About

Christine Mona, PhD, is an Assistant Adjunct Professor at UCLA in the Department of Molecular and Medical Pharmacology. She received her Ph.D. in Pharmacology in 2016 from Université de Sherbrooke. After completing her doctoral studies, she joined UCLA in 2016 as a Post-Doctoral Research Associate in Nuclear Medicine within the research group of Professor Johannes Czernin. In early 2020, Dr. Mona was promoted to Adjunct Assistant Professor at the Ahmanson Translational Theranostic Division (ATTD). Her research is focused on translational science at the intersection of Chemistry, Pharmacology, and Nuclear Medicine, contributing to the advancement of nuclear medicine research and its applications.

Research topics

• Medicine
• Internal medicine
• Cancer research
• Immunology
• Oncology
• Radiology
• Biology
• Nuclear medicine
• Pathology

Selected publications

• Metformin effects on renal function in mCRPC during PSMA radiopharmaceutical therapy (RPT): A retrospective analysis.

  Journal of Clinical Oncology · 2026-03-01

  article

  203 Background: Preclinical research indicates that metformin may mitigate renal accumulation of lutetium-177-labeled PSMA radioligands in metastatic castration-resistant prostate cancer (mCRPC) by inhibiting organic cation transporters in the kidneys, thereby offering potential protection against radiopharmaceutical-induced nephrotoxicity. Methods: In this IRB-exempt retrospective analysis, 181 mCRPC patients treated with PSMA-RPT were identified from UCLA electronic health record database (2016–2025) and stratified by metformin exposure. Data on their age at treatment onset, hypertension diagnosis, treatment cycles, estimated glomerular filtration rate (eGFR), serum creatinine (Cr), and prostate-specific antigen (PSA) were collected. The study protocol was reviewed by the Internal Scientific Peer Review Committee. Inclusion required documented baseline and post-treatment eGFR and Cr. Primary endpoints were absolute changes in eGFR (|ΔeGFR|) and Cr (|ΔCr|) from baseline to first post-treatment assessment. Missing data was addressed using complete-case analysis. Two-sided t-tests were performed at α = 0.05. Multivariate analysis of variance (MANOVA) was conducted to evaluate ΔeGFR and ΔCr from metformin exposure, with age, hypertension, treatment cycles, and PSA as predictors. Results: Metformin-exposed patients (n=23), compared to controls (n=158), exhibited better baseline renal function (eGFR 89.6 ± 11.0 vs 81.7 ± 18.8 mL/min/1.73 m², p =0.048; creatinine 0.82 ± 0.18 vs 0.98 ± 0.30 mg/dL, p =0.009) despite significantly higher hypertension prevalence (47.8% vs 23.4%, p=0.019). In univariate analyses of posttreatment changes, metformin exposure was significantly associated with lower eGFR decline (-2.2 ± 16.8 vs -9.2 ± 27.1 mL/min/1.73 m², p =0.048) and creatinine increase (0.003 ± 0.20 vs 0.124 ± 0.32 mg/dL, p =0.042). However, metformin showed no significant multivariate effect on posttreatment ΔeGFR and ΔCr (Wilks’ λ = 0.944, F (2,92) = 2.72, p = 0.071). Conclusions: Renal preservation observed in the unadjusted analysis was likely attributable to confounding factors such as indication bias. Future research will address this limitation through a randomized, placebo-controlled trial with standardized metformin dosing, serial assessment of renal biomarkers, and quantitative PET SUV with predefined imaging outcomes. Variable Metformin (n = 23) Control (n = 158) p -value Age (years), mean ± SD 74.4 ± 8.1 72.9 ± 9.2 0.45 Hypertension (%) 47.8 23.4 0.019* Baseline eGFR (mL/min/1.73 m²), mean ± SD 89.6 ± 11.0 81.7 ± 18.8 0.048* Baseline serum creatinine (mg/dL), mean ± SD 0.82 ± 0.18 0.98 ± 0.30 0.009* Baseline PSA (ng/mL), mean ± SD 189.3 ± 358.7 266.5 ± 603.3 0.55 Treatment cycles, mean ± SD 3.7 ± 2.2 3.6 ± 2.1 0.85 Posttreatment ΔeGFR (mL/min/1.73 m²), mean ± SD -2.2 ± 16.8 -9.2 ± 27.1 0.048* Posttreatment ΔCr (mg/dL), mean ± SD 0.003 ± 0.20 0.124 ± 0.32 0.042* * p <0.05.

