mischel: The concepts of glues and degraders open the therapeutic landscape in a very different way. In many ways, the landscape has been limited to enzymes that you can inhibit, and not all good cancer targets are going to be enzymes that you can inhibit, and these glues and degraders change what you can do, whether it’s getting rid of them, moving them, giving them new functions. It’s a very powerful technology that is getting ready to make an enormous difference in clinic.

Shaw:  In the opening plenary session, George Winter will speak on glues and degraders. I also wanted to highlight the “New Drugs on the Horizon” sessions. We do this every year at the annual meeting. I love these sessions because they are first time disclosures of novel cancer therapies that have just entered the clinic or they’re about to enter the clinic. These talks go deep into the biology of the disease and how the drug was discovered and developed into early clinical plans. Several talks in this session this year are going to feature molecular glue degraders. That will be a nice way to tie together this theme around the degraders and the power of this new modality.

Mischel: One other thing I want to squeeze in is why on Earth are younger people getting cancer, particularly colorectal cancer? That’s really disturbing. We have sessions that are data rich that go right at that, and the answers are interesting.

 

GEN: Will there be any programming at the meeting that addresses the current state of funding?

Shaw:  We’re fortunate that Tony Letai, MD, PhD, the NCI director, is attending and speaking at the meeting in our opening ceremony on Sunday. He’s also participating in a workshop that we’re holding on grant writing and the scientific review process. On Monday, he will give an NCI director’s address and participate in a fireside chat where I’m sure he’s going to get a lot of questions around funding.

There are also sessions within the science and health policy track at the meeting that are going to focus on federal funding of grants. There is even a researcher town hall that’s really going to talk a lot about this.

 

GEN: Do you have any advice for young cancer researchers that may be attending AACR for the first time?

Mischel: I have two bits of advice. One of them is to know that what you’re doing is incredibly important. You are welcome. You’re one of us, you’re important. Do what you need and go forward because the work that you’re doing is going to matter an enormous amount. The second thing is do not be afraid. Do not think that the senior people at the meeting, the “bigwigs,” are too busy for you. Do not think they do not want to meet you, because they do. You’re the future. Go up, introduce yourself, say hello, tell us who you are.

 

GEN: What are things you are looking forward to outside of the sessions? 

Shaw:  I love the AACR annual meeting because it’s such an opportunity not just to learn, but to network and reconnect with friends and collaborators who you may not have seen in a while. I also think it’s a great venue for many of us to have formal sit-down meetings with industry partners and talk through the latest data that were just presented and discuss new collaborations. I personally am looking forward to the 5K race that Paul and I are speaking at. I’m going to try to run the race! One of my sons runs marathons and I thought, well, the least I can do is try and run a 5K.

Mischel: I’m looking forward to having a drink with Alice after the meeting ends and debriefing on putting this meeting together, which has been an absolute pleasure. I wish I were running the 5K race. I’m doing an education session at that time. I’m looking forward to meeting the students. There are these brilliant young people from all around the world and they’re just at the start of their career and they draw inspiration from this meeting, and I really enjoy it when they come up to me and I get to meet them. You see the brilliance and excitement in these people’s faces. And I’m looking forward to that.

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Integrated Sample Preparation System Standardizes and Streamlines Pre-Analytical Workflows

Invivoscribe launched the PrepQuant™ sample preparation platform that integrates nucleic acid extraction, concentration, and quantification with a single automated instrument. The product is designed to standardize sample preparation and simplify pre-analytical workflows to reduce costs and eliminate a primary source of inconsistency in molecular testing.

Developed in collaboration with Hitachi High-Tech Corporation, PrepQuant combines Invivoscribe’s experience in developing standardized molecular assays, providing global clinical testing services, along with Hitachi High-Tech’s technological and manufacturing capabilities

The PrepQuant system is assay agnostic, generating highly concentrated genomic DNA and cell free DNA (cfDNA) yields for next-generation sequencing (NGS), qPCR, and digital PCR (dPCR) assays. By consolidating multiple steps in a single platform, the system can lab operating costs, sample variability, and lab bench space, while optimizing tests results.

“PrepQuant represents a significant advancement in our commitment to standardize the entire testing process, starting with the pre-analytical workflow,” said Jeff Miller, CEO and CSO of Invivoscribe. “This is particularly important in the era of precision medicine, where reliability of measurable residual disease and liquid biopsy results depend markedly on the quality and consistency of the starting material.”

“The concept for the [product] was driven directly by insights from LabPMM, our global network of testing laboratories,” added Jordan Thornes, vice president, global clinical lab operations. “Our teams recognized the limitations of currently available automated instruments, particularly the labor-intensive nature and increased risk of errors associated with running three separate protocols across multiple instruments. This all-in-one system was designed to reduce costs, while addressing those challenges and significantly improving operational efficiency.”

The PrepQuant is designed and validated for use with blood, plasma, and bone marrow specimens, with ongoing development for additional specimen types. Invivoscribe will officially unveil the product at the American Association for Cancer Research (AACR) Annual Meeting in San Diego, at booth #3459 from April 19–22.

 

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Landmark Pancreatic Cancer Trial Highlights Promise of RAS-Targeting Daraxonrasib

Earlier this week, Revolution Medicines reported positive results from a global Phase III trial of its RAS‑targeting inhibitor daraxonrasib (RMC-6236) in metastatic pancreatic ductal adenocarcinoma (PDAC). In the RASolute 302 trial, patients receiving daraxonrasib achieved longer progression‑free survival (PFS) and overall survival (OS) than those on standard cytotoxic chemotherapy.

The RASolute 302 trial enrolled patients with pancreatic tumors harboring a wide range of RAS variants, including those with RAS G12 mutations (such as G12D, G12V, and G12R), as well as those without an identified RAS mutation. The primary endpoints of the trial were PFS and OS in patients with tumors harboring RAS G12 mutations. Secondary endpoints assessed PFS and OS in all enrolled patients (the intent-to-treat population), including those with tumors with and without (wild type) an identified RAS mutation.

Daraxonrasib patients achieved a median OS of 13.2 months versus 6.7 months for chemotherapy. The drug was generally well tolerated, with a manageable safety profile and with no new safety signals.

“With these unprecedented results, daraxonrasib has the potential to achieve our goal of bending the mortality curve in pancreatic cancer. Unlike chemotherapy, daraxonrasib is a RAS-targeted medicine that targets RAS in its active ‘ON’ state, shutting down a key signaling pathway that drives aggressive tumor growth. This is especially important in pancreatic cancer, which is among the most RAS-driven cancers, with more than 90% of tumors harboring a RAS mutation that is the driver of the cancer,” asserted Mark A. Goldsmith, MD, PhD, CEO and chairman of Revolution Medicines.

