About

Dr. Johannes Czernin received his MD degree from the University of Vienna in 1983. He was board certified in Internal Medicine in Austria in 1989 and in Nuclear Medicine in the USA in 1996. In 1996, he was named Director of Nuclear Medicine at the David Geffen School of Medicine at UCLA and currently serves as the Chief of the Ahmanson Translational Theranostics Division at UCLA. The division includes the Nuclear Medicine Clinic, a clinical imaging research program, a drug and probe development program with a strong underpinning in tumor biology, and a preclinical imaging center. It collaborates within the department of molecular and medical pharmacology and across several other departments including medicine, surgery, radiology, neurology, and pathology. Dr. Czernin has over 25 years of experience in preclinical molecular imaging and molecular radiotherapy. He is currently the Editor-in-Chief of the Journal of Nuclear Medicine and is a past president of the Academy of Molecular Imaging. He has published more than 280 peer-reviewed research papers.

Research topics

• Medicine
• Internal medicine
• Nuclear medicine
• Oncology
• Pathology
• Computer Science
• Cancer research
• Urology
• Radiology
• Computer Security
• Immunology
• Surgery
• Political Science
• Medical emergency
• Medical physics
• Intensive care medicine
• Family medicine
• Biology
• Law
• Virology
• Emergency medicine

Selected publications

• From Physical Therapy to Pioneering Molecular Imaging Instrumentation

  Journal of Nuclear Medicine · 2026-03-26

  articleSenior author

  ![Figure][1]</img> Katherine W. Ferrara, PhD Dr. Katherine W. Ferrara is a professor of radiology at Stanford University and the division chief for the Molecular Imaging Program at Stanford (MIPS). Before her appointment at Stanford University, she served as the founding chair of the Biomedical

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• Abstract B001: Double targeted therapy PSCA-CAR-T cells and PSMA-radioligand in metastatic castration-resistant prostate cancer

  Clinical Cancer Research · 2025-01-26 · 1 citations

  article

  Abstract Targeted radioligand therapy (PSMA-RLT) extends survival in advanced castration-resistant prostate cancer (CRPC) (Sartor et al., 2021), yet half of patients experiences limited responses or relapse with additional metastases (Stuparu et al., 2020). Given that metastatic CRPC has a tumor environment lacking immune infiltration and resisting immune checkpoint therapies, combination strategies that actively bring immune cells into the tumor are urgently needed (Choudhury et al., 2024). Prostate stem cell antigen (PSCA) is another promising target, as it is frequently overexpressed in advanced CRPC. PSCA-CAR-T cells, engineered to specifically attack PSCA-expressing tumors, may complement PSMA-RLT by overcoming immune resistance (Dorff et al., 2024; Murad et al., 2021). This study explores the therapeutic potential of combining PSMA-RLT with PSCA-CAR-T cells to strengthen immune response and increase response rates and survival. For this reasons, PC3-PIP human metastatic prostate cancer cells expressing PSMA were transfected to express human PSCA. PSMA and PSCA expression was confirmed by flow cytometry. Double positive PSMA-PSCA cells were inoculated by intracardiac injection in NSG mice under ultrasound guidance. Tumor progression was followed up twice a week by bioluminescence imaging. Mice were randomized before treatment into 5 groups: (1) Control NT (2) 225Ac-PSMA-617 (15 kBq) alone (3) CAR-T (0.2 x 106 cells) alone (4) Combo 225Ac-PSMA-617 (15 kBq) + CAR-T (0.2 x 106 cells) (day 4 post-RLT) (5) Combo 225Ac-PSMA-617 (15 kBq) + CAR-T (0.2 x 106 cells) (day 6 post-RLT). 4 mice per group were used to determine blood toxicity of RLT and 8 mice in each group were followed up until the end point for efficacy study. No blood toxicity related to RLT was observed in treated mice. Compared to control group, the Combo 225Ac-PSMA-617 and PSCA-CAR-T demonstrated a synergistic effect with a significant delay in tumor growth. Comparison between 68Ga-PSMA-11 PET and bioluminescence imaging showed heterogenous localization in 3 mice randomized to Combo groups and CAR-T alone group. In conclusion, our study shows promising results from combining PSMA-RLT with PSCA-CAR-T cell therapy. In a dual prostate cancer expressing in vivo model (PC3-PIP PSMA-PSCA), we observed a delay in tumor growth. However, the increase of survival rates in combo groups compared to CAR-T alone was limited. Additional studies are required to improve overall survival. Thus, we plan to extend our study to test the combination of PSCA-CAR-T with PluvictoTM, a recent FDA approved theranostics agent for metastatic CRPC (Hennrich &amp; Eder, 2022). Moreover, we will modify the expression of PSCA to mimic the heterogeneity expression observed in patients, to validate the performance of the combination. Citation Format: Iveta Fajnorova, Pauline Jeanjean, Ines Camille Azrour, Ava Fakharpour, Venna Jiangyue Liu, Johannes Czernin, Caius Radu, Saul Priceman, Christine Mona. Double targeted therapy PSCA-CAR-T cells and PSMA-radioligand in metastatic castration-resistant prostate cancer. [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Translating Targeted Therapies in Combination with Radiotherapy; 2025 Jan 26-29; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(2_Suppl):Abstract nr B001.

