About

Caius Radu is a Professor in the Departments of Molecular and Medical Pharmacology and Surgery at the University of California Los Angeles (UCLA). He also serves as a Vice Chairman of the Department of Molecular and Medical Pharmacology and is Co-Director of the Cancer Molecular Imaging, Nanotechnology, and Theranostics Research Program (CMINT) at the Jonsson Comprehensive Cancer Center. Dr. Radu received his M.D. from the University of Medicine, Craiova, Romania, and completed his postdoctoral training in immunology and cancer biology at the University of Texas Southwestern Medical Center in Dallas, as well as at UCLA with Dr. Owen Witte. His research group aims to advance the understanding of fundamental biological processes at the interface between metabolic, signal transduction, and immune networks in cancer, leveraging this knowledge towards the development of new diagnostic and therapeutic approaches. Additional research focuses include studies of novel mechanisms regulating nucleotide metabolism in cancer, identification of targetable co-dependencies in pancreatic and prostate cancers, and the use of nucleoside imaging probes as non-invasive predictive biomarkers for treatment responses.

Research topics

• Medicine
• Cancer research
• Internal medicine
• Biology
• Immunology
• Oncology
• Cell biology
• Biochemistry

Selected publications

• Noninvasive in vivo deoxycytidine kinase (dCK)-PET identifies tumor-draining lymph nodes upon immune checkpoint inhibitor therapy

  npj Imaging · 2026-01-06

  articleOpen access

  Abstract Efficient application of immunotherapy necessitates advanced whole-body imaging techniques to monitor sites of immune cell activation. Deoxycytidine kinase (dCK), a key enzyme in the deoxynucleotide salvage pathway, is upregulated in proliferating immune cells and can be targeted by the radiotracers [ 18 F]FAC (preclinical) and [ 18 F]CFA (clinical), allowing for noninvasive monitoring of immune activation in lymphatic organs via positron emission tomography (PET). In this study, we aimed to assess the efficacy of [ 18 F]FAC in detecting immune activation upon immune checkpoint inhibitor therapy (CIT). In vitro, activated T cells and macrophages exhibited significantly higher [ 18 F]FAC uptake compared to their naïve counterparts. In vivo, preclinical [ 18 F]FAC-PET/MRI revealed a CIT-induced significant increase in [ 18 F]FAC uptake in tumor-draining lymph nodes (TDLNs) compared to contralateral lymph nodes, independent of tumor responsiveness. This phenomenon was absent in TDLNs of sham-treated experimental mice. Ex vivo cell sorting further confirmed elevated [ 18 F]FAC uptake in T cells from TDLNs following CIT. Consistently, [ 18 F]CFA-PET/CT imaging in metastatic melanoma patients demonstrated CIT-induced enhanced regional LN uptake. Together, these findings establish a strong correlation between CIT-induced immune activation and [ 18 F]FAC/[ 18 F]CFA uptake, underscoring the critical role of TDLNs in cancer immuotherapy. The radiotracers [ 18 F]FAC and [ 18 F]CFA provide valuable tools for noninvasive monitoring of immune cell activation, potentially unveiling tumor-microenvironment-related resistance mechanisms and advancing the utility of PET imaging in immunotherapy monitoring and patient stratification.

  PublisherOA PDFDOI

• Abstract 4374: A novel RNA-LNP immunotherapy platform to drive anti-tumor efficacy in solid tumors

  Cancer Research · 2026-04-03

  articleSenior author

  Abstract Nucleoside-modified RNA vaccines complexed in ionizable lipid nanoparticles (RNA-LNPs) constitute a promising immunotherapy platform for T cell-directed cancer vaccine development. A challenge in generating a proper anti-tumor CD8 T cell response with current RNA vaccine iterations remains, however, in providing optimal activation of antigen-presenting cells. Further, the presence of an immunologically cold tumor microenvironment (TME) presents an additional obstacle in designing an immunotherapeutic strategy to overcome such immunosuppression. To address these challenges, we hypothesized that an optimized RNA-LNP platform which couples an antigen-encoding RNA with a novel RNA-LNP innate immune activator will synergistically activate dendritic cells (DCs) by engaging multiple pattern recognition receptor (PRR) pathways to enhance cross-presentation and drive CD8 T cell responses. To this end, we immunized mice with our novel RNA-LNP platform and demonstrated that multiple DC subsets were activated at both local and distal secondary lymphoid organs respective to the injection site. The DCs from the immunized mice also activated and expanded antigen-specific T cells and resulted in memory T cell formation. Abrogation of these T cell responses in genetic knockout models demonstrate that such T cell activation is mediated by multiple PRRs. Systemic delivery of the novel innate immune activators activated DCs at draining lymph nodes local to the tumor site in an orthotopically implanted murine pancreatic cancer model and subsequently conferred tumor growth suppression. Collectively, these studies establish a new paradigm for RNA-LNP immunotherapy that integrates multifaceted PRR engagement to promote antigen-specific vaccination and facilitate T cell priming and reactivation at the tumor. Citation Format: Hailey R. Lee, Khalid Rashid, Tony Luu, Amanda Creech, Pu-Lin Teng, Emma Lieberman, Bridget Vause, Catherine Xie, Britney Trieu, Willy Hugo, Ting-Ting Wu, Norbert Pardi, Caius G. Radu. A novel RNA-LNP immunotherapy platform to drive anti-tumor efficacy in solid tumors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4374.