Pancreatic cancer carries one of the highest mortality rates of any solid tumor, a consequence of late-stage diagnosis and resistance to standard chemotherapy. In the United States, recent estimates point to roughly 60,000 new cases and nearly 50,000 deaths each year. With most PDAC tumors driven by RAS alterations, the early success of emerging RAS‑targeted strategies hints at how much more may be possible as this therapeutic space continues to expand.

RAS is the key oncogenic driver of pancreatic cancer. Nearly all RAS mutations occur at KRAS position G12, but RAS mutations in other isoforms and at KRAS positions G13 and Q61 are also observed. Daraxonrasib works by suppressing RAS signaling through inhibition of the interaction between both wild-type and mutant RAS(ON) proteins and their downstream effectors.

Pancreatic cancer is the most RAS-addicted of all major cancers, with more than 90% of patients harboring tumors driven by mutations in RAS proteins. These mutations span a range of RAS variants that fuel aggressive tumor behavior. Daraxonrasib, a multi-selective inhibitor of RAS(ON) proteins, is the first investigational agent in a novel class of RAS inhibitors designed to address a diverse and broad spectrum of oncogenic RAS drivers.

“For patients with metastatic pancreatic cancer, new treatment options are urgently needed to increase survival time and improve quality of life,” said Brian M. Wolpin, MD, MPH, professor of medicine at Harvard Medical School, director of the Hale Family Center for Pancreatic Cancer Research at Dana-Farber Cancer Institute, and principal investigator for the RASolute 302 trial. “The widely anticipated results of this study indicate that daraxonrasib provides a clear and highly meaningful step forward for patients with pancreatic cancer who have experienced progression on prior treatment, typically chemotherapy. I believe that this new approach is a very important advance for the field that I expect will be practice-changing for physicians and improve the care for patients with previously treated metastatic pancreatic cancer.”

Revolution Medicines now intends to submit the drug for approval by regulatory authorities, including the U.S. Food and Drug Administration as part of a future New Drug Application, and for presentation at the 2026 American Society of Clinical Oncology Annual Meeting. 

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Protocol for a randomized trial to predict the efficacy of cognitive and behavioral interventions for symptoms of depression

IntroductionCognitive behavioral therapy (CBT) is one of the most common interventions for depression and has two key components: Cognitive Restructuring (CR) and Behavioral Activation (BA). However, no evidence-based guidelines exist to help clients and clinicians decide whether CBT would be a good first-line treatment for a given individual based on their personal characteristics, and which CBT intervention would benefit them more. We propose that specific capacities to learn from new information and experiences are prerequisites for response to CBT and that BA and CR require different learning capacities. In this study, we aim to develop predictive models of symptom change based on computationally-derived variables from behavioral tasks, in addition to clinical and demographic self-report data, to identify parameters and variables that can determine which individuals with depressive symptoms would benefit from CBT-based interventions and, ideally, which specific interventions they would benefit from more.Methods and analysisWe plan to recruit at least 1,500 adult participants who report having symptoms of depression and reside in U.S. After completing a series of questionnaires and behavioral tasks to assess their learning propensities, participants will be randomly assigned to a BA or a CR group. Using an online self-help tool, participants will then engage with designated modules according to their assigned group for five weeks. We will assess symptoms 1 week post-intervention (main end point of study) and follow up at 6, 18, and 42 weeks post-intervention. Upon enrolling and consenting into the main study, participants will be randomly assigned to either the training dataset or the held-out test dataset at a ratio of 2:1. This enables a clean separation of training and test datasets and prevent data leakage. We plan to build cross-validated predictive algorithms on the training dataset, and preregister our analysis plan before we validate our models and hypotheses in the held-out, unseen, test dataset. Enrollment of the study started 23rd January, 2024.Study protocol registrationClinicalTrials.gov, identifier (NCT06631183). The protocol follows the Standard Protocol Items: Recommendations for Interventional Trials (SPIRIT) guidelines. Numbers in brackets follow subsection numbers in the guidelines.
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STAT+: Roche to launch another Elevidys trial, with eyes on European approval

In an attempt to win European approval for the controversial medicine, Roche said Thursday it would run another trial of the Duchenne muscular dystrophy gene therapy Elevidys. 

The Swiss company’s move comes after European regulators last year gave a negative review to the therapy, saying it had failed to demonstrate long-term benefits for patients with the degenerative muscle condition. Roche has rights to the therapy outside the U.S., where it is marketed by its developer, Sarepta Therapeutics.

Roche said the Phase 3 trial will generate the type of evidence that could lead to a resubmission with European officials and to applications with regulatory agencies in other parts of the world. The study will evaluate the safety and efficacy of Elevidys versus placebo over 72 weeks in roughly 100 boys at the early stages of the disease. 

Continue to STAT+ to read the full story…

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Is carbon removal in trouble?

Last week, news outlets reported that Microsoft was pausing carbon removal purchases. It was something of a bombshell.

The thing is, Microsoft is the carbon removal market. The company has single-handedly purchased something like 80% of all contracted carbon removal. If you’re looking for someone to pay you to suck carbon dioxide out of the atmosphere, Microsoft is probably who you’re after.

The company has said that it is not permanently ending its carbon removal purchases (though it didn’t directly answer further questions about this apparent pause). But with this flurry of news, there’s a lot of fear in the industry—so, it’s worth talking about the state of carbon removal, and where Big Tech companies fit in.

Carbon removal aims to reliably pull carbon dioxide out of the atmosphere and permanently store it. There’s a wide range of technologies in this space, including direct air capture (DAC) plants, which usually use some kind of sorbent or solvent to pull carbon dioxide from the air. Another important method is bioenergy with carbon capture and storage (BECCS), in which biomass like trees or waste-derived biofuels are burned for energy, and scrubbing equipment captures the greenhouse gases.

There was a huge boom of interest in carbon removal technologies in the first half of this decade. One UN climate report in 2022 found that nations may need to remove up to 11 billion metric tons of carbon dioxide every year by 2050 to keep warming to 2 °C above preindustrial levels.

One nagging problem is that the economics here have always been tricky. There’s a major potential public good to pulling carbon pollution out of the atmosphere. The question is, Who will pay for it?

So far, the answer has been Microsoft. The company is by far the largest buyer of carbon removal contracts, and it’s the only purchaser that has made megatonne-scale purchases, says Robert Höglund, cofounder of CDR.fyi, ​​a public-benefit corporation that analyzes the carbon removal sector. “Microsoft has had a huge importance, especially for getting large-scale projects off the ground and showing there is demand for large deals,” Höglund said via email.

Microsoft has pledged to become carbon-negative by 2030 and to remove the equivalent of its historic emissions by 2050. Progress on actually cutting emissions has been tough to achieve though—in the company’s latest Environmental Sustainability Report, published in June 2025, it announced emissions had risen by 23.4% since 2020.