  PublisherDOI

• From Physical Therapy to Pioneering Molecular Imaging Instrumentation

  Journal of Nuclear Medicine · 2026-03-26

  article

  ![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

  PublisherDOI

• FAP Expression in Renal Tumors Assessed by [ ⁶⁸ Ga]Ga-FAPI-46 PET Imaging and FAP Immunohistochemistry: A Case Series of Six Patients from the Prospective Exploratory Trial NCT04147494

  Journal of Nuclear Medicine · 2025-10-16

  articleOpen access

  Fibroblast activation protein (FAP) has been proposed as a pan-tumor target for PET imaging using FAP-targeted tracers. Here, we explore the potential value of FAP PET in renal tumors. <b>Methods:</b> Six patients with renal tumors (4 with clear cell renal cell carcinoma, 1 with papillary renal cell carcinoma, and 1 with renal oncocytoma) who were included in a prospective imaging study (NCT04147494) underwent [⁶⁸Ga]Ga-FAPI-46 PET before nephrectomy. FAP PET radiotracer uptake and FAP expression by immunohistochemistry were assessed in the tumors and surrounding renal parenchyma. <b>Results:</b> Tumoral FAP radiotracer uptake was highest in clear cell renal cell carcinoma (median SUV_max, 3.1; range, 2.5–5.3), followed by renal oncocytoma (SUV_max, 1.9) and papillary renal cell carcinoma (SUV_max, 1.1). The FAP PET signal strongly correlated with FAP expression by immunohistochemistry (SUV_max; <i>r</i> = 0.93; <i>P</i> = 0.007). <b>Conclusion:</b> FAP expression in different renal tumors, including renal cell carcinoma, was lower when compared with cancers with known FAP expression, such as sarcoma. Although our data do not favor FAP-based theranostic approaches in renal cell carcinoma, studies in larger cohorts are warranted for conclusive evidence.

  PublisherOA PDFDOI

• Application of a Hand-Held Czt-Based Gamma Camera for Pre-Clinical Intratherapeutic Imaging of ¹⁷⁷ Lu, ²²⁵ Ac, and ²¹² Pb

  2025-11-01

  article

  A small, portable gamma camera has been acquired for fast, easy, and quantitative imaging in preclinical radionuclide therapy studies. The camera uses a <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">$39 \times 39 \times 5 ~\text{mm}^{3}$</tex> Cadmium Zinc Telluride semiconductor crystal to produce <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">$16 \times 16$</tex>-pixel images and can be equipped with a medium-energy high-resolution collimator, two low-energy collimators (high-sensitivity or high-resolution), or a pinhole collimator. The performance of the camera was assessed for imaging of the therapeutic radionuclides <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">177</sup>Lu, <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">225</sup> Ac, and <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">212</sup> Pb using phantom and in-vivo studies. All collimators were used for <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">177</sup>Lu, while imaging of <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">225</sup> Ac and <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">212</sup> Pb utilized only the medium-energy collimator and the pinhole collimator due to the abundance of high-energy photons. A mouse-like phantom was manufactured through 3D printing with fillable cavities for the liver and a subcutaneous tumor.

  PublisherDOI

• A neurotensin receptor type 1-derived pepducin acts as a biased allosteric modulator to regulate target receptor function

  Acta Pharmaceutica Sinica B · 2025-12-31

  articleOpen access

  Pepducins are synthetic membrane-tethered lipopeptides designed to allosterically modulate G protein-coupled receptor (GPCR) signaling. Here, we characterize a series of pepducins targeting the neurotensin receptor type 1 (NTSR1), revealing their complex and multifaceted modulation properties. Using BRET-based biosensors, we show that PP-001, a pepducin derived from NTSR1’s first intracellular loop, preferentially activates G protein over β -arrestin signaling while inhibiting NT binding, NT-induced β -arrestin recruitment, and NTSR1 internalization, thereby acting as biased allosteric agonist and negative allosteric modulator. PP-001 also promotes the formation of both homo- and heteromeric multi-receptor complexes. In vivo , PP-001 elicits potent, sustained hypotensive effects, reversible by the NTSR1 antagonist SR48692. Although the precise mechanism of pepducin-receptor interaction remains unclear, we identify a critical N-terminal RKK motif for PP-001’s biological activity. Finally, thermodenaturation assays using purified NTSR1, combined with mutagenesis and molecular docking, provide evidence for the role of the receptor’s H8 domain in direct pepducin interaction. Together, these findings highlight pepducins as versatile modulators of GPCR function and as valuable pharmacological tools for GPCR-targeted drug development. The NTSR1 pepducin PP-001 biases signaling toward G proteins, inhibits neurotensin binding, and induces sustained hypotension, with functional activity dependent on an N-terminal RKK motif and interaction with the receptor H8 domain.

  PublisherDOI

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

  Clinical Cancer Research · 2025-01-26

  articleSenior author

  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

  PublisherDOI

• A neurotensin receptor type 1-derived pepducin acts as a biased allosteric modulator to regulate target receptor function

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-15

  preprintOpen access

  Abstract Pepducins are synthetic membrane-tethered lipopeptides designed to allosterically modulate G protein-coupled receptor (GPCR) signaling. Here, we characterize a series of pepducins targeting the neurotensin receptor type 1 (NTS1), revealing multifaceted modulation of this receptor class. Using BRET-based biosensors, we show that PP-001, a pepducin derived from NTS1’s first intracellular loop, preferentially activates G protein over β-arrestin signaling while inhibiting NT binding, NT-induced β-arrestin recruitment, and NTS1 receptor internalization, thereby acting as biased allosteric agonist and negative allosteric modulator. PP-001 also promotes the formation of both homo- and heteromeric multi-receptor units. In vivo, PP-001 elicits potent, sustained hypotensive effects, reversible by the NTS1 antagonist SR48692. Finally, although the mechanism of pepducin-receptor interaction remains unclear, this study identifies a critical N-terminal RKK motif for PP-001’s biological activity. Thermodenaturation assays with purified NTS1 and mutagenesis further provide evidence for the role of NTS1’s H8 domain in direct pepducin-receptor interaction. This work highlights pepducins’ modulatory potential as pharmacological tools for GPCR-targeted drug development.

