Author: "Loureiro L" - Searchworks@Jio Institute Digital Library Search Results

351 results on '"Loureiro L"'

1. The influence of simultaneous pancreas–kidney transplantation on the evolution of diabetic foot lesions and peripheral arterial disease

Author: Monteiro, S. S., Santos, T. S., Pereira, C. A., Duarte, D. B., Neto, H., Gomes, A., Loureiro, L., Martins, J., Silva, F., Martins, L. S., Ferreira, L., Amaral, C., Freitas, C., Carvalho, A. C., Carvalho, R., and Dores, J.
Published: 2023
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2. Evaluation of Ergonomic Risk of Warehouse Activities in a Telecommunications Sector Company

Author: Fernandes, J., Monteiro, R., Carneiro, Paula, Colim, Ana, Loureiro, L., Kacprzyk, Janusz, Series Editor, Arezes, Pedro M., editor, Baptista, J. Santos, editor, Carneiro, Paula, editor, Castelo Branco, Jacqueline, editor, Costa, Nélson, editor, Duarte, J., editor, Guedes, J. C., editor, Melo, Rui B., editor, Miguel, A. Sérgio, editor, and Perestrelo, Gonçalo, editor
Published: 2022
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3. CAR-MEDIATED TARGETING OF NK CELLS OVERCOMES TUMOR IMMUNE ESCAPE CAUSED BY ICAM-1 DOWNREGULATION

Author: Eitler, J., primary, Rackwitz, W., additional, Wotschel, N., additional, Gudipati, V., additional, Shankar, N. Murali, additional, Sidorenkova, A., additional, Huppa, J.B., additional, Montero, P.O., additional, Opitz, C., additional, Künzel, S.R., additional, Michen, S., additional, Temme, A., additional, Loureiro, L., additional, Feldmann, A., additional, Bachmann, M., additional, Boissel, L., additional, Klingemann, H.G., additional, Wels, W.S., additional, and Tonn, T., additional
Published: 2024
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4. UniCAR T-cell potency – A matter of affinity between Adaptor Molecules and Adaptor CAR T-cells?

Author: (0009-0004-8164-4306) Boutier, H., Rodrigues Loureiro, L. R., Hoffmann, L., (0000-0002-1285-5052) Arndt, C., Bartsch, T., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., (0009-0004-8164-4306) Boutier, H., Rodrigues Loureiro, L. R., Hoffmann, L., (0000-0002-1285-5052) Arndt, C., Bartsch, T., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Although Chimeric Antigen Receptor (CAR) T-cells have shown high efficacy in hematologic malignancies, they can cause severe to life-threatening side effects. To address these safety concerns, we have developed adaptor CAR platforms, like the UniCAR system. The redirection of UniCAR T-cells to target cells relies on a Target Module (TM), containing the E5B9 epitope and a tumor-specific binding moiety. Appropriate UniCAR-T activation thus involves two interactions: between the TM and the CAR T-cell, and the TM and the target cell. Here, we investigate if and how alterations of the amino acid sequence of the E5B9 UniCAR epitope impact the interaction between TMs and the UniCAR.We identify the new epitope E5B9L, for which the monoclonal antibody 5B9 has the greatest affinity. We then integrate the E5B9L peptide in previously established TMs directed to Fibroblast Activation Protein (FAP) and assess if such changes in the UniCAR epitope of the TMs affect UniCAR T-cell potency. Binding properties of the newly generated anti-FAP-E5B9L TMs to UniCAR and their ability to redirect UniCAR T-cells were compared side-by-side with the ones of anti-FAP-E5B9 TMs. Despite a substantial variation in the affinity of the different TMs to the UniCAR, no significant differences were observed in the cytotoxic and cytokine-release profiles of the redirected T-cells. Overall, our work indicates that increasing affinity of the UniCAR to the TM does not play a crucial role in such adaptor CAR system, as it does not significantly impact the potency of the UniCAR T-cells.
Published: 2024

5. From Suppression to T cell Activation: Targeting Immune Checkpoints with the RevCAR System

Author: Crespo, E., Rodrigues Loureiro, L. R., Stammberger, A., Rupp, L., Hoffmann, L., (0000-0002-8029-5755) Bachmann, M., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., Crespo, E., Rodrigues Loureiro, L. R., Stammberger, A., Rupp, L., Hoffmann, L., (0000-0002-8029-5755) Bachmann, M., Schmitz, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: T cells can be armed with chimeric antigen receptors (CARs) to target tumor cells, a strategy which has proven successful against some hematological cancers. To overcome some of the dangerous side-effects, a modular system termed RevCAR has been developed. Its components are the RevCAR T cells, which alone cannot bind to any targets, and a bispecific targeting molecule (RevTM). Since the presence of the RevTM is necessary for the system to be functional, it can be used as a safety switch. In addition, different RevTMs can be used with the same T cells to target different antigens, achieving more flexibility. In order to achieve a successful treatment of solid tumors, however, the immune suppression of the tumor microenvironment needs to be overcome. To do this, novel RevTMs were designed which target immune checkpoint molecules such as PD-L1, a pathway which is often exploited by cancer cells to block the immune response. We have successfully shown that, in the presence of these new RevTMs, RevCAR T cells are able to specifically target and kill a wide range of PD-L1-expressing cells, both in monolayer and 3D models. They also release pro-inflammatory cytokines and express activation markers after the co-culture. Furthermore, a combinatorial targeting approach of both a TAA and an immune checkpoint has been proven. Together, these results demonstrate a promising new strategy to apply the RevCAR platform to solid tumors.
Published: 2024

6. 64Cu tumor labeling with hexadentate picolinic acid-based bispidine immunoconjugates

Author: (0000-0001-8857-5922) Kubeil, M., (0000-0002-0646-5808) Neuber, C., Starke, M., (0000-0002-1285-5052) Arndt, C., Rodrigues Loureiro, L. R., Hoffmann, L., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., (0000-0002-1610-1493) Pietzsch, J., Comba, P., (0000-0002-2972-2803) Stephan, H., (0000-0001-8857-5922) Kubeil, M., (0000-0002-0646-5808) Neuber, C., Starke, M., (0000-0002-1285-5052) Arndt, C., Rodrigues Loureiro, L. R., Hoffmann, L., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., (0000-0002-1610-1493) Pietzsch, J., Comba, P., and (0000-0002-2972-2803) Stephan, H.
Abstract: Discussed are two picolinate appended bispidine ligands (3,7-diazabicyclo[3.3.1]nonane derivatives) in comparison with an earlier described bis-pyridine derivative, which are all known to strongly bind CuII. The radiopharmacological characterization of the two isomeric bispidine complexes includes quantitative labeling with 64CuII at ambient conditions with high radiochemical purities and yields (molar activities > 200 MBq/nmol). Challenge experiments in presence of EDTA, cyclam, human serum and SOD demonstrate high stability and inertness of the 64Cu-bispidine complexes. Biodistribution studies performed in Wistar rats indicate a rapid renal elimination for both 64Cu-labeled chelates. The bispidine ligand with the picolinate group in N7 position was selected for further biological experiments, and its backbone was therefore substituted with a benzyl-NCS group at C9. Two tumor target modules (TMs), targeting prostate stem cell antigen (PSCA), overexpressed in prostate cancer, and the fibroblast activation protein (FAP) in fibrosarcoma, were selected for thiourea coupling with the NCS-functionalized ligand and lysine residues of TMs. Small animal PET experiments on tumor-bearing mice showed very good and specific accumulation of the 64Cu-labeled TMs in tumors.
Published: 2024

7. Evaluation of Ergonomic Risk of Warehouse Activities in a Telecommunications Sector Company

Author: Fernandes, J., primary, Monteiro, R., additional, Carneiro, Paula, additional, Colim, Ana, additional, and Loureiro, L., additional
Published: 2021
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8. IMPACTOS DA COVID-19 NA SAÚDE DO IDOSO

Author: OLIVEIRA, J. R. A., primary, SOARES, G. H. S., additional, BARROS, F. M. S., additional, SANTOS, I. T. S., additional, LOUREIRO, L. M. S., additional, VALENCA, M. P. P., additional, and Arraes, Diana Caroline Diniz, additional
Published: 2021
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9. QUANTITATIVE PHARMACOKINETIC MODEL TO CHARACTERIZE AND EXTRAPOLATE LONG-TERM FVIII ACTIVITY LEVELS IN PATIENTS WITH SEVERE HEMOPHILIA A TREATED WITH VALACTOCOGENE ROXAPARVOVEC

Author: Loureiro, L, primary, Henshaw, J, additional, Agarwal, S, additional, Tiede, A, additional, and Robinson, T, additional
Published: 2023
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10. Torrefaction of woody biomasses from poplar SRC and Portuguese roundwood: Properties of torrefied products

Author: Rodrigues, A., Loureiro, L., and Nunes, L.J.R.
Published: 2018
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11. AVALIAÇÃO DA QUALIDADE DAS INFORMAÇÕES DO REGISTRO HOSPITALAR DE CÂNCER DO MUNICÍPIO DE SANTA MARIA, RIO GRANDE DO SUL, BRASIL

Author: CARDOSO, ANDREZA LIMA, primary, BICK, MIGUEL ARMANDO, additional, RIGON, ARLETE LOUREIRO L., additional, PONTES, GRACIELE, additional, CASSOL, REJANE, additional, and PEREIRA, ADRIANA DALLASTA, additional
Published: 2023
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12. Development of UniCAR TM for targeting of FAP positive cells

Author: (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., Robinson, A., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., and Robinson, A.
Abstract: Development of UniCAR TM for targeting of FAP positive cells
Published: 2023

13. Targeting immune checkpoint molecules with RevCAR platform for immunotherapy and modulation of the tumor microenvironment

Author: Crespo, E., Rodrigues Loureiro, L. R., (0000-0002-1285-5052) Arndt, C., Schmitz, M., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., Crespo, E., Rodrigues Loureiro, L. R., (0000-0002-1285-5052) Arndt, C., Schmitz, M., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Chimeric antigen receptors (CARs) are used for redirection of T cells against tumor cells and have demonstrated remarkable therapeutic eﬀects against some hematological cancers. The modular system termed RevCAR can overcome the dangerous side effects associated with conventional CAR T cell therapy, such as cytokine release syndrome. It is composed of RevCAR T cells and a bispecific molecule target module, termed RevTM. This system is highly safe since RevCAR T cell activity can be controlled by RevTM and immediately switched off if side effects are detected. It is also versatile, since the same RevCAR T cell can be directed to different tumor-associated antigens (TAA) simply by adding RevTMs with different specificities. However, to improve the effectiveness in the treatment of solid tumors, the immunosuppressive tumor microenvironment (TME) still needs to be addressed. For this purpose, we have developed novel RevTMs targeting immune checkpoint molecules such as PD-L1, which are often upregulated by cancer cells to escape the immune cells. We have demonstrated that our novel RevTMs can redirect RevCAR T cells to specifically kill cell lines expressing immune checkpoint molecules. In addition to this strategy, the combinatorial targeting of a TAA and an immune checkpoint is very promising strategy to overcome the immunosuppressive microenvironment of solid tumors and thus to improve the treatment outcome.
Published: 2023

14. Therapeutic targeting and diagnostic imaging of Fibroblast Activation Protein expressing cancers using the UniCAR system

Author: Hoffmann, L., Rodrigues Loureiro, L. R., (0000-0002-0646-5808) Neuber, C., Rupp, L., (0000-0001-8857-5922) Kubeil, M., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Hoffmann, L., Rodrigues Loureiro, L. R., (0000-0002-0646-5808) Neuber, C., Rupp, L., (0000-0001-8857-5922) Kubeil, M., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Engineered T cells that express chimeric antigen receptors (CARs) show a big potential in cancer immunological research. They are synthetic receptors that can target antigens independently from the MHC complex. However, most tumor associated antigens are not only expressed on the tumor site but also on healthy tissues. To switch off CAR T cells in case of on-target/off-tumor effects occur, an adaptor CAR platform, called the universal CAR (UniCAR), was developed. In contrast to conventional CAR systems this platform consists of the engineered T cells and a linker molecule, called target module (TM), that is both binding to the target antigen and recognized by the UniCAR T cell. With this approach there is the possibility to switch the system on and off when needed. Fibroblast activation protein (FAP) is a protein of high interest in cancer research as it is upregulated in most of epithelial cancers but shows a comparably low expression in healthy tissues. It is shown to be expressed on cancer associated fibroblasts and therefore plays an important role in the tumor microenvironment where it has pro-tumorigenic activity both in the FAP positive and surrounding cells. Given this, the goal of this work was to develop new TMs against FAP. To achieve such aim, we cloned two TM formats, either based on a single-chain variable fragment (scFv) or an IgG4 based backbone. The difference in the size of the backbones translates into different half-lifes and kinetics. These different TM formats can be used to customize UniCAR therapy according to the given circumstances. We were able to purify and perform various experiments with the mentioned TMs. We could show binding to the target cells using flow cytometry. We could also show that the TMs could be used to induce specific lysis in vitro on monolayer cells and spheroids. We were also able to show UniCAR T cell infiltration into the spheroids and their consequent activation. Moreover, in mouse models the TMs could be used for P
Published: 2023

