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Letteratura scientifica selezionata sul tema "Abstract Targeted radionuclide therapy (TRT)"

Autore: Grafiati

Pubblicato: 6 luglio 2024

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Nguyen, Thanh Phuong T., Caroline P. Kerr, Joseph J. Grudzinski, Carolina A. Ferreira, Julia Sheehan-Klenk, Ohyun Kwon, Maria Powers et al. "Abstract 6407: Radionuclide-specific effects of90Y-,177Lu-, or225Ac-NM600 targeted radionuclide therapy on tumor immunomodulation and enhanced immunotherapy response in syngeneic murine tumors". Cancer Research 83, n. 7_Supplement (4 aprile 2023): 6407. http://dx.doi.org/10.1158/1538-7445.am2023-6407.

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Abstract Background: Targeted radionuclide therapy (TRT) delivers radiation treatment systemically to tumor sites via a therapeutic radionuclide-linked tumor-selective targeting vector. NM600 is an alkylphosphocholine analog selectively taken up and retained in murine and human tumor cells. We previously showed that low dose radiation delivery with 90Y-NM600 improves tumor response to immune checkpoint inhibitors (ICIs). Understanding the effect of different radionuclide physical properties (emission type, linear energy transfer (LET), half-life, and tissue range) on immunomodulation of metastatic cancers may guide therapy development. Here, we evaluated the type 1 interferon (IFN1) response elicited by 90Y-, 177Lu-, and 225Ac-NM600 in an immunologically cold syngeneic murine tumor model, B78 melanoma. We hypothesized that the unique physical properties of radionuclides will differentially impact immunomodulation by TRT. Methods: Mice bearing B78 WT or Tmem173 -/- CRISPR deletion B78 (STING KO) tumors were randomized to receive 1.5 Gy external beam radiation (EBRT), an equivalent tumor dose of 90Y-, 177Lu-, or 225Ac-NM600 determined by the Monte Carlo-based RAPID platform, or no radiation on day 1. Tumors were harvested on days 4, 7, and 10 for RT-qPCR. Mice bearing two B78 WT or Tmem173 -/- CRISPR deletion B78 (STING KO) tumors were randomized to receive 4 Gy external beam radiation therapy (EBRT), an equivalent tumor dose of 90Y- or 177Lu-NM600, 0.5 μCi 225Ac-NM600, or no radiation +/- dual ICI (anti-CTLA4 and anti-PDL1). Mice were monitored for tumor growth and survival following these treatments. Results: Both EBRT and TRT upregulated expression of IFN1 response-associated genes (Ifnβ1, Mx1) in B78 WT tumors. Only TRT induced upregulation of Ifnβ1 and Mx1 in STING KO B78 tumors. Ddx58, which encodes RIG-I, integral to an alternative IFN1 pathway, was upregulated in both B78 WT and STING KO tumors following 225Ac-NM600, but not other treatments. TRT in B78 STING KO tumors had earlier expression of IFN1 response-associated genes than B78 WT, 225Ac-NM600 in combination with dual ICI improved overall survival over 90Y- or 177Lu-NM600 + ICI and 225Ac-NM600 monotherapy. Conclusions: The distinct physical properties of TRT radiation, γ, β or α, affect the timing, magnitude, and molecular pathways leading to this IFN1 response. Understanding TRT effects on the tumor microenvironment may optimize TRT and immunotherapy. Citation Format: Thanh Phuong T. Nguyen, Caroline P. Kerr, Joseph J. Grudzinski, Carolina A. Ferreira, Julia Sheehan-Klenk, Ohyun Kwon, Maria Powers, Paul A. Clark, Raghava N. Sriramaneni, Reinier Hernandez, Bryan Bednarz, Jamey P. Weichert, Zachary S. Morris. Radionuclide-specific effects of90Y-,177Lu-, or225Ac-NM600 targeted radionuclide therapy on tumor immunomodulation and enhanced immunotherapy response in syngeneic murine tumors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6407.

Kerr, Caroline P., Joseph J. Grudzinski, Carolina A. Ferreira, David Adam, Julia Sheehan-Klenk, Amber M. Bates, Won Jong Jin et al. "Abstract 2828: Impact of sequencing of immune checkpoint blockade and targeted radionuclide therapy on murine tumor response". Cancer Research 83, n. 7_Supplement (4 aprile 2023): 2828. http://dx.doi.org/10.1158/1538-7445.am2023-2828.

