ASCO 2026 offered a broad view of oncology’s direction of travel – from therapies moving into earlier treatment settings and the growing use of molecular monitoring to advances in cancer vaccines, RNA-targeting drugs, and precision immune modulation. But which developments could genuinely change patient care, and which areas are receiving too little attention?
We asked Wolfram Brugger, Chief Medical Officer at Asgard Therapeutics; Michael Lahn, Chief Medical Officer at iOnctura; Stephan Schann and Jean-Marie Cuillerot, Chief Scientific Officers at Kainova Therapeutics; Anthony Johnson, CEO of Outrun Therapeutics; and Jerry McMahon, CEO of STORM Therapeutics, to share their perspectives.
What drug development trends from ASCO stood out to you most, and why do they matter?
Wolfram Brugger: One of the strongest trends at ASCO was the continued movement of therapies, including immunotherapies, antibody-drug conjugates (ADCs), T-cell engagers, and targeted therapies, into earlier lines of treatment, including neoadjuvant and locally advanced disease settings. This shift reflects a growing recognition that patients should receive the most effective therapies as early as possible, when the likelihood of achieving long-term disease control or even cure is highest.
This trend matters because it has the potential to improve overall survival while reducing the need for subsequent lines of therapy. Earlier intervention may also lessen the treatment burden on patients, improve quality of life, and ultimately reduce healthcare costs.
Michael Lahn: During ASCO’s 2026 annual meeting, the most common malignancies, such as breast, lung, and colorectal cancer, remained at the centre of clinical and scientific interest. The use of immunotherapies in clinical studies also remains a major focus of novel combination therapies.
Personally, I found it exciting that approved agents are increasingly being investigated outside their initial indications. Based on the knowledge underlying rare tumour types, approved agents can be used to provide clinical benefit. One example is the study of abemaciclib in patients with the rare malignancy dedifferentiated liposarcoma. Patients who took this agent, which is approved in breast cancer, had a progression-free survival of 9.7 months, compared with 1.5 months for patients who did not take abemaciclib.
Stephan Schann: The clearest trend at ASCO 2026 was the shift from broad immunotherapy expansion to precision-guided, biology-driven immune modulation. Across plenary sessions, the central question was: “Why do patients fail immunotherapy, and how do we overcome the specific mechanisms driving resistance?” This theme was echoed in several late-phase readouts showing that more selective combination strategies, anchored in a deeper understanding of tumour–immune interactions, are now delivering meaningful clinical signals and reopening responsiveness in tumours that have remained largely refractory to standard immuno-oncology approaches.
What matters is that oncology is moving beyond “more IO” towards “smarter IO,” integrating biomarkers, deep biological knowledge, and combinations built on a clear mechanistic rationale. ASCO confirmed that precision approaches grounded in mechanistic clarity are increasingly shaping where the field is heading across multiple clinical contexts.
Jerry McMahon: A lot of development is still focused on well-known targets such as HER2, but what is changing is the range of ways in which they are being tackled. Multiple modalities are now in play. At the same time, there is growing interest in going beyond proteins to targets such as RNA, which could open up new ways to treat cancer.
What is one oncology trend you think is overhyped – or underappreciated – after ASCO?
Brugger: Although immune checkpoint inhibitors, ADCs, bispecific antibodies, and targeted therapies continue to attract significant attention – and rightly so – I believe cellular and gene therapies for solid tumours remain underappreciated. Gene therapies for solid tumours are highly innovative and offer novel mechanisms of action, including off-the-shelf products designed to generate personalised antitumour immune responses in vivo.
As an example, Asgard Therapeutics is developing AT-108, an off-the-shelf gene therapy that directly reprograms tumour cells into a rare subset of conventional type 1 dendritic cells, which are critical for mounting effective cytotoxic T-cell responses.
Lahn: ASCO will certainly be the place to learn more about tumour vaccine treatments once the data are more mature. In the past, we heard about Phase I mRNA tumour vaccines. There are now several Phase II and III studies underway, especially in combination with immunotherapy. Although it is still early, the data presented at ASCO 2026 demonstrated the potential of mRNA vaccines to induce durable antitumour responses. I am eagerly awaiting the results of the ongoing studies.