15. AND-Targeting of EpCAM+ and CEA+ colorectal cells using the modular Dual-RevCAR platform

Author: González Soto, K. E., Rodrigues Loureiro, L. R., Abken, H., Momburg, F., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., González Soto, K. E., Rodrigues Loureiro, L. R., Abken, H., Momburg, F., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Genetically engineered T cells expressing chimeric antigen receptors (CARs) have shown promising results particularly when targeting tumor associated antigens (TAAs) related to hematological malignancies. However, TAAs are usually expressed to some extend also on healthy tissues leading to on-target/off-tumor effects. To overcome this important safety issue along with improving targeting specificity and efficient killing of tumor escape variants, we adapted our Reverse CAR (RevCAR) system to follow an AND-gate Boolean logic. For that, Dual-RevCAR T cells were designed and armed with (I) a signaling (SIG) RevCAR, that includes the intracellular domain (ICD) of CD3 zeta; and (II) a costimulatory (COS) RevCAR, which contains a domain derived from CD28. Because the extracellular domains of both RevCARs are derived from the La/SS-B nuclear protein, Dual-RevCAR T cells will remain inactive until they encounter matching target modules (RevTMs). The bispecific antibody (bsAb)-like structure of the RevTMs allows their binding to RevCAR molecules and to specific antigens. However, only the simultaneous binding of RevTMs to SIG and COS RevCARs will promote the full activation of the Dual-RevCAR T cells. The epithelial cell adhesion molecule (EpCAM) and the carcinoembryonic antigen (CEA) have become appealing markers due to their overexpression in various solid tumor entities such as colorectal cancer, therefore representing promising target antigens for cancer immunotherapies following such a Dual Targeting CAR approach. Having this in mind, the aim of this work was to assess the potential therapeutic application of the Dual-RevCAR system to target EpCAM and CEA following an AND-gating approach.
Published: 2023

16. Using an Adaptor CAR System to Target Fibroblast Activation Protein for Diagnostic and Therapeutic Purposes

Author: Hoffmann, L., Rodrigues Loureiro, L. R., (0000-0002-0646-5808) Neuber, C., Rupp, L., (0000-0001-8857-5922) Kubeil, M., Hagemeyer, C., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Hoffmann, L., Rodrigues Loureiro, L. R., (0000-0002-0646-5808) Neuber, C., Rupp, L., (0000-0001-8857-5922) Kubeil, M., Hagemeyer, C., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: T-cells genetically modified to express chimeric antigen receptors (CARs) are playing a more and more important role in targeted cancer immunotherapy. However, these living drugs can also cause lifethreatening side effects. To overcome such limitations and improve the safety of CAR T-cell therapy, adaptor CAR platforms such as the universal CAR (UniCAR) have been developed. This platform consists of the UniCAR T-cell and a target module (TM) cross-linkage effector and tumor cells. Here, we have established a novel UniCAR system targeting Fibroblast Activation Protein (FAP) that is highly expressed in the tumor microenvironment of epithelial cancers and a marker for cancer-associated fibroblasts. For that, we constructed two novel FAP-directed TMs possessing different sizes and pharmacokinetic properties, in which one is based on a single-chain variable fragment (scFv), and the other is based on an IgG4 backbone. We have shown that both TMs were able to bind to FAP-expressing cells and redirect UniCAR T-cells in vitro to monolayer and spheroid target cells inducing effective killing. Furthermore, we could show infiltration and activation of T-cells in the spheroid setting. Using in vivo models, the TMs were proven to be suitable to be used for PET imaging showing FAP-specific accumulation at the tumor site. Moreover, the immunotherapeutic effect of UniCAR T-cells in combination with FAP TMs was demonstrated using mouse models. In conclusion, in this work, we could show that the two novel anti- FAP TMs prove to hold great theranostic potential for diagnostic imaging and immunotherapy.
Published: 2023

17. Turning an Immunosuppressive Marker Into a T-Cell Activating Signal: Using the RevCAR System to Target Immune Checkpoints

Author: Crespo, E., Rodrigues Loureiro, L. R., (0000-0002-1285-5052) Arndt, C., Schmitz, M., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., Crespo, E., Rodrigues Loureiro, L. R., (0000-0002-1285-5052) Arndt, C., Schmitz, M., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Immunotherapy based on chimeric antigen receptor (CAR) T-cells has demonstrated remarkable therapeutic eﬀects, particularly against some hematological cancers. A versatile adaptor CAR system called RevCAR, consisting of RevCAR T-cells and a bispecific target module (RevTM) has been developed to overcome severe side effects associated with conventional CAR T-cell therapy. As the activity of RevCAR T-cells can be steered based on the availability of RevTM, working as an on/off switch, the system can be immediately turned off if side effects occur. Furthermore, the RevCAR system is highly flexible, since the same RevCAR T-cell can be directed towards different tumor-associated antigens (TAA) simply by adding RevTMs with different specificities. However, the effectiveness of CAR T-cells against solid tumors remains limited particularly due to their immunosuppressive tumor microenvironment (TME). To overcome these hurdles, we have established a novel RevCAR system targeting immune checkpoint molecules such as PD-L1, which are frequently overexpressed by cancer cells to suppress immune responses. We have constructed novel RevTMs that can redirect RevCAR T-cells to kill tumor cells that express such immune checkpoint molecules. Furthermore, true AND gate tumor targeting was achieved by targeting a TAA in addition to PD-L1 in a combinatorial manner using our Dual-RevCAR system. In this way, targeting PD-L1 not only results in Dual-RevCAR T-cell activation but simultaneously blocks the immunosuppressive PD-L1/PD-1 axis. Altogether, we have turned an immunosuppressive marker into an immune-activating signal that might modulate the TME in a beneficial manner, showing promise for the development of an effective immunotherapy against solid tumors.
Published: 2023

18. Lisbon Summer School - Mid-term check - Innovative Target Modules for FAP-Targeting UniCAR T therapy

Author: (0009-0004-8164-4306) Boutier, H., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., (0000-0002-1285-5052) Arndt, C., Hoffmann, L., (0000-0002-8029-5755) Bachmann, M., (0009-0004-8164-4306) Boutier, H., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., (0000-0002-1285-5052) Arndt, C., Hoffmann, L., and (0000-0002-8029-5755) Bachmann, M.
Abstract: This presentation was given in Lisbon for the first OncoProTools Summer School.
Published: 2023

19. A novel ACE2 decoy for both neutralization of SARS-CoV-2 variants and killing of infected cells

Author: Kegler, A., Drewitz, L., (0000-0002-1285-5052) Arndt, C., Daglar, C., Rodrigues Loureiro, L. R., Mitwasi, N., (0000-0002-0646-5808) Neuber, C., González Soto, K. E., Bartsch, T., (0000-0003-1010-2791) Baraban, L., Ziehr, H., Heine, M., Nieter, A., Moreira-Soto, A., Kühne, A., Drexler, J. F., Seliger, B., (0000-0003-4916-3794) Laube, M., Máthé, D., Pályi, B., Hajdrik, P., Forgách, L., Kis, Z., Szigeti, K., (0000-0002-8733-4286) Bergmann, R., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Kegler, A., Drewitz, L., (0000-0002-1285-5052) Arndt, C., Daglar, C., Rodrigues Loureiro, L. R., Mitwasi, N., (0000-0002-0646-5808) Neuber, C., González Soto, K. E., Bartsch, T., (0000-0003-1010-2791) Baraban, L., Ziehr, H., Heine, M., Nieter, A., Moreira-Soto, A., Kühne, A., Drexler, J. F., Seliger, B., (0000-0003-4916-3794) Laube, M., Máthé, D., Pályi, B., Hajdrik, P., Forgách, L., Kis, Z., Szigeti, K., (0000-0002-8733-4286) Bergmann, R., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: The COVID-19 pandemic caused by SARS-CoV-2 led to millions of infections and deaths worldwide. As this virus evolves rapidly, there is a high need for treatment options, which can win the race against new emerging variants of concern. Here, we describe a novel immunotherapeutic drug based on the SARS-CoV-2 entry receptor ACE2 and provide experimental evidence that it cannot only be used for (i) neutralization of SARS-CoV-2 in vitro and in SARS-CoV-2 infected animal models, but also for (ii) clearance of virus infected cells. For the latter purpose, we equipped the ACE2 decoy with an epitope tag. Thereby, we converted it to an adapter molecule which we successfully applied in the modular platforms UniMAB and UniCAR for retargeting of either unmodified or universal chimeric antigen receptor modified immune effector cells. Our results pave the way for a clinical application of this novel ACE2 decoy, which will clearly improve COVID-19 treatment.
Published: 2023

20. Targeting colorectal cancer cells using AND-gated Adaptor RevCAR T-cells

Author: González Soto, K. E., Rodrigues Loureiro, L. R., Bartsch, T., (0000-0002-1285-5052) Arndt, C., Kegler, A., Mitwasi, N., Drewitz, L., Hoffmann, L., Abdelfatah Saleh Hassan, H. A., Crespo, E., Mehnert, M., Daglar, C., Abken, H., Momburg, F., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., González Soto, K. E., Rodrigues Loureiro, L. R., Bartsch, T., (0000-0002-1285-5052) Arndt, C., Kegler, A., Mitwasi, N., Drewitz, L., Hoffmann, L., Abdelfatah Saleh Hassan, H. A., Crespo, E., Mehnert, M., Daglar, C., Abken, H., Momburg, F., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Despite the success of chimeric antigen receptor (CAR) T-cells especially for treating hematological malignancies, critical drawbacks, such as “on-target, off-tumor” toxicities, need to be addressed to improve safety in translating to clinical application. This is especially true, when targeting tumor-associated antigens (TAAs) that are not exclusively expressed by solid tumors but also on healthy tissues. To improve the safety profile, we developed switchable adaptor CAR systems including the RevCAR system. RevCAR T-cells are activated by cross-linking of bifunctional adaptor molecules termed target modules (RevTM). In a further development, we established a Dual-RevCAR system for an AND-gated combinatorial targeting by splitting the stimulatory and co-stimulatory signals of the RevCAR T-cells on two individual CARs. Examples of common markers for colorectal cancer (CRC) are the carcinoembryonic antigen (CEA) and the epithelial cell adhesion molecule (EpCAM), while these antigens are also expressed by healthy cells. Here we describe four novel structurally different RevTMs for targeting of CEA and EpCAM. All anti-CEA and anti-EpCAM RevTMs were validated and the simultaneous targeting of CEA+ and EpCAM+ cancer cells redirected specific in vitro and in vivo killing by Dual-RevCAR T-cells. In summary, we describe the development of CEA and EpCAM specific adaptor RevTMs for monospecific and AND-gated targeting of CRC cells via the RevCAR platform as an improved approach to increase tumor specificity and safety of CAR T-cell therapies.
Published: 2023

21. Design and Biological Evaluation of Small-Molecule PET-Tracers for Imaging of Programmed Death Ligand 1

Author: Krutzek, F., Donat, C., (0000-0001-6104-6676) Ullrich, M., (0000-0002-7571-4732) Zarschler, K., Ludik, M.-C., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., (0000-0003-4846-1271) Kopka, K., (0000-0003-2276-5330) Stadlbauer, S., Krutzek, F., Donat, C., (0000-0001-6104-6676) Ullrich, M., (0000-0002-7571-4732) Zarschler, K., Ludik, M.-C., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., (0000-0003-4846-1271) Kopka, K., and (0000-0003-2276-5330) Stadlbauer, S.
Abstract: Noninvasive molecular imaging of the PD-1/PD-L1 immune checkpoint is of high clinical relevance for patient stratification and therapy monitoring in cancer patients. Here we report nine small-molecule PD-L1 radiotracers with solubilizing sulfonic acids and a linker–chelator system, designed by molecular docking experiments and synthesized according to a new, convergent synthetic strategy. Binding affinities were determined both in cellular saturation and real-time binding assay (LigandTracer), revealing dissociation constants in the single digit nanomolar range. Incubation in human serum and liver microsomes proved in vitro stability of these compounds. Small animal PET/CT imaging, in mice bearing PD-L1 overexpressing and PD-L1 negative tumors, showed moderate to low uptake. All compounds were cleared primarily through the hepatobiliary excretion route and showed a long circulation time. The latter was attributed to strong blood albumin binding effects, discovered during our binding experiments. Taken together, these compounds are a promising starting point for further development of a new class of PD-L1 targeting radiotracers.
Published: 2023

22. FLT3-directed UniCAR T-cell therapy of Acute Myeloid Leukaemia

Author: Peschke, J., (0000-0002-8733-4286) Bergmann, R., Mehnert, M., González Soto, K. E., Rodrigues Loureiro, L. R., Mitwasi, N., Kegler, A., Altmann, H., Wobus, M., Máthé, D., Szigeti, K., (0000-0001-5099-2448) Feldmann, A., Bornhäuser, M., (0000-0002-8029-5755) Bachmann, M., Fasslrinner, F., (0000-0002-1285-5052) Arndt, C., Peschke, J., (0000-0002-8733-4286) Bergmann, R., Mehnert, M., González Soto, K. E., Rodrigues Loureiro, L. R., Mitwasi, N., Kegler, A., Altmann, H., Wobus, M., Máthé, D., Szigeti, K., (0000-0001-5099-2448) Feldmann, A., Bornhäuser, M., (0000-0002-8029-5755) Bachmann, M., Fasslrinner, F., and (0000-0002-1285-5052) Arndt, C.
Abstract: Adaptor chimeric antigen receptor (CAR) T-cell therapy offers solutions for improved safety and antigen escape which represent main obstacles for the clinical translation of CAR T-cell therapy in myeloid malignancies. The adaptor CAR T-cell platform “UniCAR” is currently under early clinical investigation. Recently, first proof-of-concept of a well-tolerated, rapidly switchable, CD123-directed UniCAR T-cell product treating patients with acute myeloid leukaemia (AML) was reported. Relapsed and refractory AML is prone to a high plasticity under therapy pressure targeting one single tumour antigen. Thus, targeting of multiple tumour antigens seems to be required to achieve durable anti-tumour responses, underlining the need to further design alternative AML-specific target modules (TM) for the UniCAR platform. We here present the preclinical development of a novel FMS-like tyrosine kinase 3 (FLT3)-directed UniCAR T-cell therapy, which is highly effective for in vitro killing of both AML cell lines and primary AML samples. Furthermore, we show in vivo functionality in a murine xenograft model. PET analyses further demonstrate a short serum half-life of FLT3 TMs, which will enable a rapid on/off-switch of UniCAR T-cells. Overall, the presented preclinical data encourage the further development and clinical translation of FLT3-specific UniCAR T-cells for the therapy of AML.
Published: 2023