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• Abstract P012: PSMA-RLT and targeting the cGAS-STING pathway as a combination approach for Prostate Cancer

  Clinical Cancer Research · 2025-01-26

  article

  Abstract The VISION trial showed that 177Lu-PSMA-617 radioligand therapy (RLT) effectively reduced PSA levels and improved survival in patients with late-stage prostate cancer1. However, there is still a need to identify strategies to enhance and sustain RLT efficacy. Alpha therapy and combination of immunotherapy and radiation are emerging strategies. Herein, we focused on strategies to amplify the immune system activation to intensify the effects of PSMA-RLT in prostate cancer by combining 225Ac-PSMA-617 RLT with a STING agonist (diABZI). We compared the efficacy of alpha RLT in mice bearing STING-proficient or STING-deficient PC cell line (RM1-PGLS or Myc-CaP) alone or in combination with a STING agonist. Furthermore, we assessed the efficacy of RLT in STING knockout (Sting -/-) mice injected with RM1-PGLS. Method: Male C57BL/6 wt or STING-deficient or FVB mice were subcutaneously injected with 0.1 × 10⁶ RM1-PGLS cells in a 100 µl mixture of PBS and Matrigel (1:1) or 2 × 10⁶ MycCap cells. PSMA expression was assessed in vivo using PET/CT imaging 1h after intravenous injection of 68Ga-PSMA-617 to validate target expression prior to treatment. Once tumors reached 100 mm³, animals were treated intravenously with 30 kBq of 225Ac-PSMA. C57BL/6 mice bearing RM1 PGLS tumors and FVB mice bearing MycCap were treated with RLT alone or in combination with diABZI (1.5 mg/kg), 24h post RLT. Tumor growth and therapeutic efficacy were monitored weekly by CT. Results: In an immunocompetent syngeneic model (C57BL/6 mice bearing RM1-PGLS tumors) we observed a synergistic effect of STING agonist and RLT. At 28 days post-treatment, survival rates were: 0% for NT, 66% for RLT alone, 70% DiABZI and 89% for the combination. Contrastingly, in the MycCap model, the combination of RLT and STING agonist did not improve survival compared to the control group with 0% survival at 22 days. Same survival rate was observed with the STING agonist. Only the RLT group showed 30% of survival at day 22.In the STING-deficient host model, we observed 75% tumor-free mice (6/8). At day 22, the median survival was 50% for the control group compared to 100% for the RLT group. Rechallenged RLT-treated mice did not regrow tumors for more than a year after rechallenging. Conclusion and discussion: STING agonist and RLT synergize in certain models of PCa.Based on our results, STING proficiency in the tumor cells seems to be a critical determinant for RLT-response. Our data in the STING -/- mice suggest that host STING could have deleterious effects. We hypothesize that the acute inflammation triggered by STING activation may stimulate the accumulation of MDSCs (myeloid-derived suppressor cells), which are associated with immune suppression which may restrain the efficacy of RLT. Given this, our next strategy will focus on preventing MDSC activation to maintain the beneficial immune activation within the tumor microenvironment. The dual role of STING in both immune recruitment and activation, as well as in immunosuppression, makes it a complex mechanism that requires further exploration. Citation Format: Beatrice Louis, Marco Taddio, Clara Diaz Garcia Prada, Mathis Richard, Rachel Dove, Khalid Rashid, Evan Abt, Ethan Rosser, Thuc Le, Katharina Lueckerath, Caius Radu, Johannes Czernin, Christine Mona.PSMA-RLT and targeting the cGAS-STING pathway as a combination approach for Prostate Cancer.[abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Translating Targeted Therapies in Combination with Radiotherapy; 2025 Jan 26-29; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(2_Suppl):Abstract nr P012

