AACR Annual Meeting 2026 – Post-event summary: clinical data readouts and emerging themes

Theme 1

Second-generation targeted therapies: refinement, resistance, and reach

A consistent thread throughout the clinical trials program was the progressive maturation of targeted therapy classes that, despite representing landmark advances at the time of their introduction, are now being systematically refined to address the limitations of first-generation approaches. KRAS inhibition, antibody-drug conjugates (ADCs), and cell therapies were each represented prominently.

KRAS inhibition: moving past G12C

Two presentations at the first Clinical Trials Plenary (New Frontiers in Precision Oncology) demonstrated the pace at which KRAS inhibitor development is extending beyond the G12C subtype.

Elisrasib, a next-generation KRAS-G12C inhibitor engineered for faster and more sustained target engagement, delivered an overall response rate (ORR) of 58.8% and a disease control rate (DCR) of 98.5% in KRAS G12C inhibitor-naïve patients with locally advanced or metastatic non-small cell lung cancer (NSCLC), with a median progression-free survival (mPFS) of 12.2 months and a 12-month overall survival rate of 72%. The compound also demonstrated activity in patients with prior exposure to first-generation KRAS G12C inhibitors, with an ORR of 32.3% and a DCR of 83.9%, as well as in patients with brain metastases and KRAS gene amplification. Elisrasib has received both Breakthrough Therapy and Fast Track designation in NSCLC.

Zoldonrasib, a first KRAS-G12D-selective RAS(ON) inhibitor, addressed what many regard as the larger unmet need: G12D mutations are more prevalent than G12C across multiple tumor types, particularly pancreatic and colorectal cancer; however, until recently, no approved inhibitors targeting this variant existed. In 27 patients with G12D-mutant NSCLC, zoldonrasib achieved a confirmed ORR of 52%, DCR of 93%, and mPFS of 11.1 months, with circulating tumor DNA (ctDNA) clearance in 87% of patients who had detectable ctDNA at baseline.

Synthetic lethality beyond PARP: a new combinatorial logic

Timothy Yap (Associate Professor and Associate Director of Clinical Research, Department of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center) presented early data from a phase I trial of zedoresertib plus lunresertib, a combination of WEE1 and PKMYT1 inhibitors, in 62 heavily pretreated patients with solid tumors and CCNE1, FBXW7, or PPP2R1A genomic alterations. These alterations induce high replication stress, creating a dependency on the G2/M checkpoint that both drugs target. Within the ovarian cancer subgroup, 80% of patients demonstrated tumor shrinkage, with an ORR of 37.5% overall, increasing to 60% in the CCNE1-amplified subgroup. The combination has been granted FDA Fast Track designation in patients with ovarian cancer with confirmed CCNE1, FBXW7, or PPP2R1A alterations.

This dataset positions synthetic lethality as a clinically viable strategy in a biomarker-defined population distinct from those addressed by PARP inhibition and supports CCNE1 amplification as a clinically actionable genomic target warranting prospective biomarker-selected trial development.

Theme 2

Antibody-drug conjugates: expanding indications and refining the safety-efficacy balance

The second Clinical Trials Plenary was dedicated entirely to ADCs, a reflection of the increasing prominence of this modality in oncology drug development. Session chair Ecaterina Dumbrava, MD (Assistant Professor, Department of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center) noted that ADCs have meaningfully improved outcomes across multiple tumor types, and the four datasets presented illustrated both the diversity of tumor targets being pursued and the tolerability improvements achieved through refined ADC engineering.

Trastuzumab deruxtecan plus olaparib: synergy in HER2-positive gynecological cancers

Elizabeth Lee (Medical Oncologist, Dana-Farber Cancer Institute) reported phase I results combining trastuzumab deruxtecan with the PARP inhibitor olaparib in 28 heavily pretreated, predominantly platinum-resistant patients with recurrent or advanced HER2-positive uterine or ovarian cancer. After a median follow-up of 8.44 months, the six-month PFS rate was 88.2% and the confirmed ORR was 46%. The recommended phase II dose was established, with low-grade pneumonitis consistent with the known toxicity profile of both agents.

The scientific rationale is well-established: PARP inhibitors combined with topoisomerase-inhibiting chemotherapy have previously demonstrated synergistic activity but have been associated with dose-limiting toxicity; targeted delivery of the topoisomerase payload via ADC may preserve the synergistic mechanism while improving the therapeutic index.

