About

Antoni Ribas, M.D., Ph.D., is a physician-scientist conducting laboratory and clinical research in malignant melanoma. His work focuses on gene engineered T-cells, PD-1 blockade therapy, and BRAF targeted therapies. His laboratory, supported by the National Cancer Institute, the State of California, and foundations, develops models of disease to test new therapeutic options, studies mechanisms of action of treatments in patients, and investigates the molecular mechanisms of therapy resistance. He has played a key role in the clinical development of several agents approved by the FDA, including pembrolizumab (Keytruda), vemurafenib (Zelboraf), cobimetinib (Cotellic), dabrafenib (Tafinlar), and trametinib (Mekinist).

Research topics

• Medicine
• Internal medicine
• Biology
• Immunology
• Cancer research
• Oncology
• Surgery
• Gastroenterology
• Virology
• Cell biology
• Ecology
• Pathology
• Computational biology
• Genetics

Selected publications

• The Next Chapter of <i>Cancer Immunology Research</i>

  Cancer Immunology Research · 2026-01-08

  articleSenior author

  We are honored to serve as the new Editors-in-Chief of Cancer Immunology Research (CIR) with the opportunity to start a new chapter to guide the journal into the next frontiers of cancer immunotherapy research with a positive impact for patients. We are physician-scientists who have worked for decades studying how the immune system can be harnessed to treat cancer and conducting clinical trials to develop new immunotherapies that have shown unprecedented results in patients with cancer. These experiences shape our vision for the journal to become the leading publication for basic, translational, and clinical research in cancer immunology and immunotherapy.Through the vision of the founding Editor-in-Chief of the journal, Glenn Dranoff, which was then advanced to meet the evolving science by Editors-in-Chief Robert D. Schreiber and Philip D. Greenberg, CIR has gained a leadership position among cancer immunotherapy journals. In fact, CIR has become one of the highest Impact Factor publications in the field of cancer immunology and immunotherapy. It has published diverse articles that have expanded our knowledge of how the immune system interacts with cancer and how it can be exploited to treat patients. We intend to build on this important legacy by actively pursuing additional areas of interest. Our vision for the journal can be summarized in the following points:Expand the clinical content, including immuno-oncology clinical trials, clinical research defining biomarkers, immune mechanisms in patient samples, and understanding resistance to cancer immunotherapies;Build on our interest in studies using computational science and systems immunology, as well as those reporting technological developments to provide new insights into cancer immunology;Become more inclusive of biomedical engineering studies as they apply to cancer immunology and immunotherapy; andWelcome voices from across the globe and across disciplines to broaden access to the benefits of cancer immunotherapies for all patients with cancer.Cancer immunology is now a driving force in oncology. Since the inaugural issue of CIR in 2013, the FDA has approved 14 immune checkpoint blockade agents, nine adoptive T-cell transfer therapies, and nine bispecific and T cell–engager therapeutics. This has been driven by an ever-increasing number of immunotherapy clinical trials, which we welcome for submission to CIR. Immune checkpoint–blocking antibodies and adoptive T-cell transfer therapies have become standard-of-care treatments for multiple cancers and are among the most prescribed cancer drugs in the world. However, there is a need for further progress. The science has continued to advance, bringing new treatment strategies to the clinic, including next-generation cancer vaccines, new approaches to activate the immune system based on a refined understanding of the immune regulatory pathways and the structure of the receptors, the generation of multiple gene edits in T-cell therapies to improve their antitumor activity and control, the exciting advent of in vivo T-cell gene engineering, and the development of multifunctional antibody–drug conjugates and T-cell engagers that are providing new treatment options for patients who were not benefiting from the prior generation of immuno-oncology agents. With improved cancer immunology treatments, there is also a need to better understand mechanisms of response and resistance, both primary and after transient clinical responses. In addition, there are over 200 cancer types based on genetic and tumor microenvironment signals that subtype any given organ-derived cancer. This journal is poised to publish key studies that report both the analysis of patient-derived samples and preclinical models that study the causality of the events.It is an unprecedented time in science when multiple technologies are allowing sample analyses at previously unachievable levels. We have gone from studying one gene at a time in bulk samples to studying all genes in every single cell. The amount of knowledge derived from modern technologies provides the promise of being able to study the immune system with tools that can encompass and unravel all its complexity. It will require continued advances in computational biology, mathematical modeling, machine learning, and artificial intelligence, which will be a new focus of the journal, and we highly encourage submissions in this area.To achieve the goals of the new chapter for CIR, we have assembled an outstanding group of senior editors who are experts in all these fields. They will provide guidance to select the work that is most impactful and that advances the field toward next-generation immunotherapies in the clinic. The focus on patient impact requires that at each stage of cancer immunology research, authors and reviewers maintain very high standards for scientific rigor, reproducibility of the findings, and the interpretation of their relevance to patients with cancer. The description of data interpretation and study conclusions needs to align with the strength of the findings and their reproducibility in different model systems.In conclusion, we are excited to invite authors, reviewers, editors, and readers to join us in this next chapter to shape CIR as the journal that not only reflects the state of the science but also helps define its future.E.M. Jaffee reports personal fees from Abmeta, Adventris, HDT Bio, Dragonfly, Mestag, STIMIT, NeoTX, and NEUVOGEN; grants from Lustgarten and Genentech; and other support from Break Through Cancer and Bristol Myers Squibb outside the submitted work. A. Ribas reports personal fees from Amgen, Merck, Appia, Arcus, Compugen, Larkspur, Lutris, Lyell, MapKure, Merus, Sastra, Synthekine, Tango, Nextech, Apricity, Dispatch, and Highlight outside the submitted work and that he has a patent for Arsenal Bio licensed.