23. Immunotheranostic target modules for imaging and navigation of UniCAR T-cells to strike FAP-expressing cells and the tumor microenvironment

Author: Rodrigues Loureiro, L. R., Hoffmann, L., (0000-0002-0646-5808) Neuber, C., Rupp, L., (0000-0002-1285-5052) Arndt, C., Kegler, A., (0000-0001-8857-5922) Kubeil, M., Hagemeyer, C. E., (0000-0002-2972-2803) Stephan, H., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Rodrigues Loureiro, L. R., Hoffmann, L., (0000-0002-0646-5808) Neuber, C., Rupp, L., (0000-0002-1285-5052) Arndt, C., Kegler, A., (0000-0001-8857-5922) Kubeil, M., Hagemeyer, C. E., (0000-0002-2972-2803) Stephan, H., Schmitz, M., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Background: Chimeric antigen receptor (CAR) T-cells are a promising approach in cancer immunotherapy, particularly for treating hematologic malignancies. Yet, their effectiveness is limited when tackling solid tumors, where immune cell infiltration and immunosuppressive tumor microenvironments (TME) are major hurdles. Fibroblast activation protein (FAP) is highly expressed on cancer-associated fibroblasts (CAFs) and various tumor cells, playing an important role in tumor growth and immunosuppression. Aiming to modulate the TME with increased clinical safety and effectiveness, we developed novel small and size-extended immunotheranostic UniCAR target modules (TMs) targeting FAP. Methods: The specific binding and functionality of the anti-FAP-scFv TM and the size extended anti-FAP-IgG4 TM were assessed using 2D and 3D in vitro models as well as in vivo. Their specific tumor accumulation and diagnostic potential was evaluated using PET studies after functionalization with a chelator and suitable radionuclide. Results: The anti-FAP-scFv and -IgG4 TMs effectively and specifically redirected UniCAR T-cells using 2D, 3D, and in vivo models. Moreover, a remarkably high and specific accumulation of radiolabeled FAP-targeting TMs at the tumor site of xenograft mouse models was observed. Conclusions: These findings demonstrate that the novel anti-FAP TMs are promising immunotheranostic tools to foster cancer imaging and treatment, paving the way for a more convenient, individualized, and safer treatment of cancer patients.
Published: 2023

24. Palbociclib impairs the proliferative capacity of activated T cells while retaining their cytotoxic efficacy

Author: (0000-0002-1285-5052) Arndt, C., Tunger, A., Wehner, R., Rothe, R., Kourtellari, E., Luttosch, S., Hannemann, K., Koristka, S., Loureiro, L. R., (0000-0001-5099-2448) Feldmann, A., Tonn, T., Link, T., Kuhlmann, J. D., Wimberger, P., (0000-0002-8029-5755) Bachmann, M., Schmitz, M., (0000-0002-1285-5052) Arndt, C., Tunger, A., Wehner, R., Rothe, R., Kourtellari, E., Luttosch, S., Hannemann, K., Koristka, S., Loureiro, L. R., (0000-0001-5099-2448) Feldmann, A., Tonn, T., Link, T., Kuhlmann, J. D., Wimberger, P., (0000-0002-8029-5755) Bachmann, M., and Schmitz, M.
Abstract: The cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor palbociclib is an emerging cancer therapeutic that just recently gained Food and Drug Administration approval for treatment of estrogen receptor (ER)-positive, human epidermal growth factor receptor (Her)2-negative breast cancer in combination with the ER degrader fulvestrant. However, CDK4/6 inhibitors are not cancer-specific and may affect also other proliferating cells. Given the importance of T cells in antitumor defense, we studied the influence of palbociclib/fulvestrant on human CD3+ T cells and novel emerging T cell-based cancer immunotherapies. Palbociclib considerably inhibited the proliferation of activated T cells by mediating G0/G1 cell cycle arrest. However, after stopping the drug supply this suppression was fully reversible. In light of combination approaches, we further investigated the effect of palbociclib/fulvestrant on T cell-based immunotherapies by using a CD3-PSCA bispecific antibody or universal chimeric antigen receptor (UniCAR) T cells. Thereby, we observed that palbociclib clearly impaired T cell expansion. This effect resulted in a lower total concentration of interferon-g and tumor necrosis factor, while palbociclib did not inhibit the average cytokine release per cell. In addition, the cytotoxic potential of the redirected T cells was unaffected by palbociclib and fulvestrant. Overall, these novel findings may have implications for the design of treatment modalities combining CDK4/6 inhibition and T cell-based cancer immunotherapeutic strategies.
Published: 2023

25. Specific and safe targeting of glioblastoma using switchable and logic-gated RevCAR T cells

Author: Abdelfatah Saleh Hassan, H. A., Mitwasi, N., (0000-0001-6104-6676) Ullrich, M., (0000-0001-8857-5922) Kubeil, M., (0000-0002-1136-3857) Toussaint, M., (0000-0003-3168-3062) Deuther-Conrad, W., (0000-0002-0646-5808) Neuber, C., (0000-0002-1285-5052) Arndt, C., Rodrigues Loureiro, L. R., Kegler, A., González Soto, K. E., Belter, B., Rössig, C., (0000-0002-1610-1493) Pietzsch, J., Frenz, M., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., Abdelfatah Saleh Hassan, H. A., Mitwasi, N., (0000-0001-6104-6676) Ullrich, M., (0000-0001-8857-5922) Kubeil, M., (0000-0002-1136-3857) Toussaint, M., (0000-0003-3168-3062) Deuther-Conrad, W., (0000-0002-0646-5808) Neuber, C., (0000-0002-1285-5052) Arndt, C., Rodrigues Loureiro, L. R., Kegler, A., González Soto, K. E., Belter, B., Rössig, C., (0000-0002-1610-1493) Pietzsch, J., Frenz, M., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Glioblastoma (GBM) is still an incurable tumor that is associated with high recurrence rate and poor survival despite the current treatment regimes. With the urgent need for novel therapeutic strategies, immunotherapies, especially chimeric antigen receptor (CAR)-expressing T cells, represent a promising approach for specific and effective targeting of GBM. However, CAR T cells can be associated with serious side effects. To overcome such limitation, we applied our switchable RevCAR system to target both the epidermal growth factor receptor (EGFR) and the disialoganglioside GD2, which are expressed in GBM. The RevCAR system is a modular platform that enables controllability, improves safety, specificity and flexibility. Briefly, it consists of RevCAR T cells having a peptide epitope as extracellular domain, and a bispecific target module (RevTM). The RevTM acts as a switch key that recognizes the RevCAR epitope and the tumor-associated antigen, and thereby activating the RevCAR T cells to kill the tumor cells. However, in the absence of the RevTM, the RevCAR T cells are switched off. In this study, we show that the novel EGFR/GD2-specific RevTMs can selectively activate RevCAR T cells to kill GBM cells. Moreover, we show that gated targeting of GBM is possible with our Dual-RevCAR T cells, which have their internal activation and co-stimulatory domains separated into two receptors. Therefore, a full activation of Dual-RevCAR T cells can only be achieved when both receptors recognize EGFR and GD2 simultaneously via RevTMs, leading to a significant killing of GBM cells both in vitro and in vivo.
Published: 2023

26. Development Of A Novel ACE2 Decoy For Both SARS-CoV-2 Variant Neutralization And Infected Cell Elimination Via Unmodified Or CAR Modified Immune Cells

Author: Drewitz, L., Kegler, A., (0000-0002-1285-5052) Arndt, C., Daglar, C., Rodrigues Loureiro, L. R., Mitwasi, N., (0000-0002-0646-5808) Neuber, C., González Soto, K. E., Bartsch, T., (0000-0003-1010-2791) Baraban, L., Ziehr, H., Heine, M., Nieter, A., Moreira-Soto, A., Kühne, A., Drexler, J. F., Seliger, B., (0000-0003-4916-3794) Laube, M., Máthé, D., Pályi, B., Hajdrik, P., Forgách, L., Kis, Z., Sziget, K., (0000-0002-8733-4286) Bergmann, R., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Drewitz, L., Kegler, A., (0000-0002-1285-5052) Arndt, C., Daglar, C., Rodrigues Loureiro, L. R., Mitwasi, N., (0000-0002-0646-5808) Neuber, C., González Soto, K. E., Bartsch, T., (0000-0003-1010-2791) Baraban, L., Ziehr, H., Heine, M., Nieter, A., Moreira-Soto, A., Kühne, A., Drexler, J. F., Seliger, B., (0000-0003-4916-3794) Laube, M., Máthé, D., Pályi, B., Hajdrik, P., Forgách, L., Kis, Z., Sziget, K., (0000-0002-8733-4286) Bergmann, R., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a pandemic with millions of infections and deaths worldwide and devastating impact on global economy. Up to now, vaccines and monoclonal antibody (mAb) therapies lack to provide a long-lasting protection against rapidly evolving new emerging SARS-CoV-2 variants. Thus, novel therapeutic options are pressingly needed especially for immunocompromised patients and/or patients with high risk for developing a severe coronavirus disease 2019 (COVID-19). In that regard, we developed a novel immunotherapeutic drug based on the SARS-CoV-2 entry receptor angiotensin-converting enzyme 2 (ACE2). This ACE2 decoy potently binds to the SARS-CoV-2 receptor binding domain (RBD), neutralizes SARS-CoV-2 as well as the Delta and Omicron variant and protects hamsters from a SARS-CoV-2 infection. To additionally use this ACE2 decoy for elimination of virus infected cells, we equipped it with an epitope tag. Thus, it can be applied as adapter molecule in the modular platform technologies UniMAB and UniCAR, which already demonstrated great success in the setting of malignant diseases. As adapter molecule the ACE2 decoy is able to efficiently recruit either universal chimeric antigen receptor (UniCAR) modified T cells or, in combination with an anti-peptide epitope-anti-CD3 bispecific Ab of the UniMAB system, unmodified T cells to efficiently kill SARS-CoV-2 RBD expressing human cells. Taken together, the ACE2 decoy represents a very promising immunotherapeutic drug for both SARS-CoV-2 variant neutralization and infected cell killing via the UniMAB and UniCAR system and might, therefore, clearly improve the treatment of COVID-19 patients.
Published: 2023

27. Data publication: Design and Biological Evaluation of Small-Molecule PET-Tracers for Imaging of Programmed Death Ligand 1

Author: Krutzek, F., Donat, C., (0000-0001-6104-6676) Ullrich, M., (0000-0002-7571-4732) Zarschler, K., Ludik, M.-C., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., (0000-0003-4846-1271) Kopka, K., (0000-0003-2276-5330) Stadlbauer, S., Krutzek, F., Donat, C., (0000-0001-6104-6676) Ullrich, M., (0000-0002-7571-4732) Zarschler, K., Ludik, M.-C., (0000-0001-5099-2448) Feldmann, A., Rodrigues Loureiro, L. R., (0000-0003-4846-1271) Kopka, K., and (0000-0003-2276-5330) Stadlbauer, S.
Abstract: Bei diesem Datensatz handelt es sich um die chemische Charakterisierung der Verbindungen, die in-vitro-, in-vivo- und ex-vivo-Daten.
Published: 2023

28. Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Author: Adisa, A, Bahrami-Hessari, M, Bhangu, A, George, C, Ghosh, D, Glasbey, J, Haque, P, Ingabire, J, Kamarajah, S, Kudrna, L, Ledda, V, Li, E, Lillywhite, R, Mittal, R, Nepogodiev, D, Ntirenganya, F, Picciochi, M, Simões, J, Booth, L, Elliot, R, Kennerton, A, Pettigrove, K, Pinney, L, Richard, H, Tottman, R, Wheatstone, P, Wolfenden, J, Smith, A, Sayed, A, Goswami, A, Malik, A, Mclean, A, Hassan, A, Nazimi, A, Aladna, A, Abdelgawad, A, Saed, A, Abdelmageed, A, Ghannam, A, Mahmoud, A, Alvi, A, Ismail, A, Adesunkanmi, A, Ebrahim, A, Al-Mallah, A, Alqallaf, A, Durrani, A, Gabr, A, Kirfi, A, Altaf, A, Almutairi, A, Sabbagh, A, Ajiya, A, Haddud, A, Alnsour, A, Singh, A, Mittal, A, Semple, A, Adeniran, A, Negussie, A, Oladimeji, A, Muhammad, A, Yassin, A, Gungor, A, Tarsitano, A, Soibiharry, A, Dyas, A, Frankel, A, Peckham-Cooper, A, Truss, A, Issaka, A, Ads, A, Aderogba, A, Adeyeye, A, Ademuyiwa, A, Sleem, A, Papa, A, Cordova, A, Appiah-Kubi, A, Meead, A, Nacion, A, Michael, A, Forneris, A, Duro, A, Gonzalez, A, Altouny, A, Ghazal, A, Khalifa, A, Ozair, A, Quzli, A, Haddad, A, Othman, A, Yahaya, A, Elsherbiny, A, Nazer, A, Tarek, A, Abu-Zaid, A, Al-Nusairi, A, Azab, A, Elagili, A, Elkazaz, A, Kedwany, A, Nuhu, A, Sakr, A, Shehta, A, Shirazi, A, Mohamed, A, Sherif, A, Awad, A, Abbas, A, Abdelrahman, A, Ammar, A, Azzam, A, Ciftci, A, Dural, A, Sanli, A, Rahy-Martín, A, Tantri, A, Khan, A, Al-Touny, A, Tariq, A, Gmati, A, Costas-Chavarri, A, Auerkari, A, Landaluce-Olavarria, A, Puri, A, Radhakrishnan, A, Ubom, A, Pradhan, A, Turna, A, Adepiti, A, Kuriyama, A, Kassam, A, Hassouneh, A, El-Hussuna, A, Habeebullah, A, Mousli, A, Biloslavo, A, Hoang, A, Kirk, A, Santini, A, Melero, A, Calvache, A, Baduell, A, Chan, A, Abrate, A, Balduzzi, A, Sánchez, A, Navarrete-Peón, A, Porcu, A, Brolese, A, Barranquero, A, Saibene, A, Adam, A, Vagge, A, Maquilón, A, Leon-Andrino, A, Sekulić, A, Trifunovski, A, Mako, A, Bedada, A, Broglia, A, Coppola, A, Giani, A, Grandi, A, Iacomino, A, Moro, A, D’Amico, A, Malagnino, A, Tang, A, Doyle, A, Alfieri, A, Haynes, A, Wilkins, A, Baldwin, A, Heriot, A, Laird, A, Lazarides, A, O'Connor, A, Trulson, A, Rokohl, A, Caziuc, A, Triantafyllou, A, Anesi, A, Nikova, A, Andrianakis, A, Charalabopoulos, A, Tsolakidis, A, Chirca, A, Arnaud, A, Narvaez-Rojas, A, Kavalakat, A, Spina, A, Recordare, A, Annicchiarico, A, Conti, A, Mohammed, A, Kocataş, A, Almhimid, A, Arnaout, A, Fahmy, A, Mangi, A, Modabber, A, Ulas, A, Mohamedahmed, A, Frontali, A, Moynihan, A, Yunus, A, Ahmad, A, Kent, A, Khamees, A, Ugwu, A, Turan, A, Navarro-Barrios, A, Yebes, A, De Sousa, Á, Moreno, A, Sethi, A, Dawson, A, Kaur, A, Wolde, A, Antonelli, A, Scifo, A, Alhamad, A, Davis, A, Alderazi, A, Harky, A, Mohammed-Durosinlorun, A, Seguya, A, Okhakhu, A, Chamakhi, A, Sebai, A, Souadka, A, Asla, A, Agrawal, A, Persad, A, Gupta, A, Elgazar, A, Kulkarni, A, Coates, A, Bellés, A, Hadzibegovic, A, Jotic, A, Kowark, A, Martins, A, Pineda, A, Peral, A, Gollarte, A, Senent-Boza, A, Camarena, A, Castaño-Leon, A, Bravo, A, Musina, A, Tapia-Herrero, A, Kothari, A, Raja, A, Aljaiuossi, A, Taha, A, Majbar, A, Prodromidou, A, Kanatas, A, Gupte, A, Zakaria, A, Balla, A, Barberis, A, Bondurri, A, Bottari, A, Costantino, A, Figus, A, Lauretta, A, Mingoli, A, Romanzi, A, Sagnotta, A, Scacchi, A, Picchetto, A, Valadez, A, Luzzi, A, Älgå, A, Fontalis, A, Hecker, A, Demetriades, A, Serban, A, Văcărașu, A, Cokan, A, Isaza-Restrepo, A, Beamish, A, Schache, A, Stevenson, A, Yiu, A, Cockbain, A, Litvin, A, Abad-Motos, A, Becerra, A, Ramos, Á, Chiaradia, A, Dell, A, Romano, A, Pascale, A, Marra, A, Dimas, A, Kolias, A, Cerovac, A, Koneru, A, Tidjane, A, Agbeko, A, Bajaj, A, Gosain, A, Allan, A, Carreras-Castañer, A, D'Amore, A, Dare, A, Maffioli, A, Palepa, A, Paspala, A, Konney, A, Gatta, A, Ezanno, A, Yiallourou, A, Kinnair, A, Rayner, A, Scafa, A, Bowan, A, Veglia, A, Russo, A, Maniaci, A, Castaldi, A, Gil-Moreno, A, Maffuz-Aziz, A, Meola, A, Nenna, A, Ferrer, A, Bonilla, A, Ramos-De La Medina, A, Infante, A, Santoro, A, Laganà, A, Bateman, A, Abozid, A, Seidu, A, Lowery, A, Tantraworasin, A, Rasheed, A, Picciariello, A, Isik, A, Saif, A, Anjum, A, Ioannidis, A, Abeldaño, A, Hussain, A, Nathan, A, Bedzhanyan, A, Perfecto, A, De Virgilio, A, Galvan, A, Sablotzki, A, Böttcher, A, Pellacani, A, Gatti, A, Ibrahimli, A, Menon, A, Sahni, A, Mwenda, A, Choudhry, A, Jayawardane, A, Ramasamy, A, Mitul, A, Bawa, A, Nugur, A, Rammohan, A, Sachdeva, A, Mehraj, A, Yildirim, A, Alqaseer, A, Radwan, A, Sallam, A, Syllaios, A, Tampakis, A, Alwael, A, Samara, A, Eroglu, A, Rahman, A, Ulkucu, A, Zaránd, A, Dulskas, A, Tawiah, A, Zani, A, Vas, A, Lukosiute-Urboniene, A, Adamu, A, Aujayeb, A, İplikçi, A, Mahmud, A, Cil, A, Makanjuola, A, Akwaisah, A, Galandarova, A, Saracoglu, A, Regan, A, Barlas, A, Alhassan, B, Mostafa, B, Hamida, B, Torun, B, Abdullah, B, Balagobi, B, Banky, B, Singh, B, Alegbeleye, B, Yigit, B, Hajjaj, B, Burgos-Blasco, B, Seeliger, B, Alayande, B, Alhazmi, B, Enodien, B, Torre, B, Pérez, B, Tamayo, B, De Andrés-Asenjo, B, Quintana-Villamandos, B, Girgin, B, Barmayehvar, B, Beisenov, B, Creavin, B, Dunne, B, Marson, B, Waterson, B, Martin, B, Zucker, B, Wong, B, Ozmen, B, Hammond, B, Mbwele, B, Núñez, B, Dhondt, B, Gafsi, B, Mcleish, B, Lieske, B, Tailor, B, La Pira, B, Picardi, B, Zampogna, B, Casagranda, B, Festa, B, Panda, B, Kirmani, B, Sulaiman, B, Gurung, B, Zacharia, B, Bette, B, Ayana, B, Nikolovska, B, Vilaró, B, De Vega Sánchez, B, Hameed, B, Diaconescu, B, Kovacevic, B, Bumber, B, Sakakushev, B, Tadic, B, Malek, B, Alrayes, B, Thomas, B, Gális, B, Gallagher, B, Knowles, B, Cunningham, B, Daley, B, Mishra, B, Ashford, B, Pirozzi, B, Berselli, B, Martinez-Leo, B, Sensi, B, Nardo, B, Celik, B, Giray, B, Abud, B, Almiqlash, B, Pramesh, C, Taskiran, C, De Campos Prado, C, Cipolla, C, Kumar, C, English, C, Riccetti, C, Vanni, C, Brasset, C, Downey, C, Duffy, C, Chwat, C, 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Mostafa, Shalaby, Mostafa, Farhan-Alanie, Muhamed, Farooq, Muhammad, Musadaq, Muhammad, Arshad, Muhammad, Anjum, Muhammad Ayyub, Usman, Muhammad, Chaudhary, Muhammad Amjad, Raza, Muhammad Asif, Karim, Muhammad Fairuz Shah Abd, Chaudhary, Muhammad Hamid, Janjua, Muhammad Haris, Khokhar, Muhammad Imran, Malik, Muhammad Isfandyar Khan, Pirzada, Muhammad Taqi, Younis, Muhammad Umar, Elhadi, Muhammed, Suer, Muhammed Salih, Ergenç, Muhammer, Binnawara, Muhannud, Emmanuel, Muhawenimana, Abbasi, Mujeeb, Naimzada, Mukhammad David, Kulimbet, Mukhtar, Kusunoki, Munenori, Eugene, Muneza, Chauhan, Munish, Shokor, Muntaser Abu, Aljiffry, Murad, Kalın, Murat, Kurawa, Musbahu, Dincer, Müserref Beril, Tolani, Musliu Adetola, Soytas, Mustafa, Yakubu, Mustapha, Usman, Mustapha Ibrahim, Aremu, Muyiwa, Paranyak, Mykola, Talat, Nabila, Kausar, Nabila, Dudi-Venkata, Nagendra, Bazzi, Nagham, Hasan, Najat Ben, Van Wyk, Naomi Natasha, Shaban, Naseebah, Almgla, Naser, Kandevani, Naser Yousefzadeh, Alzerwi, Nasser, Alvarez, Natalia, Motas, Natalia, Rincón, Natalia Andrea Rivera, Blencowe, Natalie, Simon, Natalie, Aghtarafi, Natasha, Ghuman, Navdeep Kaur, Sharma, Naveen, Wijekoon, Naveen, Kumar, Navin, Hassan, Naya, Onyemaechi, Ndubuisi, Prijović, Nebojša, Özçay, Necdet, Goel, Neha, Segaren, Neil, Sharma, Neil, Kalyva, Nektaria, Palacios, Nelson Morales, Alonso, Nestor Fabian Pedraza, Onyeagwara, Ngozi, Petrucciani, Niccolò, Daddi, Niccolo’, Lightfoot, Nicholas, Power, Nicholas, Segaren, Nicholas, Starr, Nichole, Dreger, Nici Markus, Cillara, Nicola, Colucci, Nicola, Eardley, Nicola, Tartaglia, Nicola, Zanini, Nicola, Bacalbasa, Nicolae, Campuzano, Nicolas, Mouawad, Nicolas, Federico, Nicoletta Sveva Pipitone, Tamini, Nicolò, Mariani, Nicolò Maria, Beasley, Nigel, Adu-Aryee, Nii Armah, Burlov, Nikita, Dimitrokallis, Nikolaos, Gouvas, Nikolaos, Machairas, Nikolaos, Memos, Nikolaos, Thomakos, Nikolaos, Tsakiridis, Nikolaos, Schizas, Nikolaos, Börner, Nikolaus, Theochari, Nikoletta, Al-Saadi, Nina, Glass, Nina, Horesh, Nir, R, Nissi Evelyn, Gahlot, Nitesh, Ismail, Nizar, Aljirdabi, Noof, Maria, Noor Ul Huda, Trabulsi, Nora, Akeel, Nouf, Borges, Nuno, Moda, Nupur, Redondo, Nuria Villacé, Nyarko, Obed Ofori, Ginghina, Octav, Enciu, Octavian, Okere, Oghenekevwe, Ekwunife, Okechukwu Hyginus, Quadri, Oladeji, Ogundoyin, Olakayode, Tucker, Olga, Mateo-Sierra, Olga, Azzis, Olivier, Ojewuyi, Olufemi, Habeeb, Olufemi, Idowu, Olufemi, Elebute, Olumide, Agboola, Oluseyi, Ladipo-Ajayi, Oluwaseun, Oyinloye, Oluwaseun, Adebola, Oluwaseyi, Ekor, Oluwayemisi, Ogundoyin, Oluwole, Salamanca, Omar, Vergara-Fernandez, Omar, Wafi, Omar, Aladawi, Omar, Bahassan, Omar Mohammed, Tammo, Ömer, Ozkan, Omer Faruk, Williams, Omolara Modupe, Salami, Omotayo, Akinajo, Opeyemi, Sakhov, Orazbek, Gallo, Oreste, Sole, Oriol Martin, Milella, Oronzo, Alser, Osaid, Bettar, Osama Al, Alomar, Osama, Osman, Osama Saeed, Aisuodionoe-Shadrach, Oseremen, Basnayake, Oshan, Bozbiyik, Osman, Hodges, Owen, Ojo, Owolabi, Yanık, Özge, Mutlu, Özgecan Pırıl Zanbak, Kazan, Ozgur, Calavia, Pablo, García, Pablo Rodríguez, Urriza, Pablo Vallés, Lopez, Paloma Rodriguez, Christidis, Panagiotis, Dorovinis, Panagiotis, Kokoropoulos, Panagiotis, Mourmouris, Panagiotis, Papatheodorou, Panayiotis, Garg, Pankaj Kumar, Patel, Panna, Vassiliu, Panteleimon, Campennì, Paola, De Nardi, Paola, Bernante, Paolo, Ubiali, Paolo, Baroffio, Paolo, Pizzini, Paolo, Sapienza, Paolo, Myrelid, Par, Chatzikomnitsa, Paraskevi, Tsiantoula, Paraskevi, Gada, Parth, Avella, Pasquale, Cianci, Pasquale, Romero, Patricia, Méndez, Patricia Serrano, Pazmiño, Patricio Andrés Freile, Coughlin, Patrick, Kirchweger, Patrick, Pessaux, Patrick, Maguire, Patrick J, Petrone, Patrizio, Cullis, Paul, Köglberger, Paul, Marriott, Paul, Nankivell, Paul, Santos-Costa, Paulo, Martins, Paulo N, Panahi, Pedram, Botelho, Pedro, Teixeira, Pedro, Escobar, Pedro, Vázquez, Pedro José Gil, Gribnev, Petar, Nolte, Peter, Agbonrofo, Peter, Bobak, Peter, Choong, Peter, Elbe, Peter, Hutchinson, Peter, Labib, Peter, Paal, Peter, Pockney, Peter, Reemst, Peter, Szatmary, Peter, Vaughan-Shaw, Peter