On April 10, Heatmap News reported that Microsoft staff had told suppliers and partners that it was pausing future purchases of carbon removal, though it wasn’t clear whether the company would increase support for existing projects, or when purchases might resume. Bloomberg reported a similar story the next day. In one instance, Microsoft employees said that the decision was related to financial considerations, one source told Bloomberg. 

In a statement in response to written questions, Microsoft said that it was not permanently closing its carbon removal program. “At times we may adjust the pace or volume of our carbon removal procurement as we continue to refine our approach toward sustainability goals. Any adjustments we make are part of our disciplined approach—not a change in ambition,” Microsoft Chief Sustainability Officer Melanie Nakagawa said in the statement.

Whatever, exactly, is happening behind the scenes, many in the industry are nervous, says Wil Burns, Co-Director of the Institute for Responsible Carbon Removal at American University. People viewed the company as the foundational supporter of carbon removal, he adds.

“This pause—whether it’s short term or whatever it is—the way it’s been rolled out is extremely irresponsible,” Burns says. The vast majority of firms looking to get carbon removal contracts are probably seeking Microsoft deals. So, while Microsoft has every right to change its plans, the company needs to be open with the industry now, he adds.

“I don’t think you can hold yourself out as the paragon of fostering carbon removal and then treat a nascent industry that disrespectfully,” Burns says.

Carbon removal companies were already in turmoil in the US, particularly because of recent policy shifts: Funding has been cut back, and recent changes at the Environmental Protection Agency were aimed at the government’s ability to target carbon pollution.

Now, if the largest corporate backer is shifting plans or taking a significant pause, things could get rocky.

Depending on the extent of this pause, the industry may need to survive on smaller purchases and hope for support from governments and philanthropy, Höglund says. But for carbon removal to truly scale, we need policymakers to create mandates so that emitters are responsible for either storing the carbon dioxide they produce or paying for it, Burns says.

“Maybe the upside of this is Microsoft has sent a wake-up call, that you just can’t rely on the kindness of strangers to make carbon removal scale.”

This article is from The Spark, MIT Technology Review’s weekly climate newsletter. To receive it in your inbox every Wednesday, sign up here. 

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The noise we make is hurting animals. Can we learn to shut up?

When the covid-19 pandemic started, Jennifer Phillips thought about the songs of the sparrows.

They were easier to hear, because the world had suddenly become quieter. Car traffic plummeted as people sheltered at home and shifted to remote work. Air travel collapsed. Cities—normally filled with the honking, screeching, engine-gunning riot of transportation—became as silent as tombs.

For years, Phillips has studied how animals react to “anthropogenic noise,” or the racket created by human activity. Most animals really don’t like it, she and her colleagues have learned. Animals constantly listen to the world around them: They’re on the alert for the rustle of approaching predators, or a mating call from a member of their species. As human society has expanded—with sprawling cities, industrial mines, and roads crisscrossing the world—it has gotten noisier too, and animals have trouble hearing one another.

Noise is invisible; there’s no billowing smokestack, no soiled waterway. We just got used to it as it vibrated in the background.

Phillips and her colleagues had spent time in the 2010s in San Francisco recording the sound of white-crowned sparrows in the Presidio. It’s a park that is half peaceful nature and half automobile noise, since it’s filled with thick clumps of trees and grassy fields but also has two highways that slice through it, feeding onto the Golden Gate Bridge. In past recordings, starting in the 1950s, sparrows had sung with complex and lower-pitched melodies and three major “dialects.” But by the 2010s, traffic in the Presidio had exploded, and the hubbub was so loud that the birds began to sing with faster trills—and at a higher pitch—so their fellows could hear them. The two quietest dialects were either dead or on their way to extinction.

They’re “screaming at the top of their lungs,” says Phillips. “They really can’t hear the lower frequencies when the traffic noise is present.” Urban noise can even change birds’ bodies; they get thinner and more stressed out. Their mating calls aren’t as effective, because female birds, as researchers have found, generally don’t enjoy high-pitched, high-volume shouting. (It makes them wonder if the males are unhealthy.) The noise can increase bird-on-bird conflict, because when birds can’t hear warning cries they accidentally stumble into enemy territory. Perhaps worst of all, in situations like these biodiversity takes a hit: Entire species that can’t handle urban clamor simply head out of town and never come back.

But as the sudden, eerie silence of the pandemic descended, Phillips sat at home thinking, It’s really quiet. And then she wondered: Would the Presidio birds now be able to hear each other better?

She raced over to the park and started recording. Sure enough, the park was seven decibels quieter—a huge drop. (That’s like the difference between the noise of the average home and whispering.)

And remarkably, the researchers found that the songs of the white-crowned sparrows had transformed. They were singing more quietly, with a richer range of frequencies. A bird could be heard twice as far as before. And the mating calls had gotten more sultry.

“They could sing a higher performance, basically a sexier song, but not have to scream it so loud,” Phillips says. 

It was as if time had been reversed and all the damage abruptly repaired. And it proved what Phillips and her peers have been increasingly documenting: that anthropogenic noise is the newest form of pollution we need to tackle. The noise of our relentlessly on-the-move industrial society affects all life on Earth, wildlife and humans, in ways we’re just beginning to grasp. Yet strategies such as electrification and clever urban design could help. As the Presidio showed, noise can vanish overnight—once we figure out how to shut up.

Hidden impacts

Many forms of pollution are obvious to us humans. Dumping toxic goo into lakes? Sure, that’s bad. Coal smokestacks pumping soot and carbon dioxide, plastic bags and sea nets choking whales—we now understand that these, too, are problems. Even an idea as gauzy as light pollution has penetrated the public consciousness to some extent, since it’s why city dwellers can’t see many stars, and we’ve heard it confuses migratory birds.

But noise, mostly from transportation, took longer to hit our radar. This is partly because it’s invisible; there’s no billowing smokestack, no soiled waterway. We just got used to it as it vibrated in the background.

sparrow perched on a branch, singing
Sparrows in San Francisco’s Presidio began to sing with faster trills—and at a higher pitch—so their fellows could hear them over the noise of nearby traffic.
GETTY IMAGES
hummingbird in flight
The black-chinned hummingbird seems to prefer noisy areas, fledging more chicks than the same species does in quieter areas.
MDF/WIKIMEDIA COMMONS

There were a few studies in the ’70s and ’80s showing that animals were upset by our noise. But the field really began to take off in the ’00s, in part because digital technology made it easier to record long swathes of sound out in nature and analyze them. One early salvo came from the biologist Hans Slabbekoorn, who was studying doves in the city of Leiden and irritatedly noticed that he could rarely get a clean recording because of the background noise. Sometimes he’d see the doves’ throats moving as they cooed but couldn’t hear them. “If I’m having difficulty hearing them,” he thought, “what about them?”

So he and a colleague started recording ambient sound levels in different parts of Leiden. Some were quiet residential areas, which registered a soothing 42 decibels, and others were noisy intersections or areas near highways, which reached 63 decibels, about as loud as background music. Sure enough, he found that birds in the noisy areas were singing at a higher pitch.