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Abstract Background: Sequencing of immune checkpoint inhibitors (ICI) and external beam radiation therapy (EBRT) for cancer treatment has been studied, but the optimal sequencing has yet to be determined. While some studies have noted therapeutic advantages of priming the tumor immune microenvironment with EBRT prior to ICI, others have described the benefit of modulating the tumor infiltrating lymphocyte (TIL) population with ICI before EBRT. Targeted radionuclide therapy (TRT) approaches allow investigation of how irradiation by a tumor-targeted radionuclide and differences in emission type, linear energy transfer, and dose rate affect optimal timing of ICI administration. NM600 is an alkylphosphocholine analog selectively taken up by tumors capable of chelating numerous radionuclides for comparative studies. Objective: We use two immunologically cold tumor models, MOC2 head and neck squamous cell carcinoma and B78 melanoma, to describe the influence of dose rate on type I interferon (IFN1) signaling and the effect of ICI and 90Y-, 177Lu-, and 225Ac-NM600 TRT sequences on tumor response. Methods: 90Y, 177Lu, or 225Ac were added to culture media in activities estimated using GEANT4 Monte Carlo to deliver 12 Gy to the cell monolayer. qPCR was performed on cDNA from cells irradiated with EBRT, 90Y, 177Lu, or 225Ac, and harvested on days 1, 3, or 7. In vivo dosimetry was performed using the Monte Carlo-based RAPID platform utilizing serial PET/CT or SPECT/CT imaging and/or longitudinal biodistribution. Differences over time (days 4, 7, 14, 21, 28 after RT) in TIL and systemic immune cell populations were measured by flow cytometry following no treatment, 12 Gy EBRT, or 90Y-, 177Lu-, or 225Ac-NM600 in MOC2 tumors. Mice bearing B78 tumors received 1.5 Gy 90Y-, 177Lu-, or 225Ac-NM600, or no radiation on day 1 +/- ICI (anti-CTLA4 + anti-PDL1) on days -3/0/3 (early), 4/7/10 (middle), or 11/14/17 (late). Mice were monitored for tumor growth and survival. Results: TRT and EBRT induced IFN1 responses in MOC2 cells. MOC2 cells treated every 24h with EBRT-matched 90Y/225Ac dose rates led to upregulation of IFN1-associated Ifnb1 and Mx1, mimicking radionuclide-induced responses. Increased tumor CD8/Treg ratios and decreased Tregs were observed at day 7 following all RT forms in MOC2 tumors. Long half-life 225Ac-NM600 (90Y: 65h; 177Lu: 161h; 225Ac: 240h) induced similar TIL changes at day 21. For 1.5 Gy 90Y-, 177Lu-, and 225Ac-NM600, B78 tumor growth delay and statistically significant overall survival benefit over respective TRT monotherapy and control groups was observed with early (day -3/0/3) dual ICI administration. Conclusions: These studies demonstrate novel immunomodulatory effects of α- and β- emitting TRT and the capacity to achieve substantial antitumor responses with appropriate TRT + ICI sequencing. These results may inform clinical trial design of TRT + ICI regimens for patients with metastatic cancers. Citation Format: Caroline P. Kerr, Joseph J. Grudzinski, Carolina A. Ferreira, David Adam, Julia Sheehan-Klenk, Amber M. Bates, Won Jong Jin, Ohyun Kwon, Justin C. Jagodinsky, Maria Powers, Raghava N. Sriramaneni, Paul A. Clark, Luke Zangl, Thanh Phuong T. Nguyen, Anatoly N. Pinchuk, Cynthia Choi, Christopher F. Massey, Reinier Hernandez, Bryan Bednarz, Jamey P. Weichert, Zachary S. Morris. Impact of sequencing of immune checkpoint blockade and targeted radionuclide therapy on murine tumor response [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2828.

Pal, Debjani, Miguel Toro Gonzáleza, Amber N. Bibleb, Brian Sanders, Anna Plechaty, Owee Kirpekar, Mircea Podar e Sandra M. Davern. "Abstract 480: Nanotherapeutic strategies to improve targeted radionuclide therapy". Cancer Research 84, n. 6_Supplement (22 marzo 2024): 480. http://dx.doi.org/10.1158/1538-7445.am2024-480.

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Abstract Cancer is a leading cause of death worldwide. Several multidisciplinary approaches exist for cancer treatment, including radiotherapy and chemotherapy. Radiotherapy uses high-energy radiation to kill cancer cells; chemotherapy inhibits cancer cell proliferation and often kills cells by targeting the cell cycle. Resistance to radiotherapy and chemotherapy is a key determining factor in the outcome of therapeutic efficacy. Conventional nontargeted radiotherapy also affects distant nonirradiated cells, leading to DNA damage and changes in the cell cycle that are often linked to secondary carcinogenesis in patients. In recent years, targeted radionuclide therapy (TRT) has emerged as a promising personalized treatment strategy that delivers cytotoxic levels of radiation directly and specifically to cancer cells. Among radioisotopes,225Ac exhibits desirable properties for TRT: multiple α-particle emission and high cytotoxicity. One of the challenges with 225Ac is the nonspecific toxicity caused by the release and relocation of its decay daughters. Different approaches have been proposed to prevent the relocation of decay daughters, including nanoparticles. Nanoparticles have been pursued as a promising delivery vehicle of α-emitting radioisotopes to the tumor site. Here, we show specific targeting of Her2-positive breast cancer cells with 225Ac-radiolabeled lanthanum orthovanadate (LaVO4) nanoparticles. Nanoparticles’ surfaces were functionalized to improve biocompatibility and conjugated to target cancer cells, respectively. Cellular uptake and localization of these engineered nanoparticles were analyzed by a Confocal microscope and IncuCyte live cell analysis system. Results confirm its localization in the nucleus following the endolysosomal path, enhancing the nanoparticles’ effectiveness as a delivery vehicle for α-emitting radioisotopes with the potential of increased treatment efficacy. Upon addition of cancer-targeting ligands, these nanoparticles can achieve higher efficiency by delivering the radioisotope to the tumor cells with a potential of safe encapsulation of all α-emitters in the decay chain. The anticancer efficiency of 225Ac-radiolabeled nanoparticles was demonstrated by a dose-dependent effective killing of 3D breast cancer spheroids using both IncuCyte live imaging and the cell survival assays. Ultimately, the results of this study will be crucial in determining the future use of targeted radiolabeled nanoparticle-based delivery systems as an approach for more efficacious cancer treatment. Citation Format: Debjani Pal, Miguel Toro Gonzáleza, Amber N. Bibleb, Brian Sanders, Anna Plechaty, Owee Kirpekar, Mircea Podar, Sandra M. Davern. Nanotherapeutic strategies to improve targeted radionuclide therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 480.

Adhikarla, Vikram, Dennis Awuah, Alexander B. Brummer, Enrico Caserta, Amrita Krishnan, Flavia Pichiorri, Megan M. Minnix et al. "Abstract 2732: A mathematical model for optimization of combination therapy involving targeted radionuclide and CAR-T cell therapy". Cancer Research 82, n. 12_Supplement (15 giugno 2022): 2732. http://dx.doi.org/10.1158/1538-7445.am2022-2732.