G, Alexander, Philip, Pucher, Philip, Stather, Philip, Foessleitner, Philipp, Winnand, Philipp, Zehnder, Philipp, Kruse, Philippe, Matos, Philomena Alice Wawer, Lapolla, Pierfrancesco, Cicerchia, Pierfranco Maria, Solli, Piergiorgio, Di Lascio, Pierpaolo, Zarif, Pierre, Champagne, Pierre-Olivier, Anoldo, Pietro, Bertoglio, Pietro, Fransvea, Pietro, Familiari, Pietro, Lombardi, Pietro Maria, Stogowski, Piotr Tomasz, Bruzzaniti, Placido, Tripathi, Prashant, D'sa, Prashanth, Salunke, Pravin, Shah, Pritik A, Punjabi, Prof Prakash P, Christodoulou, Prokopis, Hamdan, Qusai, Tawalbeh, Ra'fat, Gadelkareem, Rabea, Awad, Rabih, Callcut, Rachael, Clegg, Rachael, Choron, Rachel, Payne, Rachel, Gefen, Rachel, Costea, Radu, Drasovean, Radu, Mirica, Radu Mihail, Ravindra, Raevin, Fajardo, Rafael Torres, Nunes, Rafael Leite, Aspide, Raffaele, Lombardi, Raffaele, Vidya, Raghavan, Elboraei, Rahma, Saaid, Rahmah, Ghodke, Rahul, Gupta, Rahul, Sharma, Rahul Deo, Lunevicius, Raimundas, Kalayarasan, Raja, Mohan, Rajashekar, Singh, Rajdeep, Sivaprakasam, Rajesh, Seenivasagam, Rajkumar Kottayasamy, Rajendram, Rajkumar, Radulescu, Raluca Bievel, Goicea, Raluca, Seshadri, Ramakrishnan Ayloor, Sarı, Ramazan, Nataraja, Ramesh, Aslam, Ramisha, Abdelemam, Rania, Shrestha, Rashmit, Bharathan, Rasiah, Pellini, Raul, Guevara, Raul, Agarwal, Ravi, Vissapragada, Ravi, Alharmi, Rawan Arahman, Sayyed, Raza, Browning, Rebecca, Critchley, Rebecca, Mallick, Rebecca, Alarabi, Rehab, Beron, Reinaldo Isaacs, Függer, Reinhold, Othman, Rema, Saad, Rema, Amores, Remedios Revilla, Colombari, Renan Carlo, Radivojević, Renata Curic, Patrone, Renato, Novysedlák, René, Huatuco, René Manuel Palacios, Baertschiger, Reto, Liang, Rhea, Luckwell, Rhys, Escrevente, Ricardo, Rezende, Ricardo Fernandes, Cruz, Ricardo Pedrini, Lenzi, Riccardo, Rosati, Riccardo, Donovan, Richard, Egan, Richard, Morris, Richard, Page, Richard, Seglenieks, Richard, Unsworth, Richard, Wilkin, Richard, Skipworth, Richard Je, Davies, Richard Justin, Bezirci, Rifat, Talwar, Rishi, Azami, Rizwan, Bohmer, Rob, Crichton, Robert, Fruscio, Robert, Hooker, Robert, Jach, Robert, Parker, Robert, Pillerstorff, Robert, Sinnerton, Robert, Stabler, Robert, O'connell, Robert Michael, Ragozzino, Roberta, Tutino, Roberta, Angelico, Roberta, Cammarata, Roberto, Colasanti, Roberto, Macchiavello, Roberto, Peltrini, Roberto, Pirrello, Roberto, Vaschetti, Roberto, Pires, Robinson Esteves, Papalia, Rocco, Arrangoiz, Rodrigo, Hompes, Roel, Salah, Rokeya, Pinto, Romina, Flumignan, Ronald, Callan, Rory, Cuthbert, Rory, Dennis, Rory, Scaramuzzo, Rosa, Macías, Rosa Montero, Sánchez, Rosa, Ogu, Rosemary, Ramely, Rosnelifaizur, Sgarzani, Rossella, Ramli, Roszalina, Hillier, Roxane, Thumbadoo, Ruben, Ooi, Rucira, Abdus-Salam, Rukiyat, Masri, Ruqaya, Hodgson, Russell, Mathew, Ryan, Wade, Ryckie, D'archi, Sabatino, Khan, Sabina, Ngaserin, Sabrina, Kale, Sachin, Hassan, Sadiq, Merghani, Safa, Benamar, Safia, Muhammad, Sagir, Badran, Saif, Elsahli, Saifaleslam, Heta, Saimir, Hammouche, Salah, Baeesa, Saleh, Paiella, Salvatore, Eldeen, Samaher Taj Eldeen Hassan Taj, Arkani, Samara, Mittal, Samarth, Hirji, Sameer, Tebha, Sameer, Emile, Sameh, Dbouk, Samer, Bandyopadhyay, Samik Kumar, Muhammad, Saminu, Olori, Samson, Asirifi, Samuel Amoako, Hailu, Samuel, Ling, Samuel, Newman, Samuel, Ross, Samuel, Wanjara, Samuel, Kumar, Sandip, Seneviratne, Sanjeewa, Tamburello, Sara, Suarez, Sara Busto, Ingallinella, Sara, Irshaidat, Sara, Konswa, Sara, Mambrilla, Sara, Nasser, Sara, Parini, Sara, Pitoni, Sara, Ornaghi, Sara, Rodrigues, Sara Castanheira, Abdelmohsen, Sarah, Aitken, Sarah, Tian, Sarah, Badiani, Sarit, Ahmad, Sarwat, Swed, Sarya, Muthu, Sathish, Lakpriya, Sathya, Alzahrani, Saud, Mikalauskas, Saulius, Lasrado, Savita, Satoskar, Savni, Bawa, Sayesha, Altiner, Saygin, Garcia, Sean, Stevens, Sean, Demir, Sebahattin, Ken-Amoah, Sebastian, Tranca, Sebastian, Ziemann, Sebastian, Awad, Selmy, Atici, Semra Demirli, Subramaniam, Sentilnathan, Erel, Serap, Jiang, Serena, Efetov, Sergey, Efremov, Sergey, Katorkin, Sergey, Valladares, Sergio Chávez, Contreras, Sergio Marcos, Meriç, Serhat, Zenger, Serkan, Safi, Seyer, Leventoğlu, Sezai, Elsalhawy, Shady, Shaikh, Shafaque, Sheik, Shahila, Islam, Shahnoor, Shamim, Shahzad, Waqar, Shahzad Hussain, Ahmad, Shahzaib, Farid, Shahzaib, Seraj, Shaikh Sanjid, Sundarraju, Shalini, Karandikar, Sharad, Sambhwani, Sharan, Chopra, Sharat, Chowdhury, Sharfuddin, Laura, Sharon, Ahmed, Sharwany, Wason, Shaun, Tan, Shawn Jia Hwang, Fraser, Sheila, Williams, Shekinah, Ghozy, Sherief, Abdelmawgoud, Sherif, Shehata, Sherif, Sharma, Shilpa, Ahmed, Shima, Al-Touny, Shimaa A, Ramzanali, Shireen, Nah, Shireen Anne, Jansen, Shirley, Rajan, Shiv, Dindyal, Shiva, Amin, Shivang, Ahmad, Shoaib, Shoukrie, Shoukrie I M, Karar, Shoura, Patkar, Shraddha, Abdulsalam, Shuaib, Lin, Shuxun, Hegde, Siddhi, Fiorelli, Silvia, Quaresima, Silvia, Redondo, Silvia Villacé, Palmisano, Silvia, Ruggiero, Silvia, Balogun, Simon, Cais, Simon, Cole, Simon, Federer, Simon, Le Roux, Simon, Ippoliti, Simona, Meneghini, Simona, Viola, Simona, Manfredelli, Simone, Novello, Simone, Gananadha, Sivakumar, Mesli, Smain Nabil, Kale, Smruti, Tani, Sobhana Iftekhar, Malik, Sobia, Anastasiadou, Sofia, Boligo, Sofia, Esposito, Sofia, Valanci, Sofia, Xenaki, Sofia, Pejkova, Sofija, Bandyopadhyay, Soham, Trungu, Sokol, Basu, Somprakas, Alkhatib, Sondos, Pérez-Bertólez, Sonia, Flores, Sonia Lopez, Donoghue, Sophie, Lunca, Sorinel, Orsoo, Soyombo, Potamianos, Spyridon, Devarakonda, Sreekar, Suresh, Sreelakshmi, Croghan, Stefanie M, Turi, Stefano, Capella, Stefano, Lucchini, Stefano, Magnone, Stefano, Salizzoni, Stefano, Scabini, Stefano, Scaringi, Stefano, Cioffi, Stefano Piero Bernardo, Seyfried, Steffen, Degener, Stephan, Potten, Stephanie, Taha-Mehlitz, Stephanie, Ali, Stephen, Angamuthu, Stephen, Mcaleer, Stephen, Knight, Stephen Richard, White, Stuart, Mantziari, Styliani, Kykalos, Stylianos, Goh, Su Kah, Chowdhury, Subhadip Pal, Ibrahim, Sufyan, Elzwai, Suha, Bansal, Sujesh, Tripathy, Sujit, Amrayev, Sultan, Anwar, Sumadi Lukman, Banerjee, Sumit, Thakar, Sumit, Saeed, Summaya, Venkatappa, Sunil Kumar, Das, Sunit, Techapongsatorn, Suphakarn, Dube, Surya Kumar, Lee, Susan, González-Suárez, Susana, Henriques, Susana, Konjevoda, Suzana, Gisbertz, Suzanne, Bravo, Sybil Lizanne, Mannan, Syed, Bukhari, Syed Imran, Zafar, Syed Nabeel, Batista, Sylvia, Chin, Synn Lynn, Arif, Tahera, Lawal, Taiwo Akeem, Aktokmakyan, Talar Vartanoglu, Osborn, Tamara, Szakmany, Tamas, Sztipits, Tamás, Triantafyllou, Tania, Valadez, Tania Abigail Cueto, Singh, Tanveer, Khaliq, Tanwir, Patel, Tapan, Fadalla, Tarig, Jichi, Tarik, Sammour, Tarik, Al-Shaiji, Tariq, Naggs, Taryn, Barišić, Tatjana, Nikolouzakis, Taxiarchis, Bisgin, Tayfun, Perra, Teresa, Uprak, Tevfik Kıvılcım, Dagklis, Themistoklis, Liakakos, Theodore, Sidiropoulos, Theodoros, Adjeso, Theophilus Justus Kofi, Dölker, Theresa, Oung, Thida, Aherne, Thomas, Diehl, Thomas, Pinkney, Thomas, Raymond, Thomas, Rhomberg, Thomas, Schmitz-Rixen, Thomas, Madhuri, Thumuluru Kavitha, Lohmann, Tibor Karl, Yeoh, Tien, Zaimis, Tilemachos, Bright, Tim, Vilz, Tim O, Glowka, Tim R, Board, Timothy, Hardcastle, Timothy, Cohnert, Tina, Mahečić, Tina Tomić, William, Tinka George, Klatte, Tobias, Abbott, Tom, Watcyn-Jones, Tom, Mendes, Tome, Kulis, Tomislav, Sečan, Tomislav, Campagnaro, Tommaso, Frisoni, Tommaso, Simoncini, Tommaso, Violante, Tommaso, Safranovs, Toms Janis, Risteski, Toni, Pang, Tony, Akinyemi, Tosin, Yotsov, Tsanko, Laeke, Tsegazeab, Kochiyama, Tsukasa, Sholadoye, Tunde T, Alekberli, Tural, Ezomike, Uchechukwu, Giustizieri, Ugo, Grossi, Ugo, Köksoy, Ülkü Ceren, Bork, Ulrich, Kisser, Ulrich, Ronellenfitsch, Ulrich, Saeed, Umar, Bracale, Umberto, Jayarajah, Umesh, Rauf, Umme Habiba Abdul, Bumbasirevic, Uros, Ferrer, Ursula María Jariod, Ahmed, Usama, Bello, Usman Mohammed, Jogiat, Uzair, Sadia, Uzma, Galandarov, Vagif, Narayanan, Vairavan, Calu, Valentin, Bianchi, Valentina, Ciniero, Valeria, Tonini, Valeria, Silvestri, Vania, Vijay, Vardhini, Dewan, Varun, Lohsiriwat, Varut, Thuduvage, Vasanthika, Mousafeiris, Vasileios, Dragisic, Vedran, Sasireka, Veerasamy, Santric, Veljko, Kusuma, Venkata Ramana Murthy, Kolli, Venkata Satish, Alonso, Veronica, De Simone, Veronica, Picotti, Veronica, Martínez, Verónica Martín, Panduro-Correa, Vicky, Kakotkin, Victor, Angulo, Victor Pinto, Turrado-Rodriguez, Victor, Krishnamoorthy, Vijay, Ban, Vin Shen, Shah, Vinay, Maiola, Vincenza, Giordano, Vincenzo, La Vaccara, Vincenzo, Lizzi, Vincenzo, Papagni, Vincenzo, Schiavone, Vincenzo, Satchithanantham, Vinojan, Garcia-Virto, Virginia, Jimenez, Virginia, Kumar, Vishal, Shelat, Vishal, Bhat, Vivek, Sodhai, Vivek, Graziadei, Vivien, Kutuzov, Vladislav, Stoyanov, Vladislav, Oktseloglou, Vlasios, Flis, Vojko, Elhassan, Wael Atif Fadl, Yang, Wah, Soon, Wai Cheong, Tashkandi, Wail, Al-Khyatt, Waleed, Mabood, Waleed, Bijou, Walid, Wijenayake, Wasantha, D, Wasim, Krawczyk, Wiktor, Atkins, William, Bolton, William, White, William, Ceelen, Wim, Vagena, Xanthoula, Gozal, Yaacov, Baba, Yabasin Iddrisu, Subramani, Yamini, Jansen, Yanina, Mittal, Yash, Kara, Yasi̇n, Zwain, Yasir, Noureldin, Yasser, Alawneh, Yazan, Aydin, Yener, Lam, Yick Ho, Tang, Yita, Lim, Yizhe, Dean, Yomna, Tanas, Yousef, Su, Yu-Xiong, Fujimoto, Yuki, Altinel, Yuksel, Frolova, Yulia, Oshodi, Yusuf, Fadel, Zahir T, Zahid, Zahra, Elahi, Zain, Djama, Zakarya, Zaheen, Zakia, Jawad, Zaynab, Demetrashvili, Zaza, Gebremeskel, Zersenay, Gudisa, Zewdie, Alyami, Ziyad, Garoufalia, Zoe, Li, Zoe, Zimak, Zoran, Radin, Zorana, and Balogh, Zsolt J
Abstract: Background: Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods: This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was coprioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low-middle-income countries. Results: In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of 'single-use' consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low-middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion: This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high- and low-middle-income countries.
Published: 2023