Over the next two decades, research in the field bloomed. Noise, the scientists found, has a few common ill effects on animals. It disrupts communication, certainly. But it also generally stresses them, reducing everything from their body weight to their receptivity to mating calls. If an animal nests closer to a road, its reproduction rates can go down; eastern bluebirds, for example, produce fewer fledglings. Truly cacophonous noise—like planes taking off at a nearby airport—can cause hearing loss in birds. And animals can wind up becoming less aware of threats from predators. They’ll wander closer to danger, because they can’t hear it coming. (And sometimes they’ll do the opposite: They’ll develop a rageaholic hair-­trigger temper, because they’re constantly on high alert and regard everything as a threat.) 

Even in deep rural areas, where things are normally pretty quiet, highways can disrupt wildlife—the noise carries far into the fields nearby. Fraser Shilling, a biologist at the University of California, Davis, has stood up to half a mile from rural highways and recorded sound as loud as 60 decibels, which is at least 20 decibels higher than you’d typically find in the wilderness. “The motorcycles and the 18-wheelers are really the ones that project a lot of noise,” he told me. 

Above 55 decibels, many skittish animals get into a fight-or-flight panic. The prevalence of bobcats—an endangered species famously rattled by noise—“starts dropping off the cliff,” says Shilling. Above 65, “you’re really starting to exclude almost all wildlife.”

And that’s not even the upper limit of what wildlife is exposed to. There are roughly a half-million natural-gas wells around the US, and piercingly loud compressors are used to shoot water down into most of them. Up close, the compressors can kick out 95 decibels, a sound as loud as a subway train; at one Wyoming gas well the sound still registered around 48 decibels nearly a quarter-mile away.

Historically, it wasn’t always easy to prove that noise was causing whatever problems the animals were experiencing. Maybe it was other factors; maybe animal populations reduce near a road because some are hit by vehicles? 

But several clever experiments have proved that noise—and noise alone—can disrupt wildlife. One was the “phantom road” experiment by the conservation scientist Jesse Barber and his team, then at Boise State University. They went out to a quiet, uninhabited area of the Boise foothills in Idaho, far away from any roads. In this valley in the mountains, thousands of migratory birds stop on their way south each year; they’ll gorge themselves on cherry bushes, gaining weight for the next days of flying. The researchers strapped 15 pairs of speakers to Douglas fir trees, in a half-kilometer line. Then they blasted recordings of highway noise. They played the noise for four days and then turned it off for four days. Then they observed thousands of birds, capturing many to measure their body mass.

The noise truly rattled the birds. When the sound was turned on, nearly a third left the area. Those that stuck around ate less: While birds should be heavier after a day of foraging, these ones didn’t gain much. The noise seemed to have so interrupted their feeding that they weren’t packing on the weight needed for their migratory trip.

Other, similarly nifty A/B tests followed. One was led by David Luther, a biologist at George Mason University (who also worked with Phillips on the covid-19 study in San Francisco). In 2015, these researchers took 17 white-crowned sparrows at birth and raised them in a lab. To teach them their species’ songs, they played the nestlings recordings of adult sparrows singing, at low and high pitches. Six of the nestlings heard the songs without any interference; with the other half, the researchers played the sounds of city noise at the same time.

The results were stark. The lucky birds that were spared the traffic noise learned to perform the quieter, sweeter, more complex songs. But the birds that had traffic noise blasted learned only the higher, faster, more stressed-out songs. From the cradle, noise changed the way they communicated.

Humans hate noise too

You can’t pull the same experiment with humans, raising them in a lab to see how noise affects them. (Not ethically, anyway.) But if we could, we’d likely find the same thing. We, too, are animals—and it appears that we suffer in similar ways from anthropogenic noise, even though we’re the ones creating it.

The sound of traffic is correlated with lousy sleep, higher blood pressure, more heart disease, and higher stress.

Stacks of research in the last few decades have found that noise—most often, as with wildlife, the sound of traffic—is correlated with lousy sleep, higher blood pressure, more heart disease, and higher stress. A Danish study followed almost 25,000 nurses for years and found that an additional 10 decibels hit them hard; over a 23-year period they had an 8% higher rate of death, plus higher rates of nearly every bad thing that could happen to you: cancers, psychiatric problems, strokes. (They controlled for other malign health influences.) As you’d probably predict by now, children fare badly too. When Barcelona researchers followed almost 3,000 elementary school kids for a year, they found that those in noisier schools performed worse on assessments of working memory and ability to pay attention.

“We think of ourselves as being ‘used to it,’” says Gail Patricelli, a professor of evolution and ecology at the University of California, Davis. “We’re not as used to it as we think we are.”

It’s also true that there’s a trade-off. Many people understand that noise from cities and highways is aggravating, but we tolerate it because we get benefits along with the hassles. Cities are crammed with jobs and connections and dating opportunities; cars and trucks bring us the things we need and increase our personal mobility.

It turns out that animals make a similar calculus. Some species appear to benefit in certain ways from proximity to noise, so they move toward it. 

Clinton Francis, a biologist at California Polytechnic State University, and a team studied bird populations near noisy gas wells in rural New Mexico. Most species avoided the riot of the well pumps. But Francis was surprised to find that some hummingbirds and finches preferred it, and by one important measure they thrived: They were nesting more in the noisy areas than in the quieter areas. Additionally, several species had more success at fledging chicks in noisier locations.

What was going on? It’s likely that the noise makes it harder for predators to hear the birds and hunt down their nests. “It’s essentially a predator shield,” Francis says. Since his research found that predators can cause as much as 76% of failures of eggs to produce healthy offspring, that’s a significant survival advantage.

Cities can offer the same protections to certain species. Consider the case of Flaco, a Eurasian eagle-owl that escaped from the Central Park Zoo in February of 2023 and found he was in a terrific place to hunt. The incessant traffic ought to have caused him trouble. “An owl like this is among the most vulnerable species to intrusions from noise pollution. They’re listening for extremely faint signals or cues that their prey provide,” Francis notes. But New York has its compensations, because prey animals abound. They’re also naïve and unguarded, never expecting an owl with a six-foot wingspan to swoop down and devour them.

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Granted, these upsides don’t cancel out the negatives. Human noise may shield some birds from predators, but in other ways it leaves them faintly miserable, with high levels of stress hormones and lower weight. 

Worse, the species that manage to thrive in cities or near highways are often the same ones all over the country.  And they represent only a minority of species; most are driven further away, with less and less land to live on as civilization spreads ever outward. 

“Overall, it’s kind of a nightmare for diversity,” says Luther.

How to silence the world

In the early ’00s, the village of Alverna in the Netherlands began to get louder. A major intercity road cut straight through the town, and traffic had gone up by two-thirds in the previous decade. Facing complaints about the din, the town offered to put up some 13-foot walls on either side of the route. Residents hated the idea. Who wants to look out the window at massive walls?