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Abstract Background: Immunotherapy with chimeric antigen receptor - T (CAR-T) cells and targeted radionuclide therapy (TRT) are two highly promising therapies in cancer treatment. Often, these therapies show limited efficacy in complete eradication of cancer cells making the combination of these two therapies an attractive cancer treatment option. The complications involved in dosing and scheduling of these therapies make mathematical modeling an appropriate method for analyzing and predicting disease response to these therapies. Here we propose a mathematical model evaluating disease response to the combination of these two therapies and explore the optimization of their dosing and scheduling. Methods: An ordinary differential equation-based formalism is proposed for simulation of tumor response to CAR-T cell therapy as well as TRT. CAR-T cell dose and injected radioactivity was input to the model. Among others, key model parameters included tumor proliferation rate, tumor cell and CAR-T cell radiosensitivity, CAR-T cell killing rate, CAR-T cell decay rate indicating persistence. Preclinical experiments involving CS1- CAR-T cell therapy and 225Ac-DOTA-Daratumumab TRT in a multiple myeloma mice model were used to parameterize the model. Sensitivity study of the model parameters using overall survival (OS) and progression-free survival (PFS) as evaluation metrics, was performed to elucidate the parameters with highest impact. Results: OS and PFS were 97 and 55 days when CAR-T cell therapy was given prior to TRT as compared to OS of 43 days for untreated control mice. Sensitivity study of model parameters showed that tumor proliferation has the highest impact on survival metrics. For a ±50% change in tumor proliferation rate, OS changed by -41%/+111% and PFS changed by -62%/+147%. Similar changes in TRT injected activity and CAR-T cell dose changed OS by ± 15% and ±21% respectively. Accordingly, PFS changed by roughly ±32% and ±45% respectively. A variation of the interval between the therapies showed that faster growing tumors required a shorter interval between the two therapies. The sequence of therapies was also changed and TRT prior to CAR-T cell therapy demonstrated shorter PFS (43 days) due to the adverse effects of radiation on CAR-T cells. Conclusion: For a fixed dose of TRT and CAR-T cells, tumor proliferation rate was found to be the prime factor impacting therapy interval. The presented work shows the key parameters required for planning and optimizing preclinical experiments and clinical trials. Using disease, CAR-T cell and radionuclide-specific parameters as shown in this work as well as incorporating immune stimulating effects of radiation would make it an extremely potent tool for optimizing combination therapies. Citation Format: Vikram Adhikarla, Dennis Awuah, Alexander B. Brummer, Enrico Caserta, Amrita Krishnan, Flavia Pichiorri, Megan M. Minnix, John E. Shively, Jeffrey Y.C. Wong, Xiuli Wang, Russell C. Rockne. A mathematical model for optimization of combination therapy involving targeted radionuclide and CAR-T cell therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2732.

Kerr, Caroline P., Amber M. Bates, Joseph J. Grudzinski, Carolina A. Ferreira, Julia Sheehan-Klenk, David Adam, Maria Powers et al. "Abstract 1306: Radionuclide-specific effects of 90Y-, 177Lu-, or 225Ac-NM600 targeted radionuclide therapy on tumor immunomodulation and enhancing immunotherapy response in murine tumor models". Cancer Research 82, n. 12_Supplement (15 giugno 2022): 1306. http://dx.doi.org/10.1158/1538-7445.am2022-1306.

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Abstract Purpose: In preclinical studies, we have demonstrated that delivering low dose radiation to all tumor sites utilizing 90Y-NM600 improves the response to immune checkpoint inhibitors (ICIs). NM600 is an alkylphosphocholine analog that is selectively taken up and retained in murine and human tumors. In this study, the immunomodulatory capacities of three distinct radionuclides (90Y, 177Lu, 225Ac) were compared using immunologically cold syngeneic murine tumor models: MOC2 head and neck squamous cell carcinoma (HNSCC) and B78 melanoma. We hypothesized that physical properties of radionuclides (e.g. emission type, linear energy transfer (LET), half-life, dose rate) would differentially impact immunomodulation by TRT and ICI treatment response. Methods: Dosimetry performed using the Monte Carlo-based RAPID platform utilizing serial 86Y-NM600 PET/CT imaging determined that 100 μCi 90Y-NM600 or 200 μCi 177Lu-NM600 delivered ~12Gy to the MOC2 tumor and ~4Gy to the B78 tumor. 225Ac-NM600 was dosed at activities ≤0.5 μCi, as determined to be safe and effective previously. Mice bearing two MOC2, B78 WT, or Tmem173 -/- CRISPR deletion B78 (STING KO) tumors were randomized to receive external beam radiation therapy (EBRT), an equivalent tumor dose of 90Y- or 177Lu-NM600, 0.25 μCi 225Ac-NM600, or no radiation +/- dual ICI (anti-CTLA4 and anti-PDL1). Tumors, blood, bone marrow, and spleen were harvested at days 4, 7, 14, and 21 post-treatment for flow cytometry and RT-qPCR. Additional mice were monitored for tumor growth and survival following these treatments. Results: TRT and EBRT induced favorable tumor-specific immune cell infiltration (increased CD8/Treg ratio) at day 7. 225Ac-NM600 additionally induced similar changes at day 21, consistent with the longer half-life radioisotope (90Y: 65h; 177Lu: 161h; 225Ac: 240h). Expression of immune susceptibility markers (Mhc1, Pdl1) and type I interferon (IFN1) response-associated genes (Ifnβ1, Mx1) was upregulated following 12 Gy EBRT or TRT both in vitro and in vivo compared to non-irradiated controls in MOC2 cells and tumors. The timing and magnitude of these effects correlated with radionuclide half-life and LET. 225Ac-NM600 + ICI improved overall survival in B78 WT mice over 90Y- or 177Lu-NM600 + ICI, 225Ac-NM600 or ICI monotherapy, and non-irradiated controls. In the B78 STING KO melanoma cell line, this 225Ac-NM600 + ICI survival benefit was decreased. Conclusions: These studies demonstrate the capacity to deliver immunomodulatory radiation to tumors using gamma-, beta- or alpha-emitting TRT. The physical properties of the delivered radionuclide dictate timing and magnitude of the IFN1 response stimulated by TRT. Understanding these effects may be critical to safely and effectively integrating TRT and immunotherapies to enhance anti-tumor immunity in cancer patients. Citation Format: Caroline P. Kerr, Amber M. Bates, Joseph J. Grudzinski, Carolina A. Ferreira, Julia Sheehan-Klenk, David Adam, Maria Powers, Wonjong Jin, Justin C. Jagodinsky, Raghava N. Sriramaneni, Paul A. Clark, Luke Zangl, Anatoly N. Pinchuk, Alejandro J. Onate, Ria Kumari, Cynthia Choi, Christopher F. Massey, Bryan Bednarz, Reinier Hernandez, Jamey P. Weichert, Zachary S. Morris. Radionuclide-specific effects of 90Y-, 177Lu-, or 225Ac-NM600 targeted radionuclide therapy on tumor immunomodulation and enhancing immunotherapy response in murine tumor models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1306.