  PublisherDOI

• Abstract LB-C001: Phase 1 Trial of Bispecific CART19/20 Cells for Relapsed or Refractory Non-Hodgkin Lymphoma: Updated Results with Over Four Years Median Follow Up

  Cancer Immunology Research · 2026-03-05

  article

  Abstract Introduction CART19/20 was developed by engineering autologous naïve/memory T (TN/MEM) cells with a bispecific anti-CD19/CD20 chimeric antigen receptor (CAR) with the goal of overcoming resistance to single-target CD19-directed CAR-T cells. We report an update of a first-in-human phase 1 clinical trial of CART19/20 for patients with relapsed/refractory non-Hodgkin lymphoma (R/R NHL) and small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) (NCT04007029) with a median follow-up of over 4 years. Methods Eligible patients were ≥18 years old with R/R NHL and SLL/CLL, with ECOG 0 or 1. Patients were included if they had 2 or more prior lines of therapy with diffuse large B cell lymphoma (DLBCL) and primary mediastinal B cell lymphoma (PMBCL) and 3 or more prior lines for CLL/SLL, follicular lymphoma (FL), and mantle cell lymphoma (MCL). Autologous leukocytes were obtained by leukapheresis and sorted for CD62L+ TN/MEM cells, followed by lentiviral transduction of the bispecific CD19/CD20 CAR, and subsequent expansion of gene-modified T-cells. The primary end point was safety, and secondary endpoints were clinical response, progression free survival (PFS), overall survival (OS), and CART19/20 persistence. Results As of the data cutoff of November 25, 2025, 15 patients had received CAR-T 19/20 cells (6 DLBCL, 4 FL, 4 MCL, 1 HGBCL). Patients were treated at two dose levels, either 50x106 +/- 30% CAR+ cells (12 patients) or 200 x106 +/- 30% CAR+ cells (3 patients). The median age was 60 (range 29 to 70). Patients had received a median of 4 prior lines of therapy (range 2 to 8). All patients except one had stage IV disease, and 11 of 15 received bridging therapy. The CART19/20 cells were enriched with central-memory T cells (TCM: CD45RA–/CD45RO+/CD62L+). Maximum CRS was grade 2 which occurred in one patient. There were 9 patients that experienced max grade 1 CRS and no ICANS or neurotoxicity. There were 12 serious adverse events and two dose limiting toxicities. Fourteen of fifteen patients achieved an objective response (93% ORR), with 12 patients (80%) achieving a complete response (CR). With a median follow up of 51 months (range: 6.4 – 73.1), the median PFS was 37.5 months (95% CI 4.8 – not estimable) and the median OS was not yet reached. The median peak CAR-T19/20 cell expansion was 592,500 cells/mL whole blood, with mean persistence of CART 19/20 from date of infusion to last date of measurable CART19/20 cells of 526 days. Conclusion Overall, this phase 1 trial demonstrates that CART19/20 is a safe and effective therapy with the potential to overcome common resistance mechanisms of CAR-T cell therapy. Citation Format: Sophie Carlson, Benjamin Puliafito, Christopher M. Walthers, Brenda Ji, Jacob Naparstek, Jia Chen, Mobina Roshandell, Caitlin Harris, Mobina Khericha Gandhi, Melanie Ayala Ceja, Christy Sidhu, Karla Nawaly, Martin Allen-Auerbach, Sven De Vos, Patricia Young, Caspian Oliai, Gary Schiller, John Timmerman, Antoni Ribas, Yvonne Chen, Sarah Larson. Phase 1 Trial of Bispecific CART19/20 Cells for Relapsed or Refractory Non-Hodgkin Lymphoma: Updated Results with Over Four Years Median Follow Up [abstract]. In: Proceedings of the AACR Immuno-Oncology Conference (AACR IO): Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2026 Feb 18-21; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2026;14(2 Suppl):Abstract nr LB-C001.