Anthony Johnson: I was impressed by two very different studies in metastatic colorectal cancer, which I believe are underappreciated and point to real progress for these patients.
The first, the CIRCULATE trial, evaluated circulating tumour DNA as a prognostic and treatment-guiding biomarker in stage II colorectal cancer. Across 1,396 patients, ctDNA proved to be an excellent prognostic marker and, when used to guide chemotherapy treatment, dramatically improved outcomes compared with observation alone. As additional data emerge, I anticipate that ctDNA could become a key part of the management of stage II colorectal cancer.
The second, the BREAKWATER trial, compared encorafenib, cetuximab, and chemotherapy with standard-of-care chemotherapy in BRAF V600E-mutant metastatic colorectal cancer, a group that is very difficult to treat. Objective response rate, progression-free survival, and overall survival were markedly improved in patients receiving encorafenib and cetuximab with chemotherapy, setting a new first-line standard for these patients. The future looks much brighter for metastatic colorectal cancer.
How can drug developers work more effectively with clinicians to make innovation more meaningful for patients?
Brugger: Drug developers can only be successful by working jointly and transparently with clinicians and health authorities, from the preclinical stages through first-in-human trials and across the entire clinical development plan.
Close collaboration between developers and clinicians will be critical to ensuring that these emerging therapies are developed in a way that delivers the greatest possible benefit to patients.
Jean-Marie Cuillerot: The most effective collaboration happens when drug developers and clinicians co-design studies around shared scientific hypotheses, rather than simply around endpoints. Clinicians navigate complex treatment sequences, often involving multiple lines of therapy, rapidly changing therapeutic options, evolving standards of care, and patients whose needs do not always fit neatly into trial designs. Developers can add value by engaging early to understand these realities and by contributing translational tools and biomarker strategies that generate evidence clinicians can act on.
Equally important is the creation of continuous feedback loops during development, with emerging data regularly reviewed alongside investigators and trial insights translated into practical, actionable guidance for the clinic and, ultimately, better treatment decisions for patients.
ASCO reinforced that translation, rather than strong science alone, is what meaningfully improves patient outcomes across diverse settings. Innovation becomes more impactful when both sides co-create development pathways in which clinicians provide real-world insight into unmet needs and drug developers bring the mechanistic depth required to address them effectively.
Which oncology modalities or platform approaches are you most excited about right now – and what still needs to be proven?
Brugger: Novel gene and cellular therapy approaches, such as in vivo CAR T, are among the oncology modalities that excite me most. These approaches have the potential to overcome some of the limitations associated with traditional cell therapies, although more clinical success stories are still needed to demonstrate their full potential.
I am also excited about the local intratumoural administration of novel drug modalities, including gene therapy approaches and cancer vaccines. By acting directly within the tumour microenvironment, these approaches could offer a powerful way to stimulate antitumour immunity while potentially enabling broader application across cancer types.
Many of these emerging modalities are now approaching clinical development, and the coming years will be an exciting period.
Lahn: Although cell therapies and ADCs continue to capture attention, I am particularly excited by the next generation of highly selective small molecules, especially when used in rational combinations.
There were two presentations: one received a standing ovation, and the other concerned an early-stage study. Both agents showed exciting improvements in survival for patients with metastatic pancreatic ductal adenocarcinoma.
The drug that received a standing ovation was daraxonrasib. This drug reduced the risk of death by 60 percent compared with chemotherapy in previously treated metastatic pancreatic cancer, with median overall survival of 13.2 months versus 6.7 months.
The second drug, atebimetinib, a MEK inhibitor, was evaluated in a Phase IIa trial with no comparator arm. Patients had a median overall survival of 17.3 months, compared with 8.5 months for patients receiving chemotherapy alone, based on historical data.
These two examples show that novel small molecules are making an impact even in malignancies that have not benefited from the drug development progress seen in other cancer types.