29. FLT3‐directed UniCAR T‐cell therapy of acute myeloid leukaemia.

Author: Peschke, J. C., Bergmann, R., Mehnert, M., Gonzalez Soto, K. E., Loureiro, L. R., Mitwasi, N., Kegler, A., Altmann, H., Wobus, M., Máthé, D., Szigeti, K., Feldmann, A., Bornhäuser, M., Bachmann, M., Fasslrinner, F., and Arndt, C.
Subjects: ACUTE myeloid leukemia, T cells, CHIMERIC antigen receptors, PROTEIN-tyrosine kinases
Abstract: Summary: Adaptor chimeric antigen receptor (CAR) T‐cell therapy offers solutions for improved safety and antigen escape, which represent main obstacles for the clinical translation of CAR T‐cell therapy in myeloid malignancies. The adaptor CAR T‐cell platform 'UniCAR' is currently under early clinical investigation. Recently, the first proof of concept of a well‐tolerated, rapidly switchable, CD123‐directed UniCAR T‐cell product treating patients with acute myeloid leukaemia (AML) was reported. Relapsed and refractory AML is prone to high plasticity under therapy pressure targeting one single tumour antigen. Thus, targeting of multiple tumour antigens seems to be required to achieve durable anti‐tumour responses, underlining the need to further design alternative AML‐specific target modules (TM) for the UniCAR platform. We here present the preclinical development of a novel FMS‐like tyrosine kinase 3 (FLT3)‐directed UniCAR T‐cell therapy, which is highly effective for in vitro killing of both AML cell lines and primary AML samples. Furthermore, we show in vivo functionality in a murine xenograft model. PET analyses further demonstrate a short serum half‐life of FLT3 TMs, which will enable a rapid on/off switch of UniCAR T cells. Overall, the presented preclinical data encourage the further development and clinical translation of FLT3‐specific UniCAR T cells for the therapy of AML. [ABSTRACT FROM AUTHOR]
Published: 2023
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30. Planejamento da Prática Pedagógica: aspectos importantes para elaboração de um planejamento com vistas a uma educação emancipatória

Author: LOUREIRO, L., primary
Published: 2023
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31. The first record of Bergamina lineolata (Chydoridae; Aloninae) from Colombia

Author: Fuentes-Reinés, J. M., primary, Eslava-Eljaiek, P., additional, and Elmoor-Loureiro, L. M. A., additional
Published: 2023
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32. 45P The RevCAR T cell platform: A switchable and combinatorial therapeutic strategy for glioblastoma

Author: Mitwasi, N., primary, Hassan, H., additional, Arndt, C., additional, Loureiro, L., additional, Neuber, C., additional, Kegler, A., additional, Kubeil, M., additional, Toussaint, M., additional, Deuther-Conrad, W., additional, Bachmann, M., additional, and Feldmann, A., additional
Published: 2022
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33. Agronomic assessment of a compost consisting of seaweed and fish waste as an organic fertilizer for organic potato crops

Author: Illera-Vives, M., Seoane Labandeira, S., Iglesias Loureiro, L., and López-Mosquera, M. E.
Published: 2017
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34. Development of a novel target module redirecting UniCAR T cells to Sialyl Tn-expressing tumor cells

Author: Loureiro, L. R., Feldmann, A., Bergmann, R., Koristka, S., Berndt, N., Arndt, C., Pietzsch, J., Novo, C., Videira, P., and Bachmann, M.
Published: 2018
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35. Extraction of biomolecules from Coelastrella sp. LRF1 biomass using Ohmic Heating technology

Author: Sousa, V., primary, Loureiro, L., additional, Carvalho, G., additional, and Pereira, R.N., additional
Published: 2022
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36. Comparison of two structurally different RevTMs for the RevCAR system to specifically target CEA expressing cells

Author: González Soto, K. E., Loureiro, L. R., (0000-0002-8733-4286) Bergmann, R., (0000-0002-1285-5052) Arndt, C., Mitwasi, N., Kegler, A., Bartsch, T., Drewitz, L., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., González Soto, K. E., Loureiro, L. R., (0000-0002-8733-4286) Bergmann, R., (0000-0002-1285-5052) Arndt, C., Mitwasi, N., Kegler, A., Bartsch, T., Drewitz, L., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Despite the fact that chimeric antigen receptor (CAR) engineered T cells have shown encouraging therapeutic effects in hematological setups, the targeting of solid tumor-related antigens still represents a challenge. One main issue is that the expression of this type of antigens is not restricted to cancer cells, but normal tissues express them as well to some degree. In order to avoid strong side-effects caused by on-target/off-tumor effects, more controllable and specific CAR T cell-derived technologies need to be developed. In this line of thought, we developed the switchable, flexible and programmable Reverse (Rev) CAR platform. This system is based on engineered T cells expressing RevCAR molecules, which have extracellular short peptide epitopes incapable of recognizing surface antigens. Thus, the RevCAR T cells are per se inert and will only recognize the target cell through the interaction with an antigen-specific target module, named RevTM. RevTMs are bispecific antibodies designed to bind simultaneously to the target antigen and the short epitopes on the RevCAR engineered T cells. This interaction triggers a specific activation and cytotoxic activity of the RevCAR T cells redirecting them to eradicate the cancer cells. Here, we adapted our RevCAR technology to target the carcinoembryonic antigen (CEA), which is a significant tumor marker for colorectal cancers and other carcinomas. Moreover, we developed two RevTMs with different structures: scFv- and IgG4-based. The first one is built by linking a scFv against CEA to a scFv that recognizes the RevCAR epitope through glycine and serine residues, resulting in a small sized molecule (<60 kDa) with two binding sites. The IgG4-based RevTM connects the same scFv-structures but in this case through the hinge and constant Fc regions (CH2 and CH3) of an IgG4 antibody. The formation of disulfide bridges on the hinge portion causes the formation of homodimers, resulting in a molecule with increased molecular weight (
Published: 2022

37. Chelator-based non-peptidic radiotracers for PET imaging of PD-L1 with copper-64

Author: Krutzek, F., Donat, C., (0000-0001-6104-6676) Ullrich, M., Loureiro, L. R., (0000-0003-4846-1271) Kopka, K., (0000-0003-2276-5330) Stadlbauer, S., Krutzek, F., Donat, C., (0000-0001-6104-6676) Ullrich, M., Loureiro, L. R., (0000-0003-4846-1271) Kopka, K., and (0000-0003-2276-5330) Stadlbauer, S.
Abstract: Objective: The programmed cell death-ligand 1 (PD-L1) is upregulated on many different cancers and allows the tumor cells to evade immune response through binding to the PD-1 receptor.[1] Monoclonal antibodies, i.e. checkpoint inhibitors, are able to break this blockade and thus reactivate the immune system.[2] However, only 30% of the patients respond to antibody-based immunotherapy. Because PD-L1 is heterogeneously expressed within and across tumor sites, there is an urgent clinical need for a non-invasive, diagnostic imaging approach helping for therapy decision. Radiotracers for PET and SPECT imaging are able to meet these requirements. Especially small molecules are favourable, because of their short clearance times and for providing high imaging contrast.[3] Methods: Modification of two literature known small molecule PD-L1 inhibitors with water-solubilizing groups, different linkers and a DOTA chelator resulted in six different radioligands. Labeling was performed with Cu-64 (HZDR, 30 MeV TR-FLEX cyclotron) and binding affinities to PD-L1 were determined in vitro on transduced PC3 cells stably overexpressing human PD-L1. Qualitative PET scans (nanoSCAN PET/CT scanner, Mediso) were performed in NMRI-FoxN1-nude mice bearing PC3-hPD-L1 xenografted tumors. Results: Organic synthesis started from biaryl building blocks (R1 = H, R2 = Br and R1 = R2 = Me), which underwent a Mitsunobu reaction with the central chloroaryl moiety. The bis(sulfonic acid) group was attached via a sarcosine spacer. Three different linker structures were synthesized and attached by Cu(I)-catalyzed click reaction. Synthesis was finished with DOTA conjugation and subsequent quantitative labeling with Cu-64 under standard labeling conditions was achieved. Using the shake flask method, log(D) values ranging from –1.5 to –2.5 were obtained. Saturation binding assays revealed that biphenyl compounds with R1 = R2 = Me showed promising binding affinities to PD-L1 (KD between 60 and 123 nM). In mic
Published: 2022

38. Immunotheranostic target modules suitable for imaging and navigation of UniCAR T-cells to strike FAP-expressing solid tumours and their microenvironment

Author: Loureiro, L. R., (0000-0002-0646-5808) Neuber, C., Hoffmann, L., (0000-0001-8857-5922) Kubeil, M., (0000-0002-1285-5052) Arndt, C., Mitwasi, N., Kegler, A., (0000-0002-8733-4286) Bergmann, R., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Loureiro, L. R., (0000-0002-0646-5808) Neuber, C., Hoffmann, L., (0000-0001-8857-5922) Kubeil, M., (0000-0002-1285-5052) Arndt, C., Mitwasi, N., Kegler, A., (0000-0002-8733-4286) Bergmann, R., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Chimeric antigen receptor (CAR) T-cells are unquestionably considered one of the most promising approaches in cancer immunotherapy. Nonetheless, mild to severe toxicities are associated with this approach which include e.g. on-target/off-tumour toxicities and cytokine release syndrome. Aiming for increased clinical safety, a modular universal CAR (UniCAR) platform was developed by our group in which UniCAR T-cells are exclusively activated in the presence of a target module (TM) that specifically establishes the cross-link between target cells and UniCAR T-cells. Fibroblast activation protein (FAP) is highly expressed on cancer-associated fibroblasts (CAFs) present in the tumour stroma and also found to be overexpressed in tumour cells. This protein plays an important role in promoting tumour growth, metastasis, and immunosuppression and has therefore been studied as a target for cancer diagnosis and treatment. Given this and the demonstrated efficacy, flexibility and switchability of the UniCAR system, currently demonstrated in phase I clinical trials, we hereby aimed to develop TMs targeting FAP that can be used for both immunotherapeutic and theranostic approaches. For that, the single-chain variable fragment (scFv) of an anti-human FAP mAb was fused to the peptide epitope E5B9 that is recognized by the UniCAR T-cells, creating low molecular weight TMs that are rapidly eliminated allowing a specific and recurrent on/off switch of UniCAR T-cell activity via TM dosing. Additionally, extended half-life anti-FAP TMs based on the human IgG4 Fc-domain, including a mutated version, were created intending to strengthen anti-tumour responses and to ease the clinical TM administration at later stages of tumour therapy. All TMs were tested in vitro based on naturally and artificially overexpressing 2D and 3D models, and proven to specifically redirect UniCAR T-cells to FAP-expressing target cells. Positron emission tomography (PET) using 64Cu radiolabelled anti-FAP IgG4 TMs
Published: 2022