Adhikarla, Vikram, Dennis Awuah, Enrico Caserta, Megan Minnix, Maxim Kuznetsov, Amrita Krishnan, Jeffrey Y. Wong et al. "Abstract 7374: Mathematical modeling of targeted radionuclide therapy and CAR-T cell immunotherapy for maximizing therapeutic efficacy in multiple myeloma". Cancer Research 84, n. 6_Supplement (22 marzo 2024): 7374. http://dx.doi.org/10.1158/1538-7445.am2024-7374.

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Abstract Background: Resistance of cancer cells to monotherapies has led to the development of sequential or combination therapy regimens. However, dosing and scheduling of these therapies is challenging due to the numerous dosing and scheduling combinations that can be given. Mathematical models are thus critical tools for addressing this challenge as multiple therapy combinations can be tested in silico to finalize a patient-specific therapeutic regimen in vivo. Here we develop a mathematical framework for combining targeted radiation therapy (TRT) with Chimeric Antigen Receptor (CAR)-T cell immunotherapy and demonstrate the use of in silico techniques to schedule these therapies for maximizing survival. Methods: In the mathematical framework tumor growth is assumed to be exponential and the effect of radiation on both tumor cells and CAR-T cells is modeled using the linear-quadratic model of cell survival to radiation. A predator-prey model is used to characterize the dynamics of tumor and CAR-T cells. Using a preclinical disseminated mouse model of multiple myeloma (MM1S), we evaluate tumor response to 200 nCi of 225Ac-DOTA-Daratumumab (TRT) and 1 million cells of CS1 CAR-T cell therapy both as monotherapies as well as in combination. Tumor burden tracked using bioluminescence imaging from six groups of mice is used to calibrate model parameters: (a) No treatment. (b) Day 7 TRT. (c) Day 7 CAR-T cell therapy. (d) Day 7 TRT + Day 18 CAR-T cell therapy. (e) Day 7 TRT + Day 25 CAR-T cell therapy. (f) Day 7 TRT + Day 32 CAR-T cell therapy. Response to therapy is evaluated using progression-free survival (PFS), overall survival (OS) and time to minimum tumor burden (tmin), all of which are calculated using the predicted in silico tumor burden dynamics and the tumor burden at the start of first therapy. We evaluate these response metrics for various dosing and scheduling regimens. Results: Therapy intervals that were too short or too long are shown to be detrimental for therapeutic efficacy. TRT too close to CAR-T cell therapy results in radiation related CAR-T cell killing, while the interval being too long results in tumor regrowth, negatively impacting tumor control and survival. If a single dose is split into multiple doses, the splitting is advantageous only if the first therapy delivered can produce a significant benefit as a monotherapy. Based on the model parameters we estimate the minimum required TRT activity and CAR-T cell dose to demonstrate an improvement in PFS. Conclusions: The proposed model demonstrates the impact of different dosing and scheduling regimens of TRT and CAR-T therapy on survival metrics. It is a potent tool for translating preclinical results to the clinic and eventually tailor therapy regimens for patients. Citation Format: Vikram Adhikarla, Dennis Awuah, Enrico Caserta, Megan Minnix, Maxim Kuznetsov, Amrita Krishnan, Jeffrey Y. Wong, John E. Shively, Xiuli Wang, Flavia Pichiorri, Russell C. Rockne. Mathematical modeling of targeted radionuclide therapy and CAR-T cell immunotherapy for maximizing therapeutic efficacy in multiple myeloma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7374.

Ruder, Samuel, Michael Sun, Andres Ricaurte Fajardo, Jones Nauseef, Zachary Davidson, Joseph Thomas, Sandra Huicochea Castellanos et al. "Abstract 7582: Descriptive analysis of patients with mCRPC and liver metastases receiving alpha and beta PSMA targeted radionuclide therapy (PSMA-TRT)". Cancer Research 84, n. 6_Supplement (22 marzo 2024): 7582. http://dx.doi.org/10.1158/1538-7445.am2024-7582.