  PublisherDOI

• Synthetic lethality between RB-loss and E2F3 inhibition in small cell cancers targeted by pyrimidine synthesis blockade

  Proceedings of the National Academy of Sciences · 2026-03-20

  articleOpen access

  Small cell carcinoma is a highly lethal cancer variant often found with neuroendocrine (NE) features, as exemplified by small cell lung cancer and small cell NE prostate cancer (SCPC). A genome-wide CRISPR dependency screen using SCPC models generated through human prostate cell transformation identifies a requirement for the transcription factor E2F3. E2F3 dependency is linked to RB inactivation, a near universal occurrence across small cell cancers. The requirement for E2F3 is shared by RB-deficient cells originating from the prostate, lung, and adnexa. In RB-deficient cancer cells, E2F3 inhibition restrains cell cycle progression, proliferation, and tumor growth in vivo. Inhibition of de novo pyrimidine synthesis limits E2F3 expression and suppresses small cell carcinoma proliferation in culture. Directly or indirectly targeting E2F3 to leverage a pan-cancer synthetic lethality resulting from RB inactivation represents a potential treatment strategy.

  PublisherDOI

• Neoadjuvant modified FOLFIRINOX plus nivolumab in borderline-resectable pancreatic ductal adenocarcinoma: a pilot phase 1 trial

  Nature Communications · 2026-01-31

  articleOpen access

  Chemotherapy and immune checkpoint inhibitor combinations have failed to improve survival in pancreatic ductal adenocarcinoma (PDAC), except in rare microsatellite instability-high cases; most studies focused on advanced disease. Here, we present clinical and translational results from a single-arm, prospective phase 1b/2 investigator-initiated study (NCT03970252) evaluating neoadjuvant modified FOLFIRINOX (mFFX) plus nivolumab in patients with borderline-resectable PDAC. The co-primary endpoints of safety and pathological response rate were met, with 22 (79%) of 28 patients proceeding to surgery and no grade ≥3 immune-related adverse events. All grade 3-4 treatment-related adverse events were chemotherapy-related. By CAP scoring, 9% of patients achieved a complete pathologic response, 9% a near-complete response, and 72% a partial response. Secondary endpoints included CA 19-9 response rate, R0 resection rate, objective response rate, and disease-free survival (median 19.7 months, 95% CI: 7.3-30.8). In post-hoc analyses, median progression-free survival was 26 months (95% CI: 14.7-34.3), and median overall survival was 38 months (95% CI: 27.9-not reached). Exploratory gene expression, immunohistochemistry and spatial transcriptomics showed increased intratumoral plasma cells and CD8 T cells in treated patients versus mFFX-only controls, and lymphoid aggregates with high plasma-cell-to-B cell ratios enriched for terminally exhausted CD8 T cells with fewer progenitor exhausted CD8 T cells and central memory CD4 T cells.

  PublisherOA PDFDOI

• Author Correction: Regulation of nucleotide metabolism by mutant p53 contributes to its gain-of-function activities

  Nature Communications · 2026-02-03

  articleOpen access
  PublisherOA PDFDOI

• Abstract 6449: Adenosine blockade combined with FOLFIRINOX chemotherapy enhances T follicular helper cell function in pancreatic adenocarcinoma draining lymph nodes from mice and humans

