Gotowe bibliografie tematyczne / CAR-T therapy

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Gotowa bibliografia na temat „CAR-T therapy”

Autor: Grafiati
Data publikacji: 12 kwietnia 2025

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Artykuły w czasopismach na temat "CAR-T therapy"

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Singh, Yuvraj. "Chimeric Antigen Receptors T Cells (CAR T) Therapy". International Journal of Science and Research (IJSR) 13, nr 5 (5.05.2024): 1563–66. http://dx.doi.org/10.21275/sr24523173932.

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San Segundo, Lucrecia Yáñez. "CAR-T cell therapy". Medicina Clínica (English Edition) 156, nr 3 (luty 2021): 123–25. http://dx.doi.org/10.1016/j.medcle.2020.05.030.

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Neff Newitt, Valerie. "CAR T-Cell Therapy". Oncology Times 39, nr 20 (październik 2017): 1. http://dx.doi.org/10.1097/01.cot.0000526653.15787.41.

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Ahmad, Aamir. "CAR-T Cell Therapy". International Journal of Molecular Sciences 21, nr 12 (17.06.2020): 4303. http://dx.doi.org/10.3390/ijms21124303.

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Jacobson, Caron, Amy Emmert i Meredith B. Rosenthal. "CAR T-Cell Therapy". JAMA 322, nr 10 (10.09.2019): 923. http://dx.doi.org/10.1001/jama.2019.10194.

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Kwon, Miji, i Hee Ho Park. "CAR-T Therapy Targeting Solid Tumor". KSBB Journal 35, nr 2 (30.06.2020): 95–104. http://dx.doi.org/10.7841/ksbbj.2020.35.2.95.

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L. Penney, Christopher, Boulos Zacharie i Jean-Simon Duceppe. "Tucaresol-Cyclophosphamide Combination Therapy: Proposal for a Safe, Affordable Alternative to CAR T-Cell Therapy". Journal of Clinical Review & Case Reports 9, nr 12 (5.12.2024): 01–04. https://doi.org/10.33140/jcrc.09.12.02.

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Chimeric Antigen Receptor (CAR) T-cell therapy is a newer immunotherapeutic process in which genetic engineering is used to incorporate a receptor protein into a patient’s T-cells thereby permitting the modified T-cells to recognize and eradicate tumors. Initially, CAR T-cell therapy was reserved as a last resort when standard cancer treatments failed to provide significant efficacy but subsequently, CAR T-cell therapy is finding use against earlier stage cancers. Since 2017, seven CAR T-cell therapies have attained FDA approval for treatment of hematological cancers. The latest approval, November 8, 2024, is for treatment of B-cell acute lymphoblastic leukemia. However, CAR T-cell therapy does not always provide a lasting anticancer response which leads to loss of tumor remission. The percent loss of tumor remission depends upon the type of hematological cancer being treated. Although currently limited to hematological cancers, CAR T-cell therapy provides cancer patients a significant increase in survival unattainable with traditional cancer treatment regimens. However, two significant issues accompany CAR T-cell therapy. The first is multiple toxicity issues which although occurring individually in a low percentage of patients, taken together constitute a significant probability of encountering a potentially fatal side effect. The second problem is the high cost of CAR T-cell therapy starting at $450,000 US per treatment. Contributing to both of these problems is the fact that CAR T-cell therapy is labor intensive which will exacerbate existing clinical facilities already challenged by a myriad of mutating pathogens and an aging population. Against this setting is proposed therapy consisting of clinical stage and FDA approved anticancer drugs with excellent safety records. Proposed herein is combination therapy with Tucaresol, up-regulates CD4+ and CD8+ T-cells, and cyclophosphamide, down-regulates Treg cells, as a convenient, cost effective cancer treatment.
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Testa, Ugo, Patrizia Chiusolo, Elvira Pelosi, Germana Castelli i Giuseppe Leone. "CAR-T CELL THERAPY FOR T-CELL MALIGNANCIES". Mediterranean Journal of Hematology and Infectious Diseases 16, nr 1 (29.02.2024): e2024031. http://dx.doi.org/10.4084/mjhid.2024.031.

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Chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of B-cell lymphoid neoplasia and, in some instances, improved disease outcomes. Thus, six FDA-approved commercial CAR-T cell products that target antigens preferentially expressed on malignant B-cells or plasma cells have been introduced in the therapy of B-cell lymphomas, B-ALLs and multiple myeloma. These therapeutic successes have triggered the application of CAR-T cell therapy to other hematologic tumors, including T-cell malignancies. However, the success of CAR-T cell therapies in T-cell neoplasms was considerably more limited to the existence of some limiting factors, such as the sharing of mutual antigens between normal T-cells and CAR-T cells, and malignant cells, determining fratricide events and severe T-cell aplasia; contamination of CAR-T cells used for CAR transduction with contaminating malignant T-cells. Allogeneic CAR-T products can avoid tumor contamination but raise other problems related to immunological incompatibility. In spite of these limitations, there has been significant progress in CD7- and CD5-targeted CAR-T cell therapy of T-cell malignancies in the last few years.
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SAYIN KASAR, Kadriye, i Yasemin YILDIRIM. "Nursing Management in CAR-T Cell Therapy". Turkiye Klinikleri