So instead town planners redesigned the road in subtle ways. They lowered it by half a meter, slightly blocking the tire sounds. They built wedges that rise up three feet on either side, and surfaced them with attractive antique stone; that blocked even more sound. They planted sound-absorbing trees. And as a final coup de grâce, they reduced the speed limit from about 50 to 30 miles per hour. When a car is moving slowly, the engine is producing most of the roar—but once it’s going 45 mph or faster, the rumble of tires on the pavement takes over and is much louder. Each intervention had only a small effect, but cumulatively they made the road a blessed 10 decibels quieter.

This tale illustrates one curious upside of noise. Compared with other forms of pollution, it can be ended quickly. Toxic pollutants or CO2 can hang around for tens of thousands of years; the microplastics in your pancreas are probably never coming out. But with noise, the instant you reduce the source, the benefits are immediate. 

Plus, most of what works is “not rocket science,” Shilling says. A tall wall at the side of a highway will cut noise by 10 decibels; fill a double-sided wall with rubble and it’s even better. That could cut the traffic noise to below 55 decibels, he notes, which would help particularly skittish forms of wildlife. Walls can block animal movement, though, so in animal-heavy areas it’s better to build berms—small hills on either side of a highway. Areas of high ecological importance could be prioritized to keep costs down. 

“If there’s a great chunk of wetland habitat and it’s the only one around for 50 miles in any direction? Well, then we should build noise walls around it,” he says. We should also build overpasses and underpasses to help animals get around. And to quiet the din of gas wells out in the countryside, states could require companies to build walls around them. (They’ll likely only do that, though, when human neighbors complain or launch lawsuits; animals don’t have lawyers.)

Cities, too, can learn to shut up, as Alverna proved. At the most ambitious, some have buried noisy highways that once cut through the downtown core. Boston put a massive elevated highway underground in its “Big Dig”; in Slabbekoorn’s hometown of Amstelveen—a suburb of Amsterdam—they’re currently enclosing the A9 highway in a tunnel and turning the surface into a verdant park with new buildings. “That’s amazing, getting back a lot of the space as well,” he says. 

Granted, this sort of reengineering can be brutally expensive, which is why politicians blanch when they’re asked to reduce road noise. The Big Dig cost $15 billion, and with interest up to $24 billion. When I mentioned cost to Shilling, he sighed. “It’s not as expensive as a B-1 bomber or tax cuts for rich people,” he says. “Environmental stuff is considered expensive just because our expectations are low, not because we can’t afford to do it.”

There are cheaper and more politically palatable fixes, though. Reducing urban speed limits is one; Paris recently cut the top speed on its ring roads from 70 to 50 kilometers per hour (43 to 31 mph), and noise at night went down by an average 2.7 decibels—a noticeable drop. Planting more trees and vegetation all around roads and cities can cut a few decibels more, and residents love it. 

Growing adoption of electricity would also bring down the volume. “Electric vehicles of all kinds have the potential to make a big difference,” Patricelli says; when the light turns green and an EV next to you accelerates away, it’s up to 13 decibels quieter than a comparable gas-­powered vehicle. These benefits won’t be felt as much on highways, because EVs still make tire noise at high speeds. But in the slower stop-and-go traffic of urban life, they are far more pleasant to the ears, both animal and human. Indeed, the electrification of everything that currently uses a gas-powered motor will make urban life quieter. Cities like Alameda, California, and Alexandria, Virginia, are increasingly banning gas-powered leaf blowers and lawn mowers, which operate at hair-raising volume while electric ones whisper along. 

We’ve engineered a civilization that roars, but the next phase is making it purr. The animals will thank us. 

Clive Thompson is a science and technology journalist based in New York City.

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Pregnancy Sickness Study Identifies New Genetic Links

The University of Southern California (USC) research team that identified the hormone-encoding gene GDF15 as a key driver of pregnancy sickness has identified nine additional genes linked to its most severe form, hyperemesis gravidarum (HG). Six of the identified genes had not been previously linked to the condition.

The Keck School of Medicine of USC team and international collaborators conducted a genome-wide association study (GWAS), scanning the entire genome for differences between women who developed HG during pregnancy and those who did not. They analyzed data from more than 10,000 women with the condition and more than 450,000 controls across European, Asian, African, and Latino ancestries. Their findings offer new clues about the condition and new hope for those affected.

Marlena Fejzo, PhD, a clinical assistant professor of population and public health sciences in the Center for Genetic Epidemiology at the Keck School of Medicine, led the present study and earlier research linking GDF15 to HG. Fejzo told GEN, “The study is much larger than previous studies and on a more diverse population allowing for identification of new genes associated with HG … The new genes give us new directions to explore for prediction, diagnosis, treatment, and response to therapies.”

Fejzo is first author of the team’s published report in Nature Genetics (“Multi-ancestry genome-wide association study of severe pregnancy nausea and vomiting”), in which the team stated, “Potential roles for candidate genes in appetite, insulin signaling, and brain plasticity provide pathways to explore etiological mechanisms and therapeutic avenues.”

HG, which affects about 2% of women, causes nausea and vomiting so severe that eating can become extremely difficult. “Most pregnancies are affected by nausea and vomiting (NVP), but in 0.3–10.8% of pregnancies the symptoms can be severe enough to cause maternal weight loss and adverse maternal and fetal outcomes,” the authors wrote. HG in its most severe form can even be life threatening.

HG was long misunderstood and often dismissed as psychological, growing evidence shows that it has a strong biological and genetic basis and can lead to severe malnourishment, putting both mother and baby at risk. Current treatments for HG are frequently ineffective in improving patient symptoms, the authors further pointed out, and so increase the risk of pregnancy termination, postpartum depression, and suicidal ideation, along with other maternal and offspring comorbidities. “Therefore, understanding of HG etiology is critical to begin to address the negative impact severe NVP has on maternal and child health.”

While historical hypotheses have previously centered around human chorionic gonadotropin (hCG), recent large-scale genetic studies have implicated the GDF15 gene encoding growth differentiation factor-15—a hormone associated with nausea and vomiting, the authors further pointed out. Earlier research by Fejzo and an international team had shown that the link between HG and GDF15 lies in women’s sensitivity to the hormone. They found that women exposed to lower levels of the hormone before pregnancy because of a mutation in the gene experience more severe symptoms, while women exposed to higher levels of the hormone before pregnancy have less severe nausea and vomiting symptoms.

“GDF15 was identified as the greatest genetic risk factor for HG in both a genome-wide and an exome-wide association study, and a rare mutation in GDF15 was associated with a greater than tenfold increased risk for HG,” the scientists noted in their newly reported study. Fejzo explained to GEN, “The mutation in GDF15 is rare. People who carry the mutation have abnormally low levels of GDF15 when they are not pregnant and that increases their risk of being hypersensitive to it during pregnancy when it is produced in massive amounts by the placenta.”