39. Adapter CARs: Estimation of the affinity between adapter and CAR domain required for function

Author: Bartsch, T., (0000-0002-1285-5052) Arndt, C., González Soto, K. E., (0000-0001-7462-7111) Wodtke, R., (0000-0001-7711-4805) Brandt, F., Loureiro, L. R., Mitwasi, N., Kegler, A., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Bartsch, T., (0000-0002-1285-5052) Arndt, C., González Soto, K. E., (0000-0001-7462-7111) Wodtke, R., (0000-0001-7711-4805) Brandt, F., Loureiro, L. R., Mitwasi, N., Kegler, A., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: As next generation for CAR T cells, adaptor CAR platforms have been developed, which are designed to improve safety, but at the same time maintain the high efficiency of the CAR T cell approach. In our lab, we developed the UniCAR system, which consists of universal (Uni)CAR T cells and tumor-specific target modules (TMs), which work as bridging molecules between the UniCAR T cells and the target cells. Until now, type 1 and type 2 UniCARs were developed. Both UniCAR types consist of an extracellular binding domain derived from a monoclonal antibody (mAb) directed to the nuclear La/SS-B protein. Type 1 UniCARs are derived from the anti-La mAb 5B9. Type 2 UniCARs from the anti-La mAb 7B6. As both anti-La mAbs are not able to precipitate native La protein, both anti-La mAbs are directed to a specific cryptic epitope which is not accessible on the cell surface. Thus, the UniCAR T cell is per se inert. To activate the UniCAR T cell for tumor cell killing a TM is needed as a second component. Typically, a TM is composed of a tumor-specific binding domain and the respective La epitope. Consequently, the affinity of the TM towards the target antigen but also towards the UniCAR T cell via the E5B9-tag plays an important role for functionality of the respective UniCAR system. In this study, we representatively aimed to elucidate if and how the affinity of the type 1 UniCAR domain to the E5B9 epitope impacts the functionality of the UniCAR system. To alter the interaction of UniCAR and TM, we designed different mutated E5B9 peptides (M1-M3) carrying one or two amino acid (aa) changes. In detail, aspartic acid and/or glutamic acid were mutated to glycine residues as they most probably are involved in epitope/paratope interactions. We subsequently fused these mutated peptides to an scFv domain, resulting in three different mutated TM versions. By conducting ELISA and flow-cytometry based binding studies, we showed that a single aa exchange (D3>G3) in M1 did not alter the affini
Published: 2022

40. As small as it can be: short peptide-derived target molecules for redirection of UniCAR T-cells and imaging of SSTR2-expressing cancers

Author: Loureiro, L. R., (0000-0002-8733-4286) Bergmann, R., (0000-0001-7462-7111) Wodtke, R., (0000-0001-7711-4805) Brandt, F., (0000-0002-1285-5052) Arndt, C., González Soto, K. E., Mitwasi, N., Kegler, A., Bartsch, T., Drewitz, L., Máthé, D., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., Loureiro, L. R., (0000-0002-8733-4286) Bergmann, R., (0000-0001-7462-7111) Wodtke, R., (0000-0001-7711-4805) Brandt, F., (0000-0002-1285-5052) Arndt, C., González Soto, K. E., Mitwasi, N., Kegler, A., Bartsch, T., Drewitz, L., Máthé, D., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Chimeric antigen receptor (CAR) T-cells are undoubtedly a promising approach in cancer immunotherapy. Nevertheless, mild to severe toxicities are associated with this approach including on-target/off-tumor effects and cytokine release syndrome. Aiming for increased clinical safety, adaptor CAR technologies were developed which include the modular universal CAR (UniCAR) platform developed by our group. UniCAR T-cells are exclusively activated in the presence of a target module (TM), which establishes the cross-link between cancer cells and UniCAR T-cells. These TMs are highly versatile molecules that can be constructed not only by using antibody fragments but also e.g. peptides specifically targeting a receptor or molecule on the cell´s surface. Somatostatin receptor (SSTR) subtype 2 is highly expressed in a variety of malignancies and has therefore been studied as a marker and target for cancer diagnosis and treatment. Currently, SSTR2 agonists and antagonists, such as Tyr3-octreotate (TATE) and BASS or JR11, respectively, are particularly well established and clinically implemented mostly used for diagnostic nuclear medicine. Given this and the proven flexibility and efficacy of the UniCAR system, we hereby aimed to develop small peptide-derived TMs targeting SSTR2 that can be used for both immunotherapeutic and diagnostic approaches. For that, the abovementioned SSTR2 agonist and antagonists were chemically linked to the E5B9 peptide and equipped with the radiometal chelator NODAGA. These TMs were tested in vitro and in vivo, in which they have proven to specifically redirect UniCAR T-cells to human neuroendocrine and breast SSTR2-expressing cancer cells. Furthermore, the enrichment of these anti-SSTR2 peptide TMs at the tumor site was confirmed by positron emission tomography (PET) studies. We hereby designed novel small peptide-derived TMs that can be used for redirection of UniCAR T-cells to SSTR2-expressing cancer cells as well as for PET imaging, proving to b
Published: 2022

41. UniCAR T cell theranostics for diagnostic imaging and therapy of prostate cancer

Author: (0000-0002-1285-5052) Arndt, C., (0000-0002-8733-4286) Bergmann, R., Striese, F., Máthé, D., (0000-0001-6921-0848) Berndt, N., Loureiro, L. R., Szöllősi, D., Kovács, N., Hegedűs, N., Kovács, T., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., (0000-0002-1285-5052) Arndt, C., (0000-0002-8733-4286) Bergmann, R., Striese, F., Máthé, D., (0000-0001-6921-0848) Berndt, N., Loureiro, L. R., Szöllősi, D., Kovács, N., Hegedűs, N., Kovács, T., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: CAR T-cell therapy achieved unparalleled clinical success rates for treatment of patients with hematological malignancies. However, progress and clinical translation towards solid tumors is slow and hampered by many factors e.g. increased complexity, high heterogeneity and an immunosuppressive tumor microenvironment. Thus, CAR T-cell therapy alone might not result in durable antitumor responses. Combinatorial approaches are promising strategies to improve CAR T-cell efficacy in solid tumor treatment. In this regard, we here aim to combine conventional cancer theranostics with CAR T-cell immunotherapy in one single approach. By using the well-established UniCAR system, a novel, multifunctional tool termed PSCA-IgG4 target module (TM) was developed for dual prostate cancer theranostics. It comprises a human PSCA-specific binding domain, the hinge and Fc-domain of human IgG4 molecules as well as the UniCAR epitope E5B9. As shown by in vitro assays with PSCA-positive and PSCA-negative prostate cancer cells, the novel TM redirected UniCAR T cells for efficient tumor cell lysis in a strictly antigen- and TM-dependent manner. After radiolabeling with copper-64 or actinium-225, the novel PSCA-IgG4 TM was successfully applied for diagnostic imaging and targeted radioimmunotherapy. The 64Cu-labeled PSCA-IgG4 TM showed maximal tumor accumulation with optimal tumor-to-background ratios after 1.5 days. Furthermore, targeted alpha-therapy with the 225Aclabeled TM significantly delayed the outgrowth of established tumors in mice. In summary, the here presented, novel PSCA-IgG4 TM is a promising candidate for dual theranostics of prostate cancer that may help to overcome present hurdles in solid tumor therapy. After radiolabeling it facilitates not only targeted alpha-therapy and diagnostic imaging of PSCA, but can be also repurposed as a TM for UniCAR T-cell immunotherapy.
Published: 2022

42. Antigen-specific redirection of off-the-shelf NK-92 cells using the universal CAR platform ‘‘UniCAR’’

Author: Mitwasi, N., (0000-0001-5099-2448) Feldmann, A., (0000-0002-1285-5052) Arndt, C., Koristka, S., Loureiro, L. R., Berndt, N., Tonn, T., (0000-0002-8733-4286) Bergmann, R., Rössig, C., Wels, W. S., (0000-0002-8029-5755) Bachmann, M., Mitwasi, N., (0000-0001-5099-2448) Feldmann, A., (0000-0002-1285-5052) Arndt, C., Koristka, S., Loureiro, L. R., Berndt, N., Tonn, T., (0000-0002-8733-4286) Bergmann, R., Rössig, C., Wels, W. S., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Modifying of immune effector cells with chimeric antigen receptors (CARs) has revealed a promising therapeutic potential for targeting cancer, especially with CAR-modified T cells. However, the use of other immune cells like primary NK cells or NK cell lines appeared as another advantageous approach that can be combined with CAR technology. Unlike T cells, established NK cell lines can be used allogenically as an off-the-shelf product with reduced risk of toxicities. We have established previously a modular Universal CAR platform (UniCAR) which can be switched on/off and allows the flexible targeting of various tumor antigens. This system consists of two parts, the UniCAR-expressing immune effector cells and a target module (TM). The UniCAR-immune cells cannot recognize surface antigens but are only redirected with the TM which contains an antigen-binding moiety on one hand and an epitope recognized by the UniCAR molecules on the other hand. Here, we provide a proof of concept for using the UniCAR system in combination with the NK-92 cell line to target disialoganglioside GD2-expressing tumors. The UniCAR NK-92 cells induced increase in lysis of neuroblastoma and melanoma cell lines in the presence of scFv- or human IgG4-based TMs, associated with specific release of pro-inflammatory cytokines. Moreover, UniCAR NK-92 cells were shown to be functional in eradicating GD2-expressing tumors in experimental mice. In order to investigate the in vivo half-life of the scFv- and IgG4-based TMs, they were radiolabeled with 64Cu and detected using PET imaging. Dynamic PET scanning has shown that the IgG4 format increased the half-life of the TM to around 24 folds in comparison to the scFv-based TMs. In summary, UniCAR NK-92 provides an off-the-shelf universal platform that can be combined with various antibody formats, and can be easily expanded for therapeutic use.
Published: 2022

43. The RevCAR T cell platform: a switchable and combinatorial therapeutic strategy for glioblastoma

Author: Mitwasi, N., Abdelfatah Saleh Hassan, H. A., (0000-0002-1285-5052) Arndt, C., Loureiro, L. R., Kegler, A., (0000-0001-8857-5922) Kubeil, M., (0000-0002-1136-3857) Toussaint, M., (0000-0003-3168-3062) Deuther-Conrad, W., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., Mitwasi, N., Abdelfatah Saleh Hassan, H. A., (0000-0002-1285-5052) Arndt, C., Loureiro, L. R., Kegler, A., (0000-0001-8857-5922) Kubeil, M., (0000-0002-1136-3857) Toussaint, M., (0000-0003-3168-3062) Deuther-Conrad, W., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Background: Glioblastoma (GBM) is a very aggressive brain tumor, associated with poor prognosis and survival. So far, the efficiency of available therapies is limited. After proving their effectiveness in targeting hematological malignancies, chimeric antigen receptor (CAR) T cells might provide a promising therapeutic approach for GBM. Here, we present our switchable Reverse CAR technology (RevCAR). Unlike conventional CAR T cells, RevCAR T cells contain an epitope in their extracellular receptor domain, and can only be activated via bispecific target modules (RevTM) which recognize the RevCAR T cells on one side and tumor cells on the other side. Once these TMs are eliminated, RevCARs are switched off. In addition, we have developed dual-targeting RevCARs allowing the control of T cells according to the AND gate logic of Boolean algebra. Methods: RevTMs directed against GMB were expressed in eukaryotic cells and purified with affinity chromatography. The ability of these RevTMs to bind GBM cells and RevCAR T cells was analyzed using flow cytometry. Moreover, the capability of the mono-specific and the dual-targeting RevCAR T cells to kill GBM cells was analyzed using luminescence-based cytotoxicity assay in the absence or presence of a range of RevTM concentrations. Secreted pro-inflammatory cytokines were also evaluated by ELISA. In addition to the in vitro assays, a proof of concept co-injection experiment was performed in vivo. Results: In this study, we show that GBM-specific RevTMs can bind both the RevCAR T cells and the GBM cells. Importantly, the RevCAR T cells can be activated to secrete pro-inflammatory cytokines and to efficiently kill GBM cells via the RevTMs. Moreover, we were able to prove that dual-targeting RevCAR T cells can be activated only upon recognition of two different GBM targets, thereby allowing a highly specific and selective killing of GBM both in vitro and in vivo. Conclusion: In conclusion, the switchable RevCAR platform is a novel t
Published: 2022

44. Development and functional characterization of a versatile radio-/immunotheranostic tool for prostate cancer management