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Abstract Introduction: Predictors of outcomes after PSMA-TRT are still being established. Liver metastases (mets) have been associated with poor response. Mutations in genes encoding DNA damage repair (DDR) and TP53 affect radiosensitivity. Here we describe a cohort of patients with mCRPC and liver metastases treated on clinical trials of PSMA-TRT. Methods: 39 patients with liver mets were enrolled on phase I/II PSMA-TRT studies between Jan 2006 to Apr 2022. Patients received alpha therapy (225Ac-J591), beta therapy (fractionated 177Lu-PSMA-617, single-dose and fractionated 177Lu-J591) or a combination of both (225Ac-591 and 177Lu-PSMA-I&T). All patients included in this analysis had CT imaging; patients enrolled after 2017 had PSMA-PET imaging. 15 patients also had genomic analysis completed. Results: Median age was 69 (range 55-93), PSA 85.7 (2.45-9614). 39 (100%) bone mets, 33 (84.6%) LN, 9 (23.1%) lung. 22 (56.4%) greater than 1 ARPI, 23 (59.0%) greater thanc 1 chemo, 13 (33.3%) sip-T, 7 (17.9%) Ra-223, 4 (10.2%) prior TRT (with concurrent liver mets). Of the 19 with both CT and PSMA PET, 18 (94.7%) were identified on PSMA PET (including 8 PET only), 10 (55.6%) on CT (1 CT only, i.e. non-PSMA PET avid). Median whole body PSMA-imaging score (PSMA-IS) was 4 (range 1-4), with 7 (17.9%) 1-2 and 32 (82.1%) 3-4. 9 (23.0%) received alpha-TRT, 26 (66.7%) beta-TRT, and 4 (10.3%) combo-TRT. Somatic or germline analysis was completed in 15 (38.5%) of 39 patients. 8 (53.3%) had mutations in DNA repair pathways (3 in BRCA2, 3 in CHEK 2, 1 in FANC, 1 in MSH2). 7 (46.7%) had mutations in TP53. 31 patients (79.5%) had PSA decline, with 15 (38.5%) achieving PSA 50. 26 (66.7%) had baseline CTC measured; 19 (73.0%) had detectable CTC at baseline. Of these 19, 3 (15.8%) converted to undetectable after therapy and 2 (10.5%) converted to favorable CTC. PSA50 rate in alpha-TRT was 4 (44.4%), beta-TRT 8 (30.7%), combo-TRT 3 (75%). PSA50 in patients with PSMA-IS 1-2 was 1 (14.2%) compared to 14 (43.9%) in PSMA-IS 3-4. 3 (37.5%) of 8 patients with mutDDR achieved PSA50, compared to 3 (42.9%) with mutTP53. Conclusions: This dataset adds to the collective literature of two subgroups of patients with mCRPC receiving TRT: those with liver disease and those with mutations in DNA repair pathways. The results of this study suggest higher rates of response in patients receiving alpha therapy, either alone or in combination with beta therapy, and in patients with high radiotracer uptake on PSMA-PET, based on PSMA-imaging score of 3 or 4. Genomic alterations in DRR proteins did not have clear implications. Citation Format: Samuel Ruder, Michael Sun, Andres Ricaurte Fajardo, Jones Nauseef, Zachary Davidson, Joseph Thomas, Sandra Huicochea Castellanos, Ana Molina, Cora Sternberg, Amie Patel, Escarleth Fernandez, Sarah Yuan, Edward Fung, Vasilios Avlonitis, Elisabeth O'Dwyer, David Nanus, Joseph Osborne, Neil Bander, Scott Tagawa. Descriptive analysis of patients with mCRPC and liver metastases receiving alpha and beta PSMA targeted radionuclide therapy (PSMA-TRT) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7582.

Sheehan-Klenk, Julia, Caroline P. Kerr, Thanh P. Nguyen, Joseph J. Grudzinski, David Adam, Maria Powers, Raghava N. Sriramaneni et al. "Abstract 6117: Dose, dose rate, and linear energy transfer influence tumor immunologic and DNA damage response following alpha- and beta-emitting radionuclides". Cancer Research 83, n. 7_Supplement (4 aprile 2023): 6117. http://dx.doi.org/10.1158/1538-7445.am2023-6117.

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Abstract Background: The low response rate to immunotherapies in poorly immunogenic cancers highlights the potential for combination therapies that propagate an anti-tumor response in metastatic settings. Targeted radionuclide therapy (TRT) can deliver radiation to metastatic tumor sites. In preclinical studies, combining low dose TRT with immune checkpoint blockade augments the anti-tumor immune response, promoting the immune susceptibility of metastatic disease sites. Radionuclides differ in their physical properties such as emission type, linear energy transfer (LET), half-life, and tissue range. In this study, clinically relevant α- and β-emitting radionuclides (225Ac, 90Y, 177Lu) were compared in vitro in MOC2 head and neck squamous cell carcinoma and B78 melanoma. We hypothesized that the unique physical properties of radionuclides would differentially impact the quantity and accumulation over time of double stranded DNA breaks, mirroring the timing of effects on tumor cell immune susceptibility markers. Methods: MOC2 or B78 cells were grown in culture and treated with external beam radiation (EBRT), or culture media containing 90Y, 177Lu, or 225Ac delivering continuous radiation at activity levels using GEANT4 Monte Carlo to deliver 12 Gy (MOC2) and 4 Gy (B78) to the cell monolayer. Cells were harvested, and cDNA was isolated for RT-qPCR one, three, and seven days after the start of irradiation. Additional cells treated in this manner were fixed and stained with DAPI/γ-H2AX antibody for confocal microscopy at the same timepoints. γ-H2AX foci/cell were quantified manually using ImageJ. Results: γ-H2AX foci counts/cell increased significantly and accumulated over time following treatment with 225Ac, but not with 90Y or 177Lu. EBRT, 90Y, and 225Ac, but not 177Lu, upregulated expression of immune response associated genes (Fas, Pdl1, Mhc1) compared to non-irradiated controls. In cells treated with EBRT every 24h at doses mimicking the interval dose delivered by continuous exponential decay of 90Y and 225Ac, but not 177Lu, the time course and magnitude of Fas and Pdl1 expression phenocopied that of these radionuclides. Conclusions: DNA damage accumulation and the timing of immunomodulation are modified by the dose, dose-rate, and LET of radiation emitted from a given radionuclide. Understanding the effects of radionuclide therapies on cancer cell immunogenicity could enable rational design of clinical trials that investigate the integration of TRT and immunotherapies into the clinical care of patients with metastatic cancers. Citation Format: Julia Sheehan-Klenk, Caroline P. Kerr, Thanh P. Nguyen, Joseph J. Grudzinski, David Adam, Maria Powers, Raghava N. Sriramaneni, Paul A. Clark, Reinier Hernandez, Bryan Bednarz, Jamey P. Weichert, Zachary S. Morris. Dose, dose rate, and linear energy transfer influence tumor immunologic and DNA damage response following alpha- and beta-emitting radionuclides [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6117.