  Cancer Research · 2026-04-03

  article

  Abstract Over 90% of all pancreatic cancer cases are pancreatic ductal adenocarcinoma (PDAC), an aggressive disease with poor prognosis and limited treatment options. Chemotherapy and immunotherapy efficacy are both limited by the immunosuppressive PDAC tumor microenvironment (TME). Treatment-related tumor cell death leads to accumulation of extracellular adenosine, a potent immunosuppressive metabolite in the PDAC TME; accordingly, we investigated the effects of blocking adenosine during chemotherapy treatment. In an orthotopic murine model of PDAC, CD73 - the primary enzyme responsible for extracellular adenosine - inhibition in combination with FOLFIRINOX reduced tumor size by 57% (P=0.04) and significantly increased survival compared to treatment with FOLFIRINOX alone. FOLFIRINOX+CD73i significantly decreased suppressive SPP1+ tumor-associated macrophages, increased Type I and Type II interferon signaling of multiple cell types in the TME, and was CD4+ and CD8+ T cell dependent. To track antigen-specific CD4+ T cells, we engineered expression of an MHC-II restricted epitope in orthotopically implanted tumor cells and found that FOLFIRINOX+CD73i treatment increased follicular helper T (Tfh) cells in tumor-draining lymph nodes but that these cells were not enriched for tetramer-positive, tumor antigen-specific cells. In contrast, Treg cells in the TME were enriched for tetramer-positive cells suggesting that CD73i may drive antigen-reactive T cells toward a suppressor phenotype. Targeting activated T cells by adding anti-CCR8 to FOLFIRINOX+CD73i significantly decreased tumor masses compared to FOLFIRINOX+CD73i alone (P=0.02). To investigate the effect of CD73i on adaptive immune responses in PDAC patients, we performed Xenium image-based spatial transcriptomics on 53 tumor-draining lymph nodes from patients treated with neoadjuvant FOLFIRINOX+anti-PD-1+CD73i, FOLFIRINOX+anti-PD-1, FOLFIRINOX alone, or untreated. In line with our mouse model, we found a significant CD73i-dependent increase in intra-follicular antigen-experienced B cell density (P=0.037) with a concomitant increase in intra-follicular CD8+ T cell density (P<0.001), which could be explained by enhanced function of Tfh cells. Accordingly, we found enrichment in IL-21 expressing Tfh cells in tumors treated with FOLFIRINOX+anti-PD-1+CD73i compared to FOLFIRINOX+anti-PD-1. These results indicate that CD73i may drive distinct immune remodeling in PDAC, boosting Tfh cell function in draining lymph nodes but favoring antigen-specific Treg enrichment in the tumor microenvironment. Citation Format: Michael K. Srienc, Serena Zheng, Jason Link, Alykhan Premji, McKensie Hammons, Shineui Kim, Evan Abt, Caius G. Radu, David W. Dawson, Zev A. Wainberg, Timothy R. Donahue. Adenosine blockade combined with FOLFIRINOX chemotherapy enhances T follicular helper cell function in pancreatic adenocarcinoma draining lymph nodes from mice and humans [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 6449.

  PublisherDOI

• Tailoring the adjuvanticity of lipid nanoparticles by PEG lipid ratio and phospholipid modifications

  Nature Nanotechnology · 2025-06-23 · 33 citations

  articleOpen access
  PublisherOA PDFDOI

• Supplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling

  2025-11-25

  articleOpen access

  <p>Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.</p>

  PublisherOA PDFDOI

• Supplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling

  2025-11-25

  articleOpen access

  <p>Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental and IFNAR1-KO cells exposed to ± 1 µM diABZI ± 100 nM trametinib for 24 h (C)Immunoblot analysis of the effects of ± 100 U/ml exogenous IFN ± 1 µM diABZI for 24 h.</p>

  PublisherOA PDFDOI

• Supplementary Figure S4 from Efficacy of a Small-Molecule Inhibitor of Kras<sup>G12D</sup> in Immunocompetent Models of Pancreatic Cancer

  2025-12-10

  articleOpen access

  <p>MRTX1133 elicits changes in the tumor stroma and vasculature</p>

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01CA160770

  NIH · $1.8M · 2014

• In Vivo Pharmacodynamics of RNAi-based Cancer Therapies

  NIH · $24.3M · 2016

• Cancer Molecular Imaging, Nanotechnology, and Theranostics (CMINT)

  NIH · $65.6M · 1996–2030

• PET Imaging-guided Personalized Therapy in Pancreatic Cancer

  NIH · $2.8M · 2014–2020

• NIH Grant P50CA086306

  NIH · $20.5M · 2015

Frequent coauthors

• Johannes Czernin

  164 shared

• Owen N. Witte

  161 shared

• Evan R. Abt

  158 shared

• Thuc Le

  Medizinische Hochschule Hannover

  152 shared

• Timothy R. Donahue

  115 shared

• Robert Damoiseaux

  99 shared

• Antoni Ribas

  Parker Institute for Cancer Immunotherapy

  95 shared

• James R. Heath

  Institute for Systems Biology

  64 shared

Education

• Postdoctoral Fellow, Cancer Immunobiology Center and Center for Immunology

  UT Southwestern

  2021

• Postdoctoral Fellow, MIMG

  University of California at Los Angeles

  2006

• MD

  University of Medicine and Pharmacy of Craiova

  1993

• Bachelor of Science

  National College Fratii Buzesti

  1987