Cuillerot: What is most exciting right now, regardless of modality, are approaches that deliver differentiated compounds built on well-defined biological mechanisms and have clearer clinical relevance for patient populations underserved by standard immuno-oncology approaches. We are seeing meaningful progress with engineered antibodies and small-molecule immune modulators, but the common thread is not the format. It is the ability to target defined biological barriers to antitumour immunity with a plausible link to clinical benefit.
Many emerging modalities show encouraging early signals, but the field must demonstrate consistent, clinically meaningful benefit, acceptable safety, and how these mechanisms integrate with existing standards of care. ASCO highlighted that progress will come from matching the right tools to the right biology.
McMahon: Targets such as METTL3, which modify RNA transcripts, are particularly exciting. They allow us to act at the level of gene expression, which represents a different approach. METTL3 inhibition has been shown to reprogramme cancer stem cells, representing a novel way to affect the growth and spread of cancers such as acute myeloid leukaemia and connective-tissue tumours, including sarcomas.
Emerging modalities often take the spotlight, but where is there still room for innovation in established approaches such as small molecules?
Lahn: Small-molecule chemistry has brought several new agents into the clinic, some of which bind to areas of the target molecule that had not previously been explored.
Johnson: Head and neck cancer remains a major unmet need and one that is expected to grow over the next 20 years, particularly among HPV-positive patients, who make up the majority of the oropharyngeal squamous cell cancer subset.
ASCO highlighted several novel treatment approaches under evaluation for head and neck cancers. Although some bispecific antibody and bifunctional fusion antibody programmes are showing real promise, others have been less encouraging.
For example, intensity-modulated radiotherapy matched the considerably more expensive intensity-modulated proton therapy in terms of quality of life, functional recovery, and tumour control in patients with locally advanced oropharyngeal squamous cell cancer, regardless of HPV status. Durvalumab plus radiotherapy was also no better than chemoradiation therapy in terms of three-year event-free survival among intermediate-risk, HPV-positive head and neck cancer patients.
There is a tremendous opportunity to leverage small-molecule approaches to address well-understood pathophysiological mechanisms, particularly in HPV-positive head and neck cancer, where the viral E6 protein hijacks E6AP to degrade the well-known tumour suppressor p53.
McMahon: Small molecules still play a huge role in innovation and drug creation. We are seeing new chemistry and scaffolds emerge, including for targets such as RAS. That shows that the approach is evolving rather than standing still and can continue to deliver new drugs against both established and emerging biology.
If current oncology development trends continue, what will cancer treatment look like in 10–20 years – and how cautious should we be when talking about “curing” cancer?
Brugger: In 10–20 years, I believe traditional systemic chemotherapy treatments will become increasingly obsolete, while immunotherapies and targeted approaches, including ADCs, bispecific antibodies, and cellular and gene therapies, will become increasingly central to cancer treatment. These approaches have the potential to provide more precise, effective, and long-lasting treatments, leading to improved outcomes for patients.
I also expect serial monitoring of treated patients using non-invasive approaches such as ctDNA assessment to become standard of care, while imaging may play a less dominant role in long-term follow-up. Molecular monitoring could enable the earlier detection of residual disease and more personalised treatment decisions.
The ultimate goal of cancer treatment is to cure patients, and we should remain ambitious in pursuing this objective. However, defining a treatment as a cure will require long-term follow-up, such as sustained undetectable ctDNA levels over time, before we can confidently confirm durable disease eradication.
Johnson: Over the next 10–20 years, it is quite possible that many cancers will become chronic diseases, managed with multiple treatment options alongside sensitive diagnostics that can measure subclinical disease burden. HIV offers a useful parallel, having evolved along similar lines over recent decades. Patients may undergo long-term treatment with much lower, better-tolerated doses, with cancer care coming to resemble the way we manage other chronic conditions.
It is also likely that cancers, and their targeted treatments, will increasingly be classified according to pathway mechanisms rather than the organ affected. Cancer therapies may be approved for the treatment of a specific pathophysiological pathway that is relevant to multiple cancer types.
An example today would be PARP inhibitors, which are approved for cancers with homologous recombination repair deficiency, including those with mutations in the BRCA1 or BRCA2 genes. These genes are relevant to several types of ovarian, cervical, prostate, and pancreatic cancer.
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