Author: (0000-0002-1285-5052) Arndt, C., (0000-0002-8733-4286) Bergmann, R., Striese, F., Merkel, K., Máthé, D., Loureiro, L. R., Mitwasi, N., Kegler, A., Fasslrinner, F., González Soto, K. E., (0000-0002-0646-5808) Neuber, C., (0000-0001-6921-0848) Berndt, N., Kovács, N., Szöllősi, D., Hegedűs, N., Tóth, G., Emmermann, J.-P., Harikumar, K. B., Kovacs, T., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., (0000-0002-1285-5052) Arndt, C., (0000-0002-8733-4286) Bergmann, R., Striese, F., Merkel, K., Máthé, D., Loureiro, L. R., Mitwasi, N., Kegler, A., Fasslrinner, F., González Soto, K. E., (0000-0002-0646-5808) Neuber, C., (0000-0001-6921-0848) Berndt, N., Kovács, N., Szöllősi, D., Hegedűs, N., Tóth, G., Emmermann, J.-P., Harikumar, K. B., Kovacs, T., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Due to its overexpression on the surface of prostate cancer (PCa) cells, the prostate stem cell antigen (PSCA) is a potential target for PCa diagnosis and therapy. Here we describe the development and functional characterization of a novel IgG4-based anti-PSCA antibody (Ab) derivative (anti-PSCA IgG4-TM) that is conjugated with the chelator DOTAGA. The anti-PSCA IgG4-TM represents a multimodal immunotheranostic compound that can be used (i) as target module (TM) for UniCAR T cell-based immunotherapy, (ii) for diagnostic PET imaging, and (iii) targeted alpha therapy. Cross-linkage of UniCAR T cells and PSCA-positive tumor cells via the anti-PSCA IgG4-TM results in efficient tumor cell lysis both in vitro and in vivo. After radiolabeling with 64Cu2+ the anti-PSCA IgG4-TM was successfully applied for high contrast PET imaging. In a PCa mouse model, it showed specific accumulation in PSCA-expressing tumors, while no uptake in other organs was observed. Additionally, the DOTAGA-conjugated anti-PSCA IgG4-TM was radiolabeled with 225Ac3+ and applied for targeted alpha therapy. A single injection of the 225Ac-labeled anti-PSCA IgG4-TM was able to significantly control tumor growth in experimental mice. Overall, the novel anti-PSCA IgG4-TM represents an attractive first member of a novel group of radio-/immunotheranostics that allows diagnostic imaging, endoradiotherapy, and CAR T cell immunotherapy.
Published: 2022

45. Combining Radiation- with Immunotherapy in Prostate Cancer: Influence of Radiation on T cells

Author: Lindner, D., (0000-0002-1285-5052) Arndt, C., Loureiro, L. R., (0000-0001-5099-2448) Feldmann, A., Kegler, A., Koristka, S., (0000-0001-6921-0848) Berndt, N., Mitwasi, N., (0000-0002-8733-4286) Bergmann, R., Frenz, M., (0000-0002-8029-5755) Bachmann, M., Lindner, D., (0000-0002-1285-5052) Arndt, C., Loureiro, L. R., (0000-0001-5099-2448) Feldmann, A., Kegler, A., Koristka, S., (0000-0001-6921-0848) Berndt, N., Mitwasi, N., (0000-0002-8733-4286) Bergmann, R., Frenz, M., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Radiation of tumor cells can lead to the selection and outgrowth of tumor escape variants. As radioresistant tumor cells are still sensitive to retargeting of T cells, it appears promising to combine radio- with immunotherapy keeping in mind that the radiation of tumors favors the local conditions for immunotherapy. However, radiation of solid tumors will not only hit the tumor cells but also the infiltrated immune cells. Therefore, we wanted to learn how radiation influences the functionality of T cells with respect to retargeting to tumor cells via a conventional bispecific T cell engager (BiTE) and our previously described modular BiTE format UNImAb. T cells were irradiated between 2 and 50 Gy. Low dose radiation of T cells up to about 20 Gy caused an increased release of the cytokines IL2, TNF and interferon-g and an improved capability to kill target cells. Although radiation with 50 Gy strongly reduced the function of the T cells, it did not completely abrogate the functionality of the T cells.
Published: 2022

46. Validation of CD98hc as a therapeutic target for a combination of radiation and immunotherapies in head and neck squamous cell carcinoma

Author: Köseer, A. S., Loureiro, L. R., Jureczek, J., Mitwasi, N., González Soto, K. E., Aepler, J., Bartsch, T., (0000-0001-5099-2448) Feldmann, A., Kunz-Schughart, L. A., Linge, A., (0000-0003-1776-9556) Krause, M., (0000-0002-8029-5755) Bachmann, M., (0000-0002-1285-5052) Arndt, C., (0000-0002-3375-1500) Dubrovska, A., Köseer, A. S., Loureiro, L. R., Jureczek, J., Mitwasi, N., González Soto, K. E., Aepler, J., Bartsch, T., (0000-0001-5099-2448) Feldmann, A., Kunz-Schughart, L. A., Linge, A., (0000-0003-1776-9556) Krause, M., (0000-0002-8029-5755) Bachmann, M., (0000-0002-1285-5052) Arndt, C., and (0000-0002-3375-1500) Dubrovska, A.
Abstract: Most patients with head and neck squamous cell carcinomas (HNSCC) are diagnosed at a locally advanced stage and show heterogeneous treatment responses. Low SLC3A2 (solute carrier family 3 member 2) mRNA and protein (CD98hc) expression levels are associated with higher locoregional control in HNSCC patients treated with primary radiochemotherapy or postoperative radiochemotherapy, suggesting that CD98hc could be a target for HNSCC radiosensitization. One of the targeted strategies for tumor radiosensitization is precision immunotherapy, e.g., the use of chimeric antigen receptor (CAR) T cells. This study aimed to define the potential clinical value of new treatment approaches combining conventional radiotherapy with CD98hc-targeted immunotherapy. To address this question, we analyzed the antitumor activity of the combination of fractionated irradiation and switchable universal CAR (UniCAR) system against radioresistant HNSCC cells in 3D culture. CD98hc-redirected UniCAR T cells showed the ability to destroy radioresistant HNSCC spheroids. Also, the infiltration rate of the UniCAR T cells was enhanced in the presence of the CD98hc target module. Furthermore, sequential treatment with fractionated irradiation followed by CD98hc-redirected UniCAR T treatment showed a synergistic effect. Taken together, our obtained data underline the improved antitumor effect of the combination of radiotherapy with CD98hc-targeted immunotherapy. Such a combination presents an attractive approach for the treatment of high-risk HNSCC patients.
Published: 2022

47. Targeting CD10 on B-Cell Leukemia Using the Universal CAR T-Cell Platform (UniCAR)

Author: Mitwasi, N., (0000-0002-1285-5052) Arndt, C., Loureiro, L. R., Kegler, A., Fasslrinner, F., (0000-0001-6921-0848) Berndt, N., Bergmann, R., HoˇRejší, V., Rössig, C., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., Mitwasi, N., (0000-0002-1285-5052) Arndt, C., Loureiro, L. R., Kegler, A., Fasslrinner, F., (0000-0001-6921-0848) Berndt, N., Bergmann, R., HoˇRejší, V., Rössig, C., (0000-0002-8029-5755) Bachmann, M., and (0000-0001-5099-2448) Feldmann, A.
Abstract: Chimeric antigen receptor (CAR)-expressing T-cells are without a doubt a breakthrough therapy for hematological malignancies. Despite their success, clinical experience has revealed several challenges, which include relapse after targeting single antigens such as CD19 in the case of B-cell acute lymphoblastic leukemia (B-ALL), and the occurrence of side effects that could be severe in some cases. Therefore, it became clear that improved safety approaches, and targeting multiple antigens, should be considered to further improve CAR T-cell therapy for B-ALL. In this paper, we address both issues by investigating the use of CD10 as a therapeutic target for B-ALL with our switchable UniCAR system. The UniCAR platform is a modular platform that depends on the presence of two elements to function. These include UniCAR T-cells and the target modules (TMs), which cross-link the T-cells to their respective targets on tumor cells. The TMs function as keys that control the switchability of UniCAR T-cells. Here, we demonstrate that UniCAR T-cells, armed with anti-CD10 TM, can efficiently kill B-ALL cell lines, as well as patient-derived B-ALL blasts, thereby highlighting the exciting possibility for using CD10 as an emerging therapeutic target for B-cell malignancies.
Published: 2022

48. Driving modular CARs through solid tumours and their microenvironment - a new era in cancer immunotherapy

Author: Loureiro, L. R. and Loureiro, L. R.
Abstract: Chimeric antigen receptor (CAR) T-cell therapies are undoubtedly a promising approach in cancer immunotherapy and have revolutionized the treatment options for hematologic malignancies. Yet, their effectiveness is more limited and challenging when it comes to tackling solid tumours. Antigen escape, on-target off-tumour effects, and the immunosuppressive tumour microenvironment (TME) of solid tumours are among the main hurdles. Aiming for increased clinical safety and effectiveness, our group works with the adaptor CAR T-cell technologies named UniCAR and RevCAR. The versatility of the adaptor molecules used in these types of approaches allows not only the targeting of antigens expressed on the surface of tumour cells but also of key molecules expressed on immunosuppressive cells as well as immune checkpoint inhibitors. Given the features of such approaches and the ease in engineering the adaptor molecules, combinatorial targeting can be exploited to pave the way for improved and personalized immunotherapies.
Published: 2022

49. CAR Technology Meets Theranostics – A New Era of Immunotheranostics for Hematological and Solid Tumors

Author: (0000-0002-1285-5052) Arndt, C., (0000-0002-8733-4286) Bergmann, R., Loureiro, L. R., Máthé, D., (0000-0002-0646-5808) Neuber, C., Mitwasi, N., Kegler, A., (0000-0001-5099-2448) Feldmann, A., (0000-0002-8029-5755) Bachmann, M., (0000-0002-1285-5052) Arndt, C., (0000-0002-8733-4286) Bergmann, R., Loureiro, L. R., Máthé, D., (0000-0002-0646-5808) Neuber, C., Mitwasi, N., Kegler, A., (0000-0001-5099-2448) Feldmann, A., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Modification of autologous T cells with tumor-specific chimeric antigen receptors (CARs) has been shown to be an effective tool for treatment of hematologic malignancies. However, clinical translation towards solid tumors is still limited as demonstrated by the suboptimal performance of CAR T cells in first in-human studies. Combining advances in CAR-T cell therapy and cancer theranostics may provide a promising multimodal approach to increase therapeutic efficacy and achieve durable responses in cancer patients. Here we present the development and functional characterization of different peptide- or antibody constructs targeting tumor-associated antigens or different structures of the tumor microenvironment. Equipment of these molecules with the E5B9 peptide epitope, enabled their use in the well-established UniCAR system. Accordingly, the constructs were able to specifically activate UniCAR T cells for efficient killing of both hematological and solid tumors in vitro and in vivo. Upon conjugation of chelators like DOTAGA and NODAGA, the peptide- or antibody derivates were further successfully applied for cancer theranostics, using e.g. 68Ga, 64Cu as diagnostic radionuclides and e.g. 67Cu, 225Ac as therapeutic radionuclides. PET imaging in xenotransplanted mice has demonstrated high contrast tumor accumulation. Consistent with the stable tumor accumulation, 225Ac-labeled molecules demonstrated therapeutic efficacy in a xenograft mouse model. In summary, E5B9-tagged peptide- or antibody constructs open a new era of cancer immunotheranostics as they can be used multimodally for (i) UniCAR-T cell therapy, (ii) non-invasive diagnostic imaging and (iii) targeted radioimmunotherapy. Prospectively, they could thus bridge the gap between the fields of CAR-T cells and cancer theranostics.
Published: 2022

50. Adaptor UniCAR and RevCAR platforms for flexible, switchable and combinatorial tumor targeting

Author: (0000-0001-5099-2448) Feldmann, A., Loureiro, L. R., Kegler, A., (0000-0002-1285-5052) Arndt, C., Mitwasi, N., (0000-0002-8733-4286) Bergmann, R., Koristka, S., Hoffmann, A., González Soto, K. E., Kittel-Boselli, E., Bartsch, T., Drewitz, L., (0000-0001-6921-0848) Berndt, N., Fasslrinner, F., Bornhäuser, M., (0000-0002-8029-5755) Bachmann, M., (0000-0001-5099-2448) Feldmann, A., Loureiro, L. R., Kegler, A., (0000-0002-1285-5052) Arndt, C., Mitwasi, N., (0000-0002-8733-4286) Bergmann, R., Koristka, S., Hoffmann, A., González Soto, K. E., Kittel-Boselli, E., Bartsch, T., Drewitz, L., (0000-0001-6921-0848) Berndt, N., Fasslrinner, F., Bornhäuser, M., and (0000-0002-8029-5755) Bachmann, M.
Abstract: Chimeric antigen receptor (CAR) T-cells show remarkable therapeutic effects especially in B-cell derived leukemias and lymphomas. However, clinical translation of such an innovative immunotherapeutic approach in highly heterogeneous hematological malignancies like acute myeloid leukemia (AML) or solid tumors is still challenging due to life-threatening side effects, immune escape and disease relapse. To overcome such major hurdles and to address the unmet need for further improvements in CAR therapy, we have established flexible, switchable and programmable adaptor CAR platform technologies named UniCAR and RevCAR. These modular strategies consist of T-cells engineered with adaptor CARs which are primarily inactive as they are incapable to recognize surface antigens. Universal adaptor CAR T-cells can be flexibly redirected to any tumor antigen and controlled by targeting modules (TMs) cross-linking adaptor CAR T- and tumor cells resulting in tumor cell lysis. As an advancement of UniCARs, RevCARs lack the extracellular antigen-binding moiety reducing the receptor size and facilitating the genetical modification of T-cells with several RevCARs possessing different specificity and functionality. Thus, the RevCAR platform enables combinatorial tumor targeting following Boolean logic gates. So far, we have successfully shown preclinical applicability of the UniCAR and RevCAR approaches to target hematological malignancies as well as solid tumors in a flexible and specific manner using tumor cell lines and patient-derived materials. Remarkably, efficiency and switchability of UniCAR T-cells were even proven for the first time in patients in a clinical phase I study. Furthermore, by targeting of two different tumor antigens, combinatorial OR and AND gate logic targeting according to the rules of Boolean algebra was accomplished using the RevCAR platform. These achievements have a high potential for an improved and personalized tumor immunotherapy.
Published: 2022

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