  PublisherOA PDFDOI

• 309 Combining radiopharmaceutical therapy with CAR T cells to overcome the heterogeneous immunosuppressive prostate tumor microenvironment

  Regular and Young Investigator Award Abstracts · 2025-11-01

  articleOpen access
  PublisherOA PDFDOI

• 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

  articleSenior author

  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.

  PublisherDOI

• Abstract P005: Fibroblast Activation Protein (FAP)-targeted radioligand therapy as a promising treatment for glioblastoma

  Clinical Cancer Research · 2025-01-26

  article

  Abstract Introduction: Glioblastoma (GBM) is the most common and aggressive primary brain tumor. The 5-year survival rate is only 4% despite the current standard treatment approaches of surgery, chemotherapy, and radiation. Fibroblast Activation Protein (FAP)-targeted radioligand therapy (RLT) has emerged as a potential alternative to traditional radiation methods. FAP is a protein highly expressed in Cancer-Associated Fibroblasts (CAFs) and on GBM cells. It can be targeted by radiolabeled molecules for selective tumor irradiation, to enhance treatment precision and reduce damage to healthy tissue. Here we evaluated the relevance of FAP inhibitor 46 (FAPi-46) as a molecular probe for Radioligand Therapy (RLT) in GBM models. Methods: U87MG, a human GBM cell line shown to express human FAP and SB28, a murine GBM cell line engineered to express murine FAP were used as GBM models. NSG and C57BL6J mice were, respectively, inoculated with U87MG and SB28 cells subcutaneously. Tumor growth was evaluated by computed tomography (CT). FAP expression was assessed by 68Ga-FAPi-46 PET imaging when tumors reached around 100 mm3 prior to treatment. Mice were subsequently randomized into 4 groups: (1) vehicle, (2) 5 mg/kg temozolomide (TMZ), (3) 60 kBq 225Ac-FAPi-46, and (4) 5 mg/kg TMZ and 60 kBq 225Ac-FAPi-46. Dose of TMZ and 225Ac-FAPi-46 were increased for the SB28 study. Overall survival was tracked. Blood was collected 24h before, after, and 7 days after RLT treatment to assess blood toxicity. Tumor were resected 24h after RLT treatment to further evaluate DNA-damage. Results: Our results show that combining TMZ with 225Ac-FAPi-46 successfully delays tumor progression and extends survival in immunocompromised mice bearing subcutaneous human U87MG GBM tumors. In the SB28 GBM model neither TMZ nor a single dose of FAPi-RLT alone affected tumor growth or survival, confirming its in vivo resistance to both chemotherapy and radiation. However, by adapting the 225Ac-FAPi-46-RLT regimen, we observed a significant reduction in tumor volume and an increase in survival in immunocompetent mice. These results suggest that higher doses of 225Ac-FAPi-46-RLT can overcome resistance in this model. Conclusion: In conclusion, our study shows that 225Ac-FAPi-46-RLT could be an effective treatment for GBM, with positive results across different tumor models. To further investigate the efficacy of FAP-targeted RLT for GBM, we have initiated an evaluation of immune cell infiltration within subcutaneous SB28 tumors. Using immunohistochemistry, RNA sequencing, and flow cytometry, ongoing studies will characterize the immunogenic response induced by RLT in this GBM model. Citation Format: Pauline Jeanjean, Rachel Dove, Ines Camille Azrour, Samantha Kwock, Sarah Taylor, Sarina Smolev, Johannes Czernin, Giuseppe Carlucci, David Nathanson, Christine Mona, Elie Besserey-Offroy. Fibroblast Activation Protein (FAP)-targeted radioligand therapy as a promising treatment for glioblastoma. [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 P005

  PublisherDOI

Frequent coauthors

• Wolfgang P. Fendler

  University of Duisburg-Essen

  42 shared

• Johannes Czernin

  40 shared

• Uwe Haberkorn

  Heidelberg University

  40 shared

• Aaron Enke

  Clovis Oncology (United States)

  36 shared

• Qin Lin

  Children's Hospital of Chongqing Medical University

  36 shared

• Marija Trajkovic‐Arsic

  Essen University Hospital

  36 shared

• Jens T. Siveke

  Heidelberg University

  36 shared

• Irene Virgolini

  Universität Innsbruck

  36 shared

Labs

• Drs. Lueckerath/Mona LabPI