Novel ADCs in difficult-to-treat populations

QLS5132, a CLDN6-targeting ADC, demonstrated an ORR of 50% across all dose levels in 18 evaluable patients with advanced platinum-resistant ovarian cancer, a population with few available treatment options following platinum failure. The DCR was 100% at doses of 3.2 mg/kg and above, and responses were observed even in patients with low or undetectable CLDN6 expression. Of note, the safety profile was favorable: no cases of interstitial lung disease, ocular toxicity, oral mucositis, or febrile neutropenia were reported. This is a clinically relevant observation given the pulmonary and ocular toxicities that have complicated other ADC programs.

In previously treated nonsquamous NSCLC, risvutatug rezetecan, a B7H3-targeting ADC, was evaluated in combination with the PD-L1 inhibitor adebrelimab in 40 patients without actionable genomic alterations. After a median follow-up of 11.7 months, the confirmed ORR was 47.1%, DCR was 94.1%, and mPFS reached 14 months, representing a clinically meaningful outcome in a population for whom no targeted therapeutic options currently exist.

SYS6010, an EGFR-targeting ADC, was evaluated in advanced nasopharyngeal carcinoma, a tumor type for which post-first-line treatment options are limited. In patients who had not previously received an EGFR monoclonal antibody, the ORR was 43–50% depending on dose. Response did not correlate with EGFR expression level, a finding with potential implications for patient selection strategies.

Theme 3

Cellular and complex immunotherapies: solid tumors and earlier intervention

The third Clinical Trials Plenary, dedicated to cellular therapies and complex immunotherapies, presented clinically significant datasets in CAR-T cell therapy and mRNA-based immunotherapy.

Earlier deployment of CAR-T cell therapy: disease interception in smoldering myeloma

The CAR-PRISM trial, presented by Omar Nadeem, MD (Associate Director, Myeloma Clinical Research Program, Dana-Farber Cancer Institute), evaluated ciltacabtagene autoleucel, a B-cell maturation antigen-directed CAR-T therapy currently approved for relapsed/refractory multiple myeloma, in 20 patients with high-risk smoldering multiple myeloma, a pre-symptomatic stage that precedes the development of active multiple myeloma. The rationale underpinning this approach is that earlier intervention, prior to the development of active disease, may yield deeper responses by virtue of a more functionally intact immune system and lower disease burden.

Across all 20 patients, 100% achieved MRD negativity within two months of a single infusion administered without induction or bridging therapy. At a median follow-up of 15.3 months, no disease progression or deaths had been observed. Six patients followed beyond 18 months retained MRD negativity. All patients experienced grade 1–2 cytokine release syndrome. Neurologic toxicities not meeting criteria for immune effector cell-associated neurotoxicity syndrome were observed in seven patients; no grade 3 or higher events of either type were recorded [2].

Addressing the solid tumor barrier in CAR-T

Janos Tanyi (Associate Professor of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine) presented first-in-human data on SynKIR-110, a multichain KIR-CAR-T cell therapy designed with a split receptor architecture that provides an inducible regulatory mechanism to prevent T cell exhaustion, the principal mechanism underlying the limited efficacy of conventional CAR-T therapy in solid tumors. In nine patients with advanced mesothelin-expressing solid tumors, no dose-limiting toxicities were observed, and a disease stabilization rate of 55% was reported at early dose levels, with one ongoing partial response. Dose escalation is continuing.

mRNA-based immunotherapy: preliminary evidence of activity in melanoma

Pavlina Spiliopoulou (Clinical Senior Lecturer and Honorary Consultant in Medical Oncology, University of Glasgow) reported results from a phase I/II study of mRNA-4359 combined with pembrolizumab in 12 previously untreated patients with locally advanced or metastatic melanoma. mRNA-4359 is designed to prime and expand T cells to kill PD-L1-positive and IDO1-positive tumor cells while depleting immunosuppressive cells. The ORR was 83% and the DCR was 92%, with a median duration of response not reached. Responses were observed irrespective of baseline PD-L1 expression.

Historically, pembrolizumab monotherapy has achieved ORRs of 35–40% in phase III trials in this setting. The limited sample size (n=12) warrants cautious interpretation; however, the consistency of response and the mechanistic rationale, using mRNA to directly program immune cell activity against immunosuppressive targets, support continued evaluation in larger prospective cohorts.