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• Comparing progression following systemic and tumor-directed therapy for <i>de novo</i> versus recurrent PSMA PET–defined oligo-M1 prostate cancer: A pooled analysis of SOLAR and SATURN clinical trials.

  Journal of Clinical Oncology · 2025-02-10

  article

  64 Background: Therapeutic strategies for oligometastatic castration sensitive prostate cancer (omCSPC) combining treatment of the primary and metastases with short-term intensified systemic therapy aim to improve survival and local control while minimizing toxicity from indefinite systemic therapy. This post-hoc analysis of the SOLAR (NCT03298087) and SATURN (NCT03902951) trials, which evaluated systemic and tumor-directed therapy in PSMA-PET defined oligo-M1 (≤5 metastases) de novo and recurrent omCSPC, respectively, aims to draw inferences on biology and oncologic outcome. Methods: All patients were treated with 6 months of systemic therapy: leuprolide, abiraterone acetate with prednisone, and apalutamide in conjunction with SBRT to oligometastatic sites. SOLAR patients were treatment naïve and underwent either radical prostatectomy (RP) with lymph node dissection followed by post-operative radiotherapy for high-risk features, or definitive radiotherapy (dRT). SATURN patients all had recurrent disease after RP with or without postoperative radiotherapy and may have also had prior hormone or metastasis-directed therapy. The primary endpoint (response rate) was the percentage of patients with an undetectable PSA (&lt;0.05 ng/mL) for post-RP patients, or a PSA &lt;2 ng/mL for post-dRT patients, six months after recovery of testosterone to &gt;150 ng/dl. Secondary endpoints included progression-free survival (PFS) and eugonadal PFS starting from time of testosterone recovery. Kaplan-Meier assessed differences in time-to-event endpoints from initiation of systemic therapy. Fischer’s Exact Test compared proportional outcomes. Results: Analysis included data from 24 SOLAR and 26 SATURN patients. Overall, median follow-up was 32 months (interquartile range 28.25-36.75 months). Response rates were higher for de novo versus oligorecurrent patients (20/24 [83%] versus 13/26 [50%], p=0.018). PFS and eugonadal PFS were also significantly longer (median not reached versus 17 months and median not reached versus 13 months, respectively, p&lt;0.05). PFS was shorter for oligorecurrent patients with prior exposure to hormone therapy (median 10 months versus not reached, p&lt;0.05). There was no PFS difference comparing patients treated in the de novo setting versus the recurrent setting who were naive to hormonal therapy (p=0.23). Conclusions: Patients with recurrent omCSPC PSMA-PET defined M1 disease had a worse response rate and shorter PFS following intensified systemic and metastasis-directed SBRT than those with de novo omCSPC. The difference was driven by recurrent patients with prior exposure to hormonal therapy, suggesting a continuum of treatment resistances over repeated courses of hormonal therapy. The majority of patients with de novo omCSPC remain in remission after gonadal recovery. Clinical trial information: NCT03298087 , NCT03902951 .

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• Advancing Tomorrow’s Cancer Medicines

  Journal of Nuclear Medicine · 2025-01-23

  articleOpen accessSenior author

  Ken Herrmann, MD, MBA, from the Universitätsklinikum Essen (Germany), and Johannes Czernin, MD, from the David Geffen School of Medicine at the UCLA, talked with Jacob S. Van Naarden, executive vice president and president of Lilly Oncology for Eli Lilly and Company (Indianapolis, IN). In this role

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• From Scientist to Analyst to Strategist