Commenting on their prior work implicating a role for GDF15 and HG, Fejzo further explained to GEN, “In our first GWAS study we found the association between the GDF15 gene and HG. Next, we published a whole-exome sequencing study that identified a mutation in GDF15 associated with HG. Then we published our study in Nature which provided strong evidence that hypersensitivity to the rise of GDF15 in pregnancy (due to low pre-pregnancy GDF15 in circulation) is the main driver of the condition.”

For their newly reported study the researchers carried out a multi-ancestry genome-wide association study of 10,974 HG/excessive vomiting in pregnancy cases and 461,461 controls across European, Asian, African, and Latino ancestries from nine contributing studies.

The results identified 10 genes that were linked to HG, including four that had previously been identified, and six new genes. “Because this is the largest study of HG ever conducted, we’ve been able to tease out important new details that were previously unknown,” said Fejzo. “The fact that we’ve studied women from multiple ancestry groups suggests that these results may be generalizable across a broad population.”

The four genes previously identified were growth differentiation factor 15 (GDF15), GFRAL, which produces the receptor for the GDF15 hormone of the same name, and IGFBP7 and PGR, both of which are involved in development of the placenta. The strongest link by far was to GDF15, which rises sharply during pregnancy. “We know that GDF15 and it’s receptor GFRAL are the main drivers and are in a signaling pathway that causes aversions, nausea, and vomiting,” Fejzo told GEN. “More work needs to be done to explore the other associations, but since studies suggest manipulating progesterone and/or IGFBP7 may not be safe in pregnancy, current studies are focusing on the GDF15 pathway.”

The six newly identified genes offer further clues that might help explain the basis of HG or point to new ways of treating it. They include FSHB, TCFL72 SLITRK1, SYN3, IGSF11, and CDH9. “Now that we’ve more than doubled the genes associated with HG, we can dig deeper into the biology behind this condition, as well as new possible pathways for treating it,” Fejzo said. Speaking to GEN, the researchers noted, “Because the new associations are novel, we need to understand the roles they may play in normal pregnancy and then compare that to pregnancies affected by HG.”

Of the newly identified genes, TCF7L2 stands out because it is one of the strongest genetic risk factors for type 2 diabetes and is also associated with gestational diabetes. “This is a brand-new target, and it’s not yet clear what it’s doing in pregnancy,” Fejzo said. In further commentary to GEN, Fejzo added, “The TCF7L2 gene is a type 2 diabetes-associated gene and a transcription factor that may control glucagon-like peptide-1 (GLP-1) expression and has been associated with liraglutide effects resulting in greater weight loss in obesity. So understanding its role in that rapidly evolving therapeutic arena has potential.”

Several of the other genes identified are involved in appetite and nausea, as well as brain plasticity, or how the brain learns and adapts to new information. Fejzo suggests the brain may learn to associate certain foods with feeling sick, leading to strong, lasting aversions during pregnancy. More research is needed to explore this possibility. “Other genes are associated with learning flexibility so we hypothesize that they may play a role in conditioned taste aversion and may provide new targets to alter or dampen learned aversions,” Fejzo told GEN. Historically, people believed the pregnancy hormone hCG was the cause, but we found no evidence to support that and instead, fascinatingly, we found a link to the follicle stimulating hormone receptor.”

Of the ten candidate genes six—GDF15, GFRAL, IGFBP7, PGR, TCF7L2 and SYN3—have been linked with cachexia—a wasting condition with similar symptoms to HG, including loss of appetite, weight loss and muscle wasting, the scientists noted. “Manipulation of GDF15, GFRAL, IGFBP7, PGR and TCF7L2 in animal models has shown effectiveness in reducing symptoms of cachexia. Thus, assuming analogous functions for these factors in HG, there is both genetic and biological support for causal and potentially reversible contributions for these genes in NVP.”

The researchers also found that some genes linked to HG were associated with other pregnancy outcomes. “This study also identified individual associations between risk genes and adverse outcomes including shorter pregnancy duration, pre-eclampsia, and birth weight,” they noted.

Several medications are available for treating HG, but even the most effective, Zofran, only partly relieves symptoms for about half of patients. The new findings reveal new potential treatment targets and could possibly also help match existing medications to patients based on their genetic profiles. “The ten genetic associations provide intriguing avenues to advance our understanding and pursue therapeutic pathways for a common pregnancy condition that in its most severe form is associated with substantial morbidity and even mortality for mothers and exposed offspring,” the scientists concluded.

Fejzo and her team just received approval to launch a clinical trial of metformin, a widely used diabetes medicine that increases GDF15 levels. The study will test whether taking metformin before pregnancy can desensitize women to the hormone, potentially reducing nausea and vomiting or preventing HG in women who have had it before. GEN was told, “We will be initiating a clinical trial to increase GDF15 prior to pregnancy in patients with a history of HG and planning to conceive to desensitize them to the hormone’s rapid rise in early pregnancy. We and others have shown preliminary evidence that this approach may work as in our retrospective study pre-pregnancy metformin use was associated with a significant reduction in HG risk.”

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Pivotal Phase III Pancreatic Cancer Trial Advances RAS-Targeting Daraxonrasib

This week, Revolution Medicines (RevMed) announced positive topline results from its global Phase III trial of RAS-targeting daraxonrasib in metastatic pancreatic ductal adenocarcinoma (PDAC) patients. In RASolute 302, patients on daraxonrasib showed improvements in progression-free survival (PFS) and overall survival (OS) compared with standard of care cytotoxic chemotherapy.

“With these unprecedented results, daraxonrasib has the potential to achieve our goal of bending the mortality curve in pancreatic cancer. Unlike chemotherapy, daraxonrasib is a RAS-targeted medicine that targets RAS in its active ‘ON’ state, shutting down a key signaling pathway that drives aggressive tumor growth. This is especially important in pancreatic cancer, which is among the most RAS-driven cancers, with more than 90% of tumors harboring a RAS mutation that is the driver of the cancer,”  Mark A. Goldsmith, MD, PhD, told Inside Precision Medicine. He is chief executive officer and chairman of Revolution Medicines.

Daraxonrasib patients achieved a median OS of 13.2 months versus 6.7 months for chemotherapy. The drug was generally well tolerated, with a manageable safety profile and with no new safety signals.

RAS is the key oncogenic driver of pancreatic cancer. Nearly all RAS mutations occur at KRAS position G12, but RAS mutations in other isoforms and at KRAS positions G13 and Q61 are also observed.  

RevMed now intends to submit the drug for approval by regulatory authorities, including the U.S. Food and Drug Administration as part of a future New Drug Application, and for presentation at the 2026 American Society of Clinical Oncology Annual Meeting. Information about current trials of the drug are available at  https://revmedclinicaltrials.com/.