Vorontsova, M., T. Karmakova, A. Pankratov e A. Kaprin. "Current Trends in Targeted Radionuclide Therapy Development". Medical Radiology and radiation safety 66, n. 6 (17 dicembre 2021): 63–70. http://dx.doi.org/10.12737/1024-6177-2021-66-6-63-70.

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Introduction 1. Features of Targeted Delivery of Therapeutic Radionuclides 2. Design of Pharmaceuticals for Targeted Radionuclide Therapy (TRT) 2.1. Radionuclides 2.2. Synthesis of Radioconjugates 2.3. Targeting Carriers 4. Subcellular Targeting of Radionuclides 5. TRT Dosimetry Conclusion

van der Wal, Bart C. H., e Ekaterina Dadachova. "Targeted Radionuclide Therapy of Cancer and Infections". International Journal of Molecular Sciences 24, n. 10 (22 maggio 2023): 9081. http://dx.doi.org/10.3390/ijms24109081.

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Rouanet, Jacques. "Radiothérapie interne du mélanome métastatique pigmenté : mécanismes et associations". Electronic Thesis or Diss., Université Clermont Auvergne‎ (2017-2020), 2019. http://www.theses.fr/2019CLFAS033.

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La radiothérapie interne vectorisée ou RIV consiste à adresser spécifiquement un isotope radioactif aux tumeurs grâce à un vecteur spécifique. Dans le cas du mélanome, le vecteur utilisé pour la RIV peut être un anticorps ciblant des antigènes de surface ou la mélanine, des analogues peptidiques capables de se fixer sur des récepteurs tumoraux (comme le récepteur à la melanocyte-stimulating hormone) ou des petites molécules se liant à la mélanine (dérivées des benzamides). Ainsi, notre équipe travaille sur cette dernière stratégie depuis 15 avec la molécule phare [ 131 I]ICF01012. De nombreuses études précliniques ont permis un essai clinique de phase I, MELRIV1, qui est ouvert depuis juillet 2019 (NCT03784625). En parallèle de cet essai,nous avons poursuivi la caractérisation préclinique des effets d’[ 131 I]ICF01012 en monothérapie et en association avec les traitements actuels du mélanome, dans la perspective d’essais cliniques de phase II.Ce travail est divisé en deux axes :1) étudier les effets de la RIV par [ 131 I]ICF01012 sur les principaux mécanismes impliqués dans la progression du mélanome : la dissémination métastatique et la pseudo-transition épithélio-mésenchymateuse, l’activation de la voie des MAPK et l’échappement à la réponse immunitaire antitumorale ;2) évaluer des combinaisons d’[ 131 I]ICF01012 avec les traitements actuels du mélanome métastatique : thérapies ciblant la voie des MAPK et inhibiteurs de checkpoints immunitaires.Pour le premier axe, grâce à un modèle de sphéroïdes, nous avons montré que la RIVpar [ 131 I]ICF01012 modifiait l’expression de gènes et de protéines impliquées dans la pTEM et pouvait donc permettre de limiter la dissémination métastatique. Ces modifications s’accompagnaient également d’une différentiation des cellules de mélanome, associée à l’induction d’une pigmentation. Nous avons également mis en évidence, dans les sphéroïdes BRAF et NRAS mutés, une activation de la voie des MAPK dans les suites de la RIV, qui peut traduire l’installation d’une radiorésistance. L’association de la RIV aux inhibiteurs de MEK dans le modèle de sphéroïdes a démontré la possibilité d’utiliser ces molécules pour radiosensibiliser les cellules de mélanome présentant une activation constitutionnelle de la voie des MAPK avec une augmentation majeure de l’apoptose. Nous avons également montré l’impact d’[ 131 I]ICF01012 sur la dissémination métastatique par voie hématogène, notamment, par ciblage des cellules circulantes, et par voie lymphatique, par diminution du nombre de métastases ganglionnaires. Nous avons également montré in vitro et in vivo la très grande radiosensibilité de la lignée NRAS 1007, qui présente une mutation Q61K du gène NRAS.Pour la deuxième partie, le modèle murin syngénique B16F10 a permis de montrer que les effets immunitaires de la RIV s’appuient sur le déclenchement d’une mort immunogénique,permettant la mise en place d’une réponse immunitaire adaptative et le recrutement de cellules T cytotoxiques au sein de la tumeur. Cependant, la mise en place de cette réponse s’accompagnait aussi du recrutement de lymphocytes T régulateurs, qui peuvent contribuer à l’échappement de la tumeur à la réponse immunitaire. L’association de la RIV aux inhibiteurs de checkpoints immunitaires a permis de montrer que la mise en place de la tolérance immunologique était un phénomène majeur induit [ 131 I]ICF01012 alors que l’épuisement des cellules T semblait plus anecdotique. De plus, nous avons montré dans notre modèle, que la réduction de la tolérance immunologique par un anticorps anti-CTLA-4 conduisait à un accroissement de l’épuisement des cellules T. Nous avons également obtenu des résultats très prometteurs en termes de survie, notamment pour l’association de la RIV avec un anticorps anti-CTLA-4, qui conduisait à un allongement significatif de la survie par rapport aux monothérapies,sans augmentation de la toxicité. (...)
Targeted radionuclide therapy (TRT) is a therapeutic strategy which consists in specificallyaddressing a radionuclide to tumor by targeting, through a specific vector. For melanoma TRT,the vector could be an antibody targeting surface antigens or melanin, a peptidomimetic ableto bind to receptors (i.e. the melanocyte-stimulating hormone receptor) or some smallmolecules which specifically bind to melanin (benzamides). Our research is focused on the latterclass with the lead molecule [ 131 I]ICF01012 developed in our unit for 15 years. Promisingpreclinical studies have resulted in a phase I clinical trial, MELRIV1, opened since July 2019(NCT03784625). In line with this trial, we pursued the preclinical characterization of [ 131 I]ICF01012effects in monotherapy and in combination with current melanoma treatments.We then defined two main axes:1) [ 131 I]ICF01012 impact on main mechanisms involved in melanomagenesis: metastaticdissemination and epithelial-mesenchymal-like transition, activation of the MAPK pathway andescape from anti-tumor immune response;2) [ 131 I]ICF01012 combination with current treatments: potential benefit assessmentIn the first axis, we developed a spheroid model and showed that [ 131 I]ICF01012 alteredthe expression of genes and proteins involved in pTEM and could therefore limit metastaticdissemination. These modifications brought also melanoma cell differentiation and induction ofpigmentation. Importantly, we showed the efficiency of [ 131 I]ICF01012 on metastaticdissemination by hematogenous route, targeting circulating cancer cells, and by lymphaticroute, decreasing number of lymph node metastases. We also demonstrated in vitro and in vivothe very high radiosensitivity of Q61K mutated NRAS 1007 cells. We also demonstrated, in themutated BRAF and NRAS spheroids, an activation of the MAPK pathway following TRT irradiation,traducing radioresistance appearance.For the second part, combination of TRT with MEK inhibitors in the spheroid modeldemonstrated the possibility of using these molecules to radiosensitize melanoma cells withconstitutional activation of the MAPK pathway. This radiosensitization lead to a major increase ofapoptosis. In the B16F10 syngeneic mouse model, we showed that TRT immune effects rely onimmunogenic cell death initiation, leading to adaptive immune response and cytotoxic T cellrecruitment. These mechanisms come with recruitment of regulatory T-cells which can contributeto tumor escape from immune response. Combination of TRT with immune checkpoint inhibitorsevidenced that immunological tolerance was a major induced mechanism following[ 131 I]ICF01012 irradiation while T-cell exhaustion appeared as a minor phenomenon. In addition,we were able to show that the reduction of immunological tolerance by an anti-CTLA-4antibody increases T-cell exhaustion. Furthermore, TRT combined with immune checkpointinhibitors, especially with anti-CTLA-4, led to a significant increase of survival compared tomonotherapies, with no increase of toxicity.Taken together, these results confirm the potential role of TRT using [ 131 I]ICF01012 in themanagement of metastatic melanoma. Notably, association with inhibitors of checkpointsinhibitors appears to be very promising for further clinical trials following the Phase I trial of[ 131 I]ICF01012