  PublisherDOI

• Cellular neighborhoods govern antitumor T-cell infiltration following anti-CTLA-4 in melanoma with primary resistance to anti-PD-1

  Cancer Discovery · 2026-04-21

  articleSenior author

  In the phase 2 trial SWOG S1616 (NCT03033576), patients with advanced melanoma with primary resistance to anti-PD-1/L1 therapies had improved outcomes on the combination of the anti-CTLA-4 antibody ipilimumab with continued anti-PD-1 with nivolumab, over ipilimumab alone. Baseline biopsies from patients responsive to combination therapy had increased transcriptomic expression of complement by myeloid cells, interferon pathways by endothelial cells, and oxidative phosphorylation and lipid metabolism by melanoma cells. Using spatial proteomics, some on-therapy biopsies from patients responding to combination therapy had networks of activated CD8 T cells nearby melanoma cells, while others had T cells and myeloid cells, reflective of different timepoints in a dynamic antitumor response. Conversely, biopsies from patients progressing on combination immunotherapy displayed impaired T-cell infiltration adjacent to plasma cells. Our results define cellular neighborhoods and transcriptomes in melanoma biopsies when reversing resistance to anti-PD-1 with the addition of anti-CTLA4, and plasma cell sheets in non-responding biopsies.

  PublisherDOI

• 26-CCC-10655-ACC SEVERE HYPERCHOLESTEROLEMIA MEDIATED BY LIPOPROTEIN X IN A PATIENT WITH IMMUNE CHECKPOINT INHIBITOR-ASSOCIATED HEPATITIS

  Journal of the American College of Cardiology · 2026-03-27

  article
  PublisherDOI

• Whole-protein screening and multi-modal profiling of antigen-specific CD4+ T cells at single-cell resolution

  Nature Communications · 2026-05-12

  articleOpen access

  Systematic whole-protein screening and comprehensive profiling of antigen-specific CD4+ T cells are crucial for advancing vaccine design and cancer immunotherapies, yet remain technically challenging. Here, we present a high-throughput platform that utilizes large-scale class II single-chain trimer libraries to detect antigen-specific CD4+ T cells, while simultaneously profiling their antigen specificity, TCRα/β sequences, MHC restriction, whole transcriptomes, and patient/timepoint origins at single-cell resolution. Upon rigorous platform validation, we screened the full SARS-CoV-2 spike receptor binding domain in a longitudinal cohort of 22 participants, identifying 2,188 antigen-specific CD4+ T cells and showing key metrics defining the immunogenicity of class II-restricted viral antigens. We further extended the platform to whole-protein screening of HPV-16 E6/E7 in a cohort of precancerous patients, indicating HPV-specific CD4 TCRs that, upon extensive characterization, demonstrate strong therapeutic potential. By integrating high-throughput antigen screening with high-dimensional, multi-modal cellular characterization, our approach provides detailed insight into CD4+ T cell immunity, potentially guiding vaccine design and next-generation TCR-based cancer immunotherapies. Rapid methods to identify antigen-specific T cells are essential for developing targeted immunotherapies. Here the authors present a high-throughput MHC class II single-chain trimer platform for the comprehensive profiling of CD4+ T cells, enabling the rapid identification and characterization of virus- and tumour-specific T cell receptors (TCR) at single-cell resolution.

  PublisherOA PDFDOI

• Rewiring STAT signaling from the cell surface with Trikine immunotherapeutics

  Science · 2026-02-19 · 5 citations

  articleOpen access

  Cytokines dimerize two receptor chains to activate Janus kinases and signal transducer and activator of transcription (STAT) transcription factors that regulate immune cells, but they have therapeutic liabilities. We engineered “Trikines” to compel cis formation of three-chain cytokine receptor complexes at the cell surface that induce bespoke STAT transcriptional signaling programs. Trikines coactivated phosphorylation of STAT5 (pSTAT5) and pSTAT3 signatures distinct from natural cytokines by assembling trimeric combinations of interleukin-2 (IL-2), IL-10, and IL-21 receptors. In preclinical models, an IL-2–based Trikine restrained terminal differentiation of T cells, promoted stemness, and enhanced durability of tumor control without observable toxicity. An IL-10–based Trikine induced immune infiltration into poorly immunogenic tumors, showing efficacy in preclinical models of small cell lung cancer and pancreatic cancer. Trikines obviate the need for cell engineering to customize STAT signatures and may hold potential for immunotherapy.