Theme 4 

Immunotherapy: resistance, new combinations, and the question of earlier use

The fourth Clinical Trials Plenary, dedicated to advances in immunotherapy, addressed several dimensions of resistance to immune checkpoint inhibitor therapy, a challenge that increasingly shapes the clinical development of this modality.

Organ preservation in gastric cancer: a two-year landmark

The INFINITY trial (cohort 2), presented by Alberto Leone (Medical Oncologist, Fondazione IRCCS Istituto Nazionale dei Tumori), assessed tremelimumab plus durvalumab as a non-surgical alternative for patients with resectable microsatellite instability-high gastric or gastroesophageal junction cancer. At two years, 100% of the 17 evaluable patients were alive, the clinical complete response rate was 71%, PFS rate was 94.1%, and the gastrectomy-free survival rate was 70.6%. ctDNA clearance was achieved in 11 of 13 patients with baseline positivity.

This represents a highly selected patient population; microsatellite instability-high gastric cancer represents a histologically and molecularly distinct subgroup accounting for a minority of cases. Nevertheless, the two-year outcomes provide proof-of-concept support for organ preservation using immunotherapy in a solid tumor type where surgery has historically been the standard of care [5].

Understanding resistance as a targetable vulnerability

Two presentations addressed the biology of immunotherapy resistance in NSCLC from complementary angles.

Archana Balan (PhD Candidate, Biomedical Engineering, Johns Hopkins University) presented a multiomic analysis of biospecimens from 951 patients in the HUDSON trial, comparing primary and acquired resistance to immune checkpoint inhibitors. Acquired resistance was characterized by subclonal genomic alterations distinct from those seen in primary resistance, alongside hallmarks of phenotypic plasticity including neuroendocrine differentiation. Stem-like CD8+ T cell clusters were enriched in tumors with acquired resistance. These findings are consistent with the hypothesis, advanced during the Opening Plenary, that acquired resistance generates distinct evolutionary vulnerabilities that may be therapeutically exploited.

Fabrice Barlesi (General Director, Gustave Roussy) presented the MATISSE trial, testing the CD39-targeting antibody IPH5201 alongside durvalumab and chemotherapy in perioperative NSCLC. The overall pathological complete response rate was 27.5%, rising to 50% in patients with PD-L1 expression of 50% or greater. Elevated baseline CD39+ and CD8+ cell density in tumors correlated with treatment response, identifying a potential predictive biomarker.

Theme 5

The biology of residual disease: a platform for the next generation of trials

The Discovery Science Plenary, titled The Next Frontier in Minimal Residual Disease: Solid Tumors, provided mechanistic and translational context for several clinical themes that recurred across the meeting program.

Aaron Hata (Clinical Investigator and Associate Professor, Massachusetts General Hospital) introduced the concept of drug-tolerant persister cells in EGFR-mutant and ALK-positive lung cancer, defined as cells that acquire resistance through epigenetic rather than pre-existing genetic mechanisms. His team identified a transitional cell population, arising through lineage-specific injury repair responses, that links untreated cellular states to those observed in residual and relapsed disease. Furthermore, EGFR inhibitors were shown to induce APOBEC3A enzyme activity, increasing mutational burden in persister cells and offering a mechanistic explanation for the emergence of late resistance mutations.

Jean-Christophe Marine (Director, VIB-KU Leuven Center for Cancer Biology) applied this framework to melanoma, presenting evidence that cell plasticity, not just genetic neo-Darwinian selection, drives drug tolerance and proposing that phenotypic plasticity generates targetable dependencies. His team’s ORIGAMI framework, which monitors phenotypic diversity through cell morphology metrics, identified a four-drug combination targeting persister cell vulnerabilities that is under development as a clinically translatable combination regimen.

Dan Landau (Associate Professor of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine and New York Genome Center) presented new single-cell multiomics tools for tracing the evolutionary history of cancer and highlighted whole-genome mutational integration as a strategy to detect ctDNA at lower concentrations, a strategy with potential applicability to early detection and MRD monitoring in solid tumors.

Jeanne Tie (Medical Oncologist, Peter MacCallum Cancer Centre and Walter and Eliza Hall Institute of Medical Research) translated this biology directly to clinical trial design, arguing that ctDNA-based MRD status should replace traditional risk stratification for patient selection in adjuvant trials. She identified three landmark clinical windows for ctDNA-guided decision-making: post-surgery, end of treatment, and surveillance. She noted that the FDA has explicitly recognized ctDNA as a potential endpoint for drug approval and urged the research community to generate the prospective randomized evidence required to validate it.