Capitoli di libri sul tema "Abstract Targeted radionuclide therapy (TRT)":

"Monoclonal antibody targeted radionuclide therapy". In Targeted Therapy for Cancer, a cura di Surinder K. Batra, Apollina Goet Gabriela Pavlinkova e David Colcher, 57–75. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198508960.003.0005.

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Abstract The pivotal work by Kohler and Milstein (1) on the development of hybridoma technology has made the production of an unlimited supply of monoclonial antibody (mAb) molecules possible. A wide range of mAbs has been generated for applications in research and health care. mAbs have made an impact in clinical medicine for the treatment of cancer, infectious diseases, and the immunomodulation of transplant rejection.

Sharma, Vipasha, Suman Khurana, Mukesh Rani, Arun Mittal e Parveen Kumar Goyal. "RADIOPHARMACEUTICALS". In Futuristic Trends in Pharmacy & Nursing Volume 3 Book 20, 59–78. Iterative International Publisher, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/v3bgpn20p2ch3.

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Radiopharmaceuticals (RPs) have revolutionized the fields of nuclear medicine, diagnostic imaging, and targeted therapy. The chapter begins by elucidating the brief explanation of production and design of RPs. This chapter focuses on newly produced diagnostic & therapeutic radiopharmaceuticals that are being employed in normal clinical settings as well as innovative, exciting technologies and agents for the treatment of cancer and other chronic diseases. In this chapter, we delve into the introduction and key applications of therapeutic RPs, with a focus on radio immunotherapy (RIT) and targeted radionuclide therapy (TRT). Subsequently, the chapter delves into the diverse imaging modalities where RPs play a pivotal role including SPECT (Single-Photon Emission Computed Tomography) and PET (Positron Emission Tomography), where radiopharmaceuticals are crucial. It draws attention to the developments in molecular imaging that have made it possible to diagnose diseases early, stage them accurately, and track treatment outcomes. Moreover, this chapter also addresses the concept of personalized medicine as the potential of RPs to target specific molecular pathways in the treatment of various disease such as cancer, cardiac and neurodegenerative disorders also highlights the most recent developments in neuroimaging and examine their possible effects on the detection of various neurodenegenerative disorders. The most significant RPs pharmaceutical elements are discussed in this chapter.

Bhandare, Manish S., Vikas Gupta, Vikram A. Chaudhari e Shailesh V. Shrikhande. "Neuroendocrine Tumours of the Pancreas". In Pancreas, a cura di Shailesh V. Shrikhande, Markus W. Büchler, Samiran Nundy e Dirk J. Gouma, 87—C11.P151. Oxford University PressOxford, 2022. http://dx.doi.org/10.1093/med/9780192858443.003.0011.

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Abstract Most pancreatic neuroendocrine tumours (p-NETs) have a sporadic occurrence and less than 10% form a part of various familial syndromes. Broadly, they can be classified as functional and non-functional tumours, based on the presence or absence of hormone secretion. Biological aggressiveness of p-NETs is determined by their degree of differentiation and rate of proliferation, and they are graded as per the World Health Organization’s classification into three grades (G1, G2, and G3). For evaluation and accurate staging of p-NETs, functional imaging has become an integral part of work-up and also guides treatment planning. Treatment decisions largely depend on the patient’s functional status and symptoms, the histological grade and size of the lesions, and the presence or absence of metastatic disease. Treatment options for p-NETs range from curative surgery to observation with close follow-up to palliation and medical therapies, including somatostatin analogues, peptide receptor radionuclide therapy (PRRT), chemotherapy, and targeted treatments.