  PublisherOA PDFDOI

• Sequential transcriptional waves and NF-κB-driven chromatin remodeling direct drug-induced dedifferentiation in cancer

  Nature Communications · 2026-04-15

  articleOpen access

  Drug-induced dedifferentiation towards drug-tolerant persister states is a common mechanism cancer cells exploit to escape therapies, hindering durable responses. How early epigenomic and transcriptomic programs coordinate to initiate these reversible transitions remains largely unexplored. Here we employ high-temporal-resolution multi-omics profiling, information-theoretic approaches, and dynamic system modeling to probe these processes in BRAF-mutant melanoma models and patient specimens. We uncover a hysteretic transition trajectory in response to oncogene inhibition and subsequent release, driven by two tightly coupled transcriptional waves that orchestrate genome-scale chromatin reconfiguration. Modeling of these waves suggests NF-κB/RelA-driven chromatin remodeling as the underlying mechanism of cell-state dedifferentiation, which we validate experimentally. We identify RelA-target genes epigenetically modulated to drive this process and define a quantitative epigenome gauge of melanoma cell-state plasticity that supports targeting epigenetic machineries to potentiate oncogene inhibition. Across additional cancer models, oxidative stress-mediated NF-κB/RelA activation emerges as a common driver of transitions into drug-tolerant persister states, revealing a central role for NF-κB axis in coupling oxidative stress to cancer progression. The mechanisms driving reversible dedifferentiation events towards a drug-tolerant persister (DTP) state remain to be explored. Here, multi-omics, information-theoretic approaches and dynamic systems modelling highlight the role of the oxidative-stress–mediated NF-κB/RelA axis in driving the transition towards DTP across multiple cancer types.

  PublisherOA PDFDOI

• Abstract LB-B005: No effect of the time-of-day infusion of adjuvant pembrolizumab in the outcomes of patients with resectable melanoma in the NCI/SWOG trial S1404

  Cancer Immunology Research · 2026-03-05

  article

  Abstract Background: Multiple reports have suggested that receiving immunotherapy infusions “earlier” in the day is associated with improved outcomes, including longer overall survival and lower toxicity rates. However, the definition of “early” varies between publications. Reports also fail to account for confounding factors (including distance to infusion center), are subject to survivor bias (analyzing post-baseline factors at baseline), and do not adjust p-values for multiple comparisons when evaluating multiple potential thresholds for early versus late time-of-day of infusion. Methods: We analyzed a previously reported multi-center clinical trial evaluating pembrolizumab as adjuvant therapy for patients with resectable high-risk melanoma. Standard statistical methodologies that account for potential biases were used to evaluate the association between time-of-day of infusion and clinical outcomes. Results: 628 participants received pembrolizumab and had time of first infusion recorded. Median age was 55 years, range 20-82. Odds of infusion before 11:00 hours increased by 32% over 12 months of therapy (p=0.013). Participants living further from their treating institution had later infusion times on average: odds of infusion before 11:00 decreased by 9% for each additional 50 miles (p=0.017). The optimal cut-point for first infusion time for OS was 15:48 with hazard ratio (HR)=1.40; changing the cut-point by 30 minutes earlier to 15:18 decreased HR to 0.98, indicating lack of robustness of the threshold. No significant association was identified between proportion of early infusions and outcomes in multivariable time-dependent Cox regression models. Conclusions: In this multi-center trial of adjuvant pembrolizumab for patients with high-risk melanoma, analyses that account for common sources of bias found no significant association between recurrence-free or overall survival and time-of-day of infusion. Clinical trial identification: NCT02506153 Funding: NIH/NCI grants U10CA18088, U10CA180819 Citation Format: Megan Othus, Thach-Giao Truong, Elad Sharon, Kari Kendra, Kenneth Grossman, Elizabeth Buchbinder, Nikhil Khushalani, Zeynep Eroglu, Sunandana Chandra, Gary Doolittle, John M. Kirkwood, Alexandra P. Ikeguchi1, Catalin Mihalcioiu, C. Lance Cowey, Sunil A. Reddy, Douglas B. Johnson, Matthew Taylor, Vernon K. Sondak, Antoni Ribas, Sapna P. Patel. No effect of the time-of-day infusion of adjuvant pembrolizumab in the outcomes of patients with resectable melanoma in the NCI/SWOG trial S1404 [abstract]. In: Proceedings of the AACR Immuno-Oncology Conference (AACR IO): Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2026 Feb 18-21; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2026;14(2 Suppl):Abstract nr LB-B005.