Theme 6

Cancer vaccines: long-term data and a field coming of age

The Cancer Vaccines major symposium, chaired by Vinod Balachandran (Founding Director, The Olayan Center for Cancer Vaccines, Memorial Sloan Kettering Cancer Center), addressed one of the most prominent emerging narratives in oncology: whether therapeutic cancer vaccines, a modality with demonstrated immunological activity but historically limited clinical efficacy, have now reached a meaningful clinical threshold.

Personalized mRNA vaccine in pancreatic cancer: six-year survival data

Updated long-term follow-up results from a phase I trial of a personalized mRNA vaccine in pancreatic ductal adenocarcinoma, a cancer type associated with poor prognosis with a five-year survival rate of approximately 12%, represented the central dataset of the symposium.

Sixteen patients received the vaccine, designed to target neoantigens unique to each patient’s tumor, alongside atezolizumab and chemotherapy in the adjuvant setting. Eight patients developed vaccine-induced T cell responses. After a median follow-up of 4.2 years, those eight vaccine responders had significantly prolonged survival compared to non-responders: median survival of 3.4 years in non-responders versus not reached in responders. Seven of the eight responders (87.5%) remained alive six years after surgery, compared to two of eight non-responders (25%).

The mechanistic basis is supported by prior work: Balachandran and colleagues have previously shown that long-term pancreatic cancer survivors mount neoantigen-specific immune responses, suggesting inherent immunological responsiveness in a subset of patients; the vaccine is designed to elicit and expand equivalent responses more broadly [3][4].

The broader vaccine landscape: interception, prophylaxis, and prevention

The meeting’s Presidential Select Symposium on precision-based prevention added further context, with Mary (Nora) L. Disis (Professor, Clinical Research Division, Fred Hutchinson Cancer Center) presenting an overview of three vaccine strategies under active clinical investigation: interception vaccines targeting precancerous lesions (with early clinical data in ductal carcinoma in situ, targeting HER2 or MUC1); prophylactic vaccines for high-risk individuals (with Lynch syndrome frameshift mutation-targeting vaccines (Nous-209), the results of which were published in Nature Medicine); and adipocyte-directed vaccination to reduce cancer risk by targeting inflammation [7]. Taken together, the symposium framed cancer vaccination not as a single modality but as a spectrum of interventions operating at different disease stages, consistent with the meeting’s broader emphasis on earlier therapeutic intervention.

Theme 7

Cell therapy at a crossroads: autologous, allogeneic, and in vivo engineering

The dedicated forum on cell therapy, Cell Therapy at a Crossroads: Exploring the Evolving Landscape between Autologous, Allogeneic, and In Vivo Engineering, chaired by Christine Brown (Deputy Director, T Cell Therapeutics Research Laboratories, City of Hope National Medical Center), and the AACR-ASCO Joint Session on next-generation CAR-T cell therapies addressed the central scalability challenge facing the CAR-T field: having established clinical proof-of-concept with autologous approaches, how can the modality be made accessible at scale?

The principal challenge facing the field is well-established: autologous CAR-T therapy requires patient-specific manufacturing, is expensive, time-consuming, and inaccessible to patients who progress rapidly or require immediate treatment. Allogeneic approaches using donor or iPSC-derived cells offer scalability and immediate availability but have historically struggled to match autologous efficacy due to immune rejection and reduced persistence.

In vivo CAR-T engineering, delivering the CAR-encoding genetic construct directly into the patient rather than manufacturing cells ex vivo, represents a third approach with the potential to circumvent both limitations. Early-stage programs using lipid nanoparticle or viral delivery of CAR constructs directly into circulating T cells represent an area of active investigation and significant current investment. The potential advantages are considerable: if CAR-T cells can be programmed in vivo, the modality becomes analogous to a conventional pharmaceutical: manufacturable at scale, stable, and administrable without complex cell processing infrastructure.

The forum also addressed the emerging relationship between gut microbiome composition and CAR-T cell therapy outcomes, a topic explored in a dedicated session on the role of the intestinal microbiome in CAR-T cell therapy, with evidence that these microbial factors influence CAR-T expansion, persistence, and clinical response, and are increasingly being considered in the design of clinical trials and patient management protocols.