  Journal of Nuclear Medicine · 2025-01-16

  articleOpen accessSenior author

  Ken Herrmann, MD, MBA, from the Universitätsklinikum Essen (Germany), and Johannes Czernin, MD, from the David Geffen School of Medicine at UCLA, talked with Aharon (Ronny) Gal, PhD, about his career across a range of scientific, analytic, consulting, and leadership positions. Dr. Gal is Chief

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• Early changes of PSMA PET expression after initiation of androgen receptor signaling inhibitors in CRPC: an international multicenter retrospective study

  European Journal of Nuclear Medicine and Molecular Imaging · 2025-03-26 · 6 citations

  article
  PublisherDOI

• Clinical Impact of Changes in Tumor Uptake and Volume on PSMA PET/CT During [ ¹⁷⁷ Lu]Lu-PSMA Therapy in Metastatic Castration-Resistant Prostate Cancer

  Journal of Nuclear Medicine · 2025-10-30

  article

  Although tumor volume and new lesions (NLs) have been investigated previously as measures of response, the clinical impact of changes in tumor uptake on prostate-specific membrane antigen (PSMA) PET remains largely unknown. <b>Methods:</b> This multicenter retrospective study investigated the clinical impact of changes in tumor uptake and volume on PSMA PET during [¹⁷⁷Lu]Lu-PSMA in metastatic castration-resistant prostate cancer (mCRPC). The primary outcomes were the associations of changes in SUV_max (ΔSUV_max) and SUV_mean(ΔSUV_mean), changes in total tumor volume (ΔTTV), and occurrence of NLs with prostate-specific antigen (PSA) progression-free survival (PSA-PFS) and overall survival (OS). The study included patients with mCRPC who received [¹⁷⁷Lu]Lu-PSMA between 2014 and 2019. PSMA PET/CT was performed at baseline and after 2 cycles of therapy. Whole-body analyses (SUV_max, SUV_mean, TTV, and NLs) were performed and calculated using qPSMA software. <b>Results:</b> In total, 124 patients with mCRPC (median age, 73 y; interquartile range, 67–76 y) were included in the study. Whole-body ΔTTV and the occurrence of NLs were significantly associated with shorter PSA-PFS (hazard ratio [HR], 5.7; 95% CI, 3.59–9.06; and HR, 1.6; 95% CI, 1.4–1.8; <i>P</i> &lt; 0.0001) and with OS (HR, 2.3; 95% CI, 1.61–3.43; and HR, 1.3; 95% CI, 1.1–1.4; <i>P</i> &lt; 0.001). Patient-based analysis showed that ΔSUV_max and ΔSUV_mean were not associated with outcome (HR, 1.00; 95% CI, 0.99–1.00; <i>P</i> = 0.30; and HR, 0.90; 95% CI, 0.99–1.00; <i>P</i> = 0.11). Region-based analysis found that only ΔSUV_max in visceral lesions was significantly associated with PSA-PFS (<i>P</i> = 0.007) but not with OS. <b>Conclusion:</b> Only ΔTTV and the occurrence of NLs provided significant prognostic value and should be considered when evaluating treatment response to [¹⁷⁷Lu]Lu-PSMA therapy.

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• A comparative study of preclinical and clinical molecular imaging response to EGFR inhibition using osimertinib in glioblastoma

  Neuro-Oncology Advances · 2025-01-01 · 1 citations

  articleOpen access

  Abstract Background To demonstrate the potential value of 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) as a rapid, non-invasive metabolic imaging surrogate for pharmacological modulation of EGFR signaling in EGFR-driven GBM, we synchronously conducted a preclinical imaging study using patient-derived orthotopic xenograft (PDOX) models and validated it in a phase II molecular imaging study in recurrent GBM (rGBM) patients using osimertinib. Methods A GBM PDOX mouse model study was performed concurrently with an open-label, single-arm, single-center, phase II study of osimertinib (NCT03732352) that enrolled 12 patients with rGBM with EGFR alterations. Patients received osimertinib daily and 3 18F-FDG PET scans: two 24 h apart prior to dosing, and one 48 h after dosing. Results GBM PDOX models suggest osimertinib has limited impact on both 18F-FDG uptake (+ 9.8%–+25.9%) and survival (+ 15.5%; P = .01), which may be explained by insufficient exposure in the brain (Kpuu: 0.30) required to robustly inhibit the EGFR alterations found in GBM. Treatment with osimertinib had subtle, but measurable decreases in the linear rate of change of 18F-FDG nSUV growth rate averaging −4.5% per day (P = .01) and change in 18F-FDG uptake was correlated with change in tumor growth rate (R2 = 0.4719, P = .0195). No metabolic (PERCIST) or radiographic (RANO) responses were seen, and no improvements in PFS or OS were observed. Conclusions This study demonstrated the feasibility of using FDG PET as a clinically reliable imaging biomarker for assessing EGFR inhibition in GBM, while revealing osimertinib’s limited impact on both metabolic activity and tumor growth in GBM, findings that were concordant between preclinical and clinical observations.