  PublisherDOI

• MONETTE: A Randomized Phase II Study of Ceralasertib plus Durvalumab or Ceralasertib Monotherapy in Patients with Advanced Melanoma Resistant to PD-(L)1 Inhibition

  Clinical Cancer Research · 2026-04-21

  articleOpen accessSenior author

  INTRODUCTION: Data suggest that ceralasertib, a potent and selective oral inhibitor of the ATR DNA damage response kinase, may overcome resistance to prior immunotherapy. METHODS: In this phase II study, patients with unresectable or metastatic melanoma of cutaneous, acral or mucosal subtype and confirmed progression during anti-PD-(L)1 therapy with or without anti-CTLA-4 were randomized 2:1 to ceralasertib 240 mg BID on days 1-7 then durvalumab 1500 mg IV on day 8, every 28 days or ceralasertib 240 mg BID on days 1-7, every 28 days. The primary endpoint was objective response rate (ORR). Key secondary endpoints included progression-free survival (PFS), overall survival (OS), and safety. Exploratory analyses of baseline (tumor and circulating) and on-treatment (circulating only) biomarkers were conducted. RESULTS: ORR was 9.3% (95% confidence interval [CI], 4.3-16.9) for ceralasertib plus durvalumab (below the prespecified minimum threshold) and 5.8% (95%CI, 1.2-15.9) for ceralasertib monotherapy; median PFS was 2.0 months (95%CI, 1.9-3.5) versus 1.9 months (95%CI, 1.9-3.1) (hazard ratio [HR], 0.80; 95%CI, 0.54-1.18); and median OS was 16.0 months (95%CI, 10.5-NC) versus 12.3 months (95%CI, 9.5-NC) (HR, 0.81; 95%CI, 0.49-1.37). Both regimens were well tolerated. Exploratory analyses indicated a possible link between higher baseline pre-treatment tumor CD8+ T cell counts and improved overall survival across both arms and suggested that ceralasertib treatment may induce transient, cyclical changes in circulating CD14+ monocytes and GDF-15 plasma levels. CONCLUSION: Both ceralasertib plus durvalumab and ceralasertib monotherapy demonstrated low response rates in anti-PD-(L)1-resistant advanced melanoma.

  PublisherOA PDFDOI

• SpaceBender: Denoising Spatial Transcriptomics Data to Enhance Biological Signals

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-23

  articleOpen access

  Abstract Spatial transcriptomics (ST) allows for the simultaneous profiling of cell phenotype (e.g. transcriptome) and physical position. Although ST data has brought about numerous new biological insights, it remains limited by noise, largely in the form of RNA diffusion. Here, we introduce SpaceBender which leverages spatial-specific information (e.g. spatial ambient RNA niches) to build upon single-cell denoising strategies. SpaceBender outperforms current ST denoising methods in simulations and in vivo chimeric tissues. Through case studies, we demonstrate how SpaceBender unveils hidden biological insights and increases the significance of said insights as evaluated by statistical testing. Finally, we reveal how SpaceBender may also be applied to subcellular resolution data where it removes off-target expression of neighboring cell type specific marker genes. In all, we present SpaceBender as an ST denoising method, freely available as an open-source package, that may enhance the insights the field may draw from various ST data types.

  PublisherOA PDFDOI

Recent grants

• NIH Grant U54CA199090

  NIH · $22.6M · 2021

• NIH Grant T32CA009297

  NIH · $5.2M · 2014

• NIH Grant P01CA168585

  NIH · $16.9M · 2019

• NIH Grant P01CA132681

  NIH · $28.7M · 2016

• Next Generation Cancer Immunotherapies to Defeat Melanoma

  NIH · $9.5M · 2015–2029

Frequent coauthors

• Georgina V. Long

  University of Sydney

  635 shared

• Bartosz Chmielowski

  425 shared

• Grant A. McArthur

  Victorian Comprehensive Cancer Centre

  414 shared

• Jeffrey A. Sosman

  Northwestern University

  411 shared

• Roger S. Lo

  411 shared

• Richard Kefford

  386 shared

• Begoña Comı́n-Anduix

  Parker Institute for Cancer Immunotherapy

  378 shared

• James S. Economou

  University of California, Los Angeles

  339 shared

Labs

• Antoni Ribas LaboratoryPI

Awards & honors

• President 2020, American Association for Cancer Research – A…