“For patients with metastatic pancreatic cancer, new treatment options are urgently needed to increase survival time and improve quality of life,” said Brian M. Wolpin, MD, MPH, professor of medicine at Harvard Medical School, director of the Hale Family Center for Pancreatic Cancer Research at Dana-Farber Cancer Institute, and principal investigator for the RASolute 302 trial. “The widely anticipated results of this study indicate that daraxonrasib provides a clear and highly meaningful step forward for patients with pancreatic cancer who have experienced progression on prior treatment, typically chemotherapy. I believe that this new approach is a very important advance for the field that I expect will be practice-changing for physicians and improve the care for patients with previously treated metastatic pancreatic cancer.”

Pancreatic cancer is the most RAS-addicted of all major cancers, with more than 90% of patients harboring tumors driven by mutations in RAS proteins. These mutations span a range of RAS variants that fuel aggressive tumor behavior. Daraxonrasib, a multi-selective inhibitor of RAS(ON) proteins, is the first investigational agent in a novel class of RAS inhibitors designed to address a diverse and broad spectrum of oncogenic RAS drivers.

The RASolute 302 trial enrolled patients with pancreatic tumors harboring a wide range of RAS variants, including those with RAS G12 mutations (such as G12D, G12V, and G12R), as well as those without an identified RAS mutation. The primary endpoints of the trial were PFS and OS in patients with tumors harboring RAS G12 mutations. Secondary endpoints assessed PFS and OS in all enrolled patients (the intent-to-treat population), including those with tumors with and without (wild type) an identified RAS mutation.

Daraxonrasib is an oral RAS(ON) multi-selective, non-covalent inhibitor. Cancers driven by a broad range of common RAS mutations include PDAC, non-small cell lung cancer (NSCLC), and colorectal cancer. The drug is currently being evaluated in four global Phase III registrational trials, including three in PDAC and one in NSCLC.

Daraxonrasib works by suppressing RAS signaling through inhibition of the interaction between both wild-type and mutant RAS(ON) proteins and their downstream effectors.

Pancreatic cancer is one of the deadliest malignancies, because of its typically late-stage diagnosis, resistance to standard chemotherapy, and high mortality rate. In the U.S., recent estimates indicate that each year approximately 60,000 people will be diagnosed with pancreatic cancer, and about 50,000 people will die from it.

The post Pivotal Phase III Pancreatic Cancer Trial Advances RAS-Targeting Daraxonrasib appeared first on Inside Precision Medicine.

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It’s HAMMR Time: Duracyte Launches with “Living Pharmacy” Platform

For many patients, especially those with chronic or life-threatening diseases, treatment is not a single intervention but a relentless routine.

Cancer patients can spend years tethered to infusion schedules, returning weekly for IV therapies that dictate where they can live, travel, and work. Children with rare metabolic disorders may rely on frequent enzyme infusions, with entire rooms of supplies needed to sustain their care. And for patients in low-resource settings, life-saving biologic drugs often remain out of reach altogether due to cost and infrastructure.

These realities highlight a critical challenge in modern medicine: some of the most potent therapies are the most difficult to deliver, necessitating repeated dosing at centralized locations.

Duracyte, a newly launched biotechnology company, is pioneering a potentially transformative approach to medicine by developing a “living pharmacy” inside the human body. Its core technology, the Hybrid Advanced Molecular Manufacturing Regulator (HAMMR), is an implantable bioreactor designed to produce biologic drugs directly within patients. This innovation could fundamentally change how medicines are manufactured, delivered, and even conceived.

HAMMR
A prototype of Hybrid Advanced Molecular Manufacturing Regulator (HAMMR), a rechargeable implantable device capable of sensing biological signals, monitoring tumor environments and dynamically adjusting therapeutic output in real time. [Rice University]

The founding team combines expertise across bioengineering, medicine, and biotech. Omid Veiseh, PhD, is a Rice University professor and RBL LLC managing partner focused on implantable cell therapies, while Paul Wotton, PhD, is a veteran biotech CEO with deep commercialization experience. Jonathan Rivnay, PhD, of Northwestern specializes in bioelectronics; Robert Langer, ScD, and Daniel Anderson, PhD, are MIT leaders in drug delivery and gene therapy; and Siddharth Krishnan, PhD, of Stanford, contributes expertise in wireless power and implantable devices.

Duracyte is the third venture created by RBL LLC, a Houston-based biotech studio founded by Rice University in 2024. Operating from Helix Park, RBL focuses on rapidly translating breakthrough research into real-world therapies, particularly in areas like oncology and autoimmune disease. Duracyte’s progress is further supported by ARPA-H’s THOR project, a nationwide collaboration aimed at advancing implantable biohybrid therapies from research to clinical application.

Honey, I shrunk the bioreactor

Biologic drugs, including antibodies, hormones, and enzymes, have become a cornerstone of modern medicine. They now represent a substantial share of the pharmaceutical market, treating conditions ranging from cancer to autoimmune diseases. But their production and delivery remain cumbersome.

Traditionally, biologics are manufactured in large-scale industrial bioreactors, purified, stabilized, and shipped to clinics, where they are administered via injection or intravenous infusion. This process is expensive, logistically demanding, and often burdensome for patients, who may require frequent hospital visits over months or years.

Veiseh, a professor of bioengineering at Rice University, has spent much of his career questioning whether this paradigm could be fundamentally reimagined. “What if we could bring this biomanufacturing to the patients and develop implantable bioreactors or injectable bioreactors whereby the biologic could be produced in the body?” Veiseh told Inside Precision Medicine. That question now underpins HAMMR.

At its core, HAMMR is a miniaturized, implantable bioreactor. Roughly the size of a small medical implant, the device houses genetically engineered human cells capable of producing therapeutic proteins. Unlike traditional drug delivery systems, which release pre-manufactured compounds, HAMMR generates biologics inside the patient’s body.

To accomplish this, the device replicates key functions of industrial bioreactors, but in a compact, implantable form. It supplies nutrients and oxygen to the cells, supports their viability, and allows for controlled production of therapeutic molecules.

One of the key technological innovations lies in how HAMMR generates oxygen. Using electrolysis—a well-established chemical engineering process—the device splits water molecules into hydrogen and oxygen. This hybrid oxygenation bioelectronics system for implanted therapy (HOBIT) component provides a steady, localized oxygen supply to sustain the embedded cells. “We’ve got a way to do electrolysis with low power and in a safe manner that actually allows this to be viable for the engineered cells,” Veiseh explained.

Real-time, feedback-controlled medicine

The device also incorporates electronic controls and sensors. Electrical signals can activate or deactivate the cells, effectively turning drug production on or off. Meanwhile, onboard sensors monitor pharmacokinetic and pharmacodynamic data.