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• Study protocol: Phase 2 trial of re-treatment with 177Lu-PSMA-617 molecular radiotherapy for metastatic castration resistant prostate cancer (RE-LuPSMA trial).

  Journal of Clinical Oncology · 2025-05-28

  article

  TPS5110 Background: The phase III VISION trial demonstrated that 177 Lu-PSMA-617 radioligand therapy (RLT) improved overall survival (OS) in patients with metastatic castration-resistant prostate cancer (mCRPC) who previously received taxane-based chemotherapy and at least one androgen receptor pathway inhibitor (ARPI). As a result, 177 Lu-PSMA-617 therapy has been approved in this patient population by the U.S. Food and Drug Administration for up to six cycles (7.4 GBq per cycle) every 6 weeks. Unfortunately, this treatment is not curative and patients relapse even after initially favorable responses. When this occurs, patients have limited treatment options given they have had prior chemotherapy and ARPI regimens. Re-administration of 177 Lu-PSMA-617 in patients who previously benefited from therapy and had limited toxicity seems to be a promising option. Small retrospective studies have reported favorable outcomes. Further prospective data with larger sample sizes are needed to confirm these findings. Methods: RE-LuPSMA is an investigator-initiated, single-arm, single-center, open-label, phase 2 clinical trial (NCT06288113). This study plans to enroll 40 patients with progressive mCRPC who previously completed 4-6 cycles of 177 Lu-PSMA-617 therapy with a favorable response. Favorable response is defined as a prostate-specific antigen (PSA) decline ≥50% during the first regimen. Progression following the first regimen is defined using imaging or PSA (two consecutive PSA increases ≥3 weeks apart). Patients who received another line of prostate cancer therapy within two months of completing the first regimen of 177 Lu-PSMA-617 are excluded. Patients must meet PSMA PET/CT VISION criteria. PSMA PET/CT must have been completed within 8 weeks of the planned first cycle of re-challenge therapy. Upon enrollment, participants will receive up to 6 additional cycles of 177 Lu-PSMA-617 (7.4GBq every 6 weeks). Patients will follow-up every 6 months until 2 years from the end of re-challenge therapy. The primary endpoint is 12-month OS measured from the start of re-challenge therapy. The study will have 80% power to detect a difference between the null hypothesis of 50% and the study hypothesis of 71%. Secondary endpoints include adverse event rates, PSA response rates (proportion of patients with a PSA decrease of ≥50%), biochemical progression-free survival (time until PSA level increases 25% and 2 ng/mL above the nadir), radiographic progression-free survival, and health-related quality of life changes (measured using Functional Assessment of Cancer Therapy - Radionuclide Therapy [FACT-RNT] and Brief Pain Inventory [Short Form]). Enrollment has started with a planned study duration of 4 years of which subject accrual occurs in the first 12 months. Clinical trial information: NCT06288113 .

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Recent grants

• NIH Grant R01CA160770

  NIH · $1.8M · 2014

• NIH Grant P01CA132681

  NIH · $28.7M · 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

• Jérémie Calais

  Molecular Theranostics (United States)

  245 shared

• Caius G. Radu

  University of the Witwatersrand

  164 shared

• Ken Herrmann

  143 shared

• Wolfgang P. Fendler

  University of Duisburg-Essen

  137 shared

• Matthias Eiber

  109 shared

• Michael E. Phelps

  104 shared

• Martin Allen-Auerbach

  Molecular Theranostics (United States)

  89 shared

• Matthew B. Rettig

  72 shared

Awards & honors

• Past president of the Academy of Molecular Imaging
• Editor-in-Chief of the Journal of Nuclear Medicine