Theme 8

RNA biology and translation in cancer: a scientific foundation for the therapeutic pipeline

Two symposia, RNA Biology in Cancer (chaired by Paul Boutz, Assistant Professor, Department of Biochemistry and Biophysics, University of Rochester Medicine) and The Role of mRNA Translation Reprogramming in Cancer (chaired by Ivan Topisirovic, Professor, Department of Biochemistry, McGill University), provided important mechanistic context for several of the therapeutic approaches presented across the meeting program.

The mRNA translation reprogramming symposium addressed how cancer cells dysregulate the translational machinery governing which mRNAs are translated into proteins, and the fidelity and selectivity of that process. These dysregulatory mechanisms are relevant to both oncogenesis, where aberrant translation selectively amplifies oncogenic protein output independent of transcriptional changes, and to therapeutic development, where translation-level dependencies represent candidate targets in the context of resistance to established therapies.

The RNA biology symposium covered non-coding RNA, RNA modifications (the epitranscriptome, addressed separately in the symposium on The Epitranscriptome in Cancer), RNA-binding proteins, and splicing dysregulation. Together, these sessions reflect the progressive maturation of RNA biology as a cancer research discipline, advancing from largely descriptive characterization of RNA alterations in tumors toward mechanistic understanding and therapeutic application.

These sessions are of particular relevance to the nucleic acid therapeutics field. The mRNA-4359 melanoma data and the Balachandran pancreatic vaccine data both depend on the capacity to design, manufacture, and deliver mRNA constructs that reliably elicit defined immune responses. The foundational biology explored in these symposia, encompassing the regulation of mRNA stability, translation efficiency, and protein output, informs both the rational design of such constructs and the mechanistic understanding of interpatient response variability. The session Chemistry to the Clinic Part 4: From Transcript to Protein: New Frontiers in Drug Discovery (chaired by Ryan Potts, Vice President, Amgen, Inc.) addressed this interface most directly from a drug development perspective, covering emerging approaches to modulating gene expression at the transcript-to-protein step, including RNA-targeted small molecules, translation inhibitors, and mRNA-based therapeutics.

Pipeline

New drugs on the horizon: first disclosures

The AACR New Drugs on the Horizon series, organized by the Chemistry in Cancer Research Working Group, featured the first public disclosure of four novel oncology drug candidates approaching first-in-human clinical evaluation.

Philip Chamberlain (Co-Founder, President and CEO, Neomorph, Inc.) presented NEO-811, a molecular glue degrader of ARNT (HIF-1β), a transcription factor central to the HIF signaling pathway. NEO-811 is being developed for clear cell renal cell carcinoma, where VHL loss drives constitutive HIF activation. The compound induced single-agent tumor regression in VHL-deficient xenograft models and demonstrated activity in HIF-2α inhibitor-resistant models. A phase I/II trial in locally advanced or metastatic unresectable disease is ongoing.

Suzanne I. Sitnikova (Director, AstraZeneca) presented AZD8359, a CD8-biased T cell engager targeting STEAP2 in prostate cancer, designed to preferentially activate cytotoxic CD8+ T cells over CD4+ cells to reduce the cytokine release syndrome that has limited first-generation T cell engagers. Preclinical data confirmed selective CD8+ engagement and a wider preclinical therapeutic window than conventional T cell engagers. The compound has entered clinical evaluation.

Hilary Elaine Nicholson (Associate Director, Discovery Biology, Tango Therapeutics) presented TNG961, a first-in-class oral molecular glue degrader of HBS1L, exploiting synthetic lethality created by FOCAD protein loss, a consequence of chromosome 9 deletions common across multiple cancer types. TNG961 caused complete tumor regression in pancreatic and lung cancer models and demonstrated combinatorial activity with inhibitors targeting MTAP deletion, which frequently co-occurs. Data were concurrently published in Cancer Discovery [6]. TNG961 has completed preclinical characterization and is entering clinical development for FOCAD-deleted cancers.

Shyra J. Gardai (Chief Scientific Officer, EpiBiologics) presented EPI-326, a tissue-selective EGFR-targeted bispecific antibody that degrades extracellular EGFR, including mutant, overexpressed, and wild-type forms, using the EpiTAC platform. ITGB6 was selected as the degrader receptor on the basis of its enriched expression in EGFR-responsive tumor types, conferring tumor selectivity. EPI-326 achieved a 90% complete response rate in EGFR-mutant NSCLC xenograft models and demonstrated enhanced antitumor activity in combination with osimertinib and sotorasib. A phase I trial in patients with EGFR-mutated tumors is ongoing.