Bharati, Dr Deepak, Prajwal Bari, Sakshi Nirhali, Jishaan Alam Khan e Pratiksha Umale. "RADIOPHARMACEUTICAL SCIENCE". In Futuristic Trends in Pharmacy & Nursing Volume 3 Book 12, 193–249. Iterative International Publisher, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/v3bgpn12p5ch4.

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Radiopharmaceutical science is a multidisciplinary field that plays a pivotal role in nuclear medicine, utilizing radiopharmaceutical agents for diagnostic imaging, therapeutic applications, and molecular target-specific therapy. This abstract provides an overview of the key aspects and advancements in radiopharmaceutical science. In the realm of diagnostic imaging, radiopharmaceuticals are employed to visualize and assess physiological and pathological processes at the molecular level. Techniques such as Single-Photon Emission Computed Tomography (SPECT) and Positron Emission Tomography (PET) have revolutionized medical imaging by enabling the non-invasive evaluation of organ function and the early detection of diseases like cancer, cardiovascular disorders, and neurological conditions. On the therapeutic front, radiopharmaceuticals are utilized for targeted radiation therapy, known as Radionuclide Therapy or Molecular Radiotherapy. This approach involves administering radiopharmaceuticals that selectively accumulate in specific disease sites, delivering precise and localized radiation to cancerous cells or diseased tissues. The development of innovative alpha and beta-emitting radionuclides has significantly expanded the therapeutic potential, allowing for personalized treatment strategies and improved patient outcomes. Furthermore, the synthesis, production, and quality control of radiopharmaceuticals poses unique challenges. Advanced radiochemistry techniques and automated systems have streamlined the production process, enhancing the availability and accessibility of these vital agents. Ensuring strict adherence to regulatory guidelines and radiopharmaceutical-specific safety protocols is crucial to guaranteeing the highest standard of patient care. The integration of artificial intelligence, machine learning, and image processing algorithms has propelled radiopharmaceutical science into the era of precision medicine. These cutting-edge technologies enable more accurate image analysis, patient-specific dosimetry, and treatment planning, optimizing therapeutic efficacy while minimizing potential side effects.

Atti di convegni sul tema "Abstract Targeted radionuclide therapy (TRT)":

Gill, Martin R., Jyothi U. Menon, Robert Carlisle e Katherine A. Vallis. "Abstract 994: Combining ruthenium metallo-intercalators and targeted radionuclide therapy for EGFR-overexpressing oesophageal cancer". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-994.

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Jensen, Mette Munk, Jesper Fonslet, Camilla S. Knudsen, Troels E. Jeppesen, Andreas I. Jensen, Gregory W. Severin, Carsten H. Nielsen e Andreas Kjær. "Abstract 5203: Tissue factor targeted radionuclide therapy with177Lu-FVIIai inhibits tumor growth of human pancreatic cancer xenografts". In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5203.

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Jagodinsky, Justin C., Ian S. Arthur, Juliana S. Castillo, Ishan Chakravarty, Luke M. Zangl, Ryan J. Brown, Ravi B. Patel et al. "Abstract 477: Comparing type 1 interferon activation in tumor cells following external beam radiotherapy versus targeted radionuclide therapy". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-477.

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Sun, Michael, Muhammad Niaz, Charlene Thomas, Ariel Schaap, Kristine Lacuna, Panagiotis Vlachostergios, Paul Christos et al. "Abstract 6511: Androgen receptor (AR) genomic alterations and clinical outcome with prostate-specific membrane antigen (PSMA)-targeted radionuclide therapy". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6511.

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Jagodinsky, Justin C., Amber M. Bates, Reinier Hernandez, Joseph J. Grudzinski, Ian R. Marsh, Ishan Chakravarty, Ian S. Arthur et al. "Abstract 3060: Temporal analysis of type 1 interferon activation in tumor cells following external beam radiotherapy or targeted radionuclide therapy". In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-3060.

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Potluri, Hemanth Kumar, Reinier Hernandez, Christopher D. Zahm, Joseph Grudzinski, Christopher Massey, Jamey Weichert e Douglas G. McNeel. "Abstract 2262: Low-dose targeted radionuclide therapy has favorable local and systemic effects on immune populations in a murine prostate cancer model". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2262.

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Sosa, Gustavo A., Amber M. Bates, Ravi Patel, Reinier Hernandez, Joseph J. Grudzinski, Ian Marsh, Bryan Bednarz et al. "Abstract 903:In vivoefficacy of bempegaldesleukin, immune checkpoint inhibition, and targeted radionuclide therapy in immunocompetent murine model of head and neck cancer". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-903.

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Kwan, Tanya T., Minh Nguyen, Dirk Zboralski, Anne Schumann, Anne Bredenbeck, Matthias Paschke, Christian Haase et al. "Abstract LBA032: Pan-cancer analysis of fibroblast activation protein alpha (FAP) expression to guide tumor selection for the peptide-targeted radionuclide therapy FAP-2286". In Abstracts: AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; October 7-10, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1535-7163.targ-21-lba032.

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Emma, Sarah E., Amber M. Bates, Reinier Hernandez, Joseph J. Grudzinski, Ian R. Marsh, Justin C. Jagodinsky, Bryan P. Bednarz et al. "Abstract 508: Mechanisms of cooperative response to bempegaldesleukin (BEMPEG) and90Y-NM600 targeted radionuclide therapy in the treatment of a syngeneic murine model of head and neck squamous cell carcinoma". In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-508.

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