This data is transmitted wirelessly to an external interface, enabling clinicians to adjust dosing in real time. Veiseh said, “The implanted device also communicates with an app that allows us to control dosing and get a lot of data from the patient as far as their physiological conditions, meaning the impact the drug is having on the body.”

One of the most transformative aspects of HAMMR is its potential to enable feedback-controlled drug delivery. Rather than administering fixed doses on a set schedule, clinicians could tailor therapy dynamically based on continuous biological data. “For the first time ever, we can create feedback drug delivery systems where you can dose to a pKa level or, better yet, to a pharmacodynamic level, which allows for that precise dosing for every patient,” said Veiseh.

This capability could be especially impactful in oncology, where patients often receive complex combinations of biologics. Current regimens may involve multiple drugs administered on different schedules, requiring frequent clinic visits and careful coordination.

Veiseh described a typical scenario: patients receiving checkpoint inhibitors such as ipilimumab and nivolumab, along with additional biologics like bevacizumab. These therapies often require weekly infusions over extended periods. “The vast majority of patients are getting IV infusions weekly and they are living longer, which is great,” he said. “But now you have patients that are on this regimen for three years.”

HAMMR aims to replace this model with a single implanted device capable of producing multiple drugs, with dosing adjusted digitally rather than through repeated clinical visits. “We’re moving away from physical prescriptions to a world of digital prescriptions,” Veiseh said.

The convergence of components

The idea of implantable bioreactors has been explored for years, but only recently have the necessary technologies matured enough to make it feasible. According to Veiseh, advances in several fields have converged: electronic miniaturization, wireless power transfer, synthetic biology, and biomaterials engineering. Together, these innovations enable the integration of complex functionalities into a small, biocompatible device.

By leveraging established technologies and adapting them for medical use, the team aims to reduce development risk and accelerate regulatory approval.

Wotton, a seasoned biotech executive working with the team, emphasized that many of the underlying components are not entirely new; they are adapted from existing technologies. “One of the advantages here is that these guys have been really intelligent when they’ve taken off-the-shelf technologies,” Wotton told Inside Precision Medicine. “The oxygen technology is lifted from what’s already used in submarines… The battery charging work is being done… The RPE cell lines that we work with… have successfully gotten into the clinic.”

Looking ahead, the team envisions integrating artificial intelligence into the platform. With continuous data collection from implanted devices, machine learning algorithms could identify patterns in treatment response and optimize therapy over time. “You can imagine… this device could now cycle through different therapies, and as it starts seeing efficacy responses, it starts learning,” Veiseh said.

Such a system could enable highly personalized medicine, adapting treatment strategies based on real-time data and accumulated experience across patients.

The HAMMR platform is built around the preparation of polymer-encapsulated cells, obtained from the human immortalized retinal pigment epithelia (RPE) cell line ARPE-19, which has already been used to generate cytokines for treating intraperitoneal tumors with oversight from the U.S. Food and Drug Administration (FDA). This provides a regulatory advantage, as the cells have an established safety profile. These preparations of ARPE-19 cells can be engineered to produce a wide range of biologics beyond cytokines.

A cost-cutting catalog

Veiseh noted that there are more than 300 FDA-approved biologics in the United States, and his team has already created versions of over 150 within this system. “This platform has the potential to really disrupt the biotech market as it exists today,” he said.

The implications extend beyond oncology. Wotton highlighted potential applications in autoimmune diseases, infectious diseases, and metabolic disorders. “There are so many applications of this technology,” he said. “Whether it’s in oncology… or… delivering antibodies like Humira to treat chronic diseases… there are applications where you can treat type two diabetes… HIV.” In each case, the goal is the same: replace repeated injections or infusions with a long-lasting implant that continuously produces therapeutic proteins.

HAMMR could have significant implications for the cost and accessibility of biologic therapies. Biologics are among the most expensive treatments in medicine, with some costing hundreds of thousands of dollars per year. Much of this cost stems from manufacturing, purification, and distribution. By producing drugs directly inside the body, HAMMR could dramatically reduce these costs. “The cost of goods is actually quite low relative to manufacturing today,” Veiseh said. “This is like one-tenth of the price.”

Wotton echoed this point, suggesting that the platform could replace expensive annual treatment regimens with lower-cost implantable devices. “Imagine what you could do if you could replace the $250,000 a year injectable schedule,” Wotton said.

This cost reduction could be particularly impactful in low-resource settings. Veiseh noted that the Gates Foundation has supported the project in part because of its potential to expand access to biologics in developing countries. “Biologics are way too expensive for sub-Saharan Africa,” he said. “But a device that can produce HIV treatments… once yearly… now it becomes… practical for that world too.”

Houston, we have clinical liftoff

Backed by more than a decade of research funding exceeding $100 million from agencies and organizations including DARPA, ARPA-H, the NIH, and the Gates Foundation, Duracyte is preparing to bring its first device into clinical trials. Duracyte plans to initiate a Phase I clinical trial this year evaluating patients with recurrent ovarian cancer. The company has already held multiple meetings with the FDA and completed a pre-IND (Investigational New Drug) meeting. “We have a clear plan as to what it takes to file an IND,” Veiseh said. “We’re on track to actually file… before the end of this year.”

If all goes as planned, the first patients could receive the implant by late this year or early next year. The trial will be conducted in Houston, leveraging partnerships with leading medical institutions, including the renowned MD Anderson Cancer Center. “Our partners at MD Anderson… will be running the first clinical trial,” Wotton said. “Taking advantage of the ecosystem down in Houston.” The proximity of Veiseh’s lab to the clinical site has helped accelerate development, enabling close collaboration between researchers and clinicians.

Despite its promise, the HAMMR platform faces significant challenges. Integrating multiple complex technologies into a single device is inherently difficult, and clinical validation will be critical. Execution risk remains high, particularly in selecting initial indications and navigating regulatory pathways. “We can’t do everything all at once,” Veiseh said. “It’s really thinking about what the value creation is at early stages.”

Prioritization will be key, given the platform’s broad potential. With hundreds of possible biologics and numerous disease targets, choosing the right starting point could determine the company’s trajectory. Wotton emphasized this challenge as well. “What are the challenges we have? Making the right choices with respect to where we go next,” Wotton said.

If successful, HAMMR could mark a fundamental shift in how medicines are delivered and even defined. Instead of prescribing drugs as physical products, physicians could prescribe programmable devices that manufacture therapies on demand. In this model, the distinction between drug and device blurs, giving rise to a new category of therapeutics. “This is so different than what pharma does,” Veiseh said. “I think it’s really interesting to see whether they are also eager to imagine a future of medicine, which gets away from the injectables.”

For now, that future remains speculative. But with clinical trials imminent and a strong foundation of research behind it, Duracyte’s “living pharmacy” is poised to test whether the idea can move from concept to clinical reality.

As Wotton put it, “This is just the tip of the iceberg.”

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