Analysis

What AACR 2026 tells us about the direction of the field

Viewed across the full program, five narratives emerge as defining the scientific character of AACR 2026.

Modality refinement, not revolution. KRAS inhibitors, ADCs, and CAR-T cells were all present not as novel technologies but as established therapeutic platforms being systematically improved: addressing resistance, expanding indications, engineering better therapeutic indices. The field is in a phase of consolidation and maturation, not fundamental reconceptualization.

Earlier intervention is associated with improved outcomes. The CAR-PRISM smoldering myeloma data, the INFINITY gastric cancer organ-preservation dataset, and the Presidential Select Symposium on Stage 0 prevention collectively support earlier deployment of high-efficacy therapies. This aligns directly with the ctDNA-guided trial design framework presented by Jeanne Tie: the tools to identify candidates for earlier intervention are now maturing in parallel with therapies of sufficient potency to act on that information clinically.

Resistance as scientific opportunity. From Charles Sawyers’ data on prostate cancer lineage switching, to the multiomic resistance analysis from the HUDSON trial, to Aaron Hata’s work on APOBEC-driven persister cell evolution, the meeting consistently reframed therapy resistance not as a clinical failure but as a source of mechanistic insight and new targets. This reframing reflects the field’s increasing mechanistic understanding of resistance as a dynamic and exploitable biological process.

mRNA therapeutics: early but significant clinical evidence. The Balachandran pancreatic cancer vaccine six-year survival data and the mRNA-4359 melanoma combination results collectively represent some of the most significant early-phase clinical evidence to date that mRNA-based immunotherapy can generate durable, clinically meaningful responses. These are still small early-phase trials, but the immunological correlates are well-characterized, the durability data are substantive, and the mechanistic foundation is supported by concurrent work in RNA biology.

Cell therapy: converging developmental strategies. Autologous optimization, allogeneic platform advancement, and in vivo engineering represent the three principal developmental trajectories currently shaping the CAR-T field. The CAR-PRISM data suggests that autologous CAR-T therapy may be deployable significantly earlier in the disease course than current approved indications permit. The in vivo delivery discussion suggests that the manufacturing constraints inherent to ex vivo cell processing may eventually be circumvented. Together, these developmental strategies will likely define the cell therapy landscape for the next decade.

No single dataset presented at AACR 2026 is likely to prompt immediate revision of clinical practice guidelines; taken collectively, however, the meeting presented a substantial accumulation of maturing clinical evidence across modalities, tumor types, and disease stages, combined with foundational science that is now progressively translating into therapeutic programs. The meeting’s theme of Precision, Partnership, Purpose accurately reflected the current character of the field: evidence-based, mechanistically driven, and advancing systematically across multiple therapeutic modalities and scientific domains.

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References

1. American Association for Cancer Research. AACR Annual Meeting 2026; April 17–22, 2026; San Diego, CA.  Link

2. Nadeem O, Cordas dos Santos DM, Nikiforow S, et al. Ciltacabtagene autoleucel in high-risk smoldering multiple myeloma: the CAR-PRISM phase 2 trial. Nat. Med. 2026; Epub ahead of print.  Crossref

3. Rojas LA, Sethna Z, Soares KC, et al. Personalized RNA neoantigen vaccines stimulate T cells in pancreatic cancer. Nature 2023; 618, 144–150.  Crossref

4. Sethna Z, Guasp P, Reiche C, et al. RNA neoantigen vaccines prime long-lived CD8+ T cells in pancreatic cancer. Nature 2025; 639, 1042–1051.  Crossref

5. Raimondi A, Lonardi S, Murgioni GG, et al. Tremelimumab and durvalumab as neoadjuvant or non-operative management strategy in microsatellite instability-high resectable gastric or gastroesophageal junction adenocarcinoma: the INFINITY study by GONO. Ann. Oncol. 2025; 36(3), 285–296.  Crossref

6. Nicholson HE, Whittington DA, Bruzzese FJ, et al. TNG961 is a selective oral HBS1L molecular glue degrader for the treatment of FOCAD-deleted cancers. Cancer Discov. 2026; Epub ahead of print.  Crossref

7. D’Alise AM, Willis J, Duzagac F, et al. Nous-209 neoantigen vaccine for cancer prevention in Lynch syndrome carriers: a phase 1b/2 trial. Nat. Med. 2026; 32, 1002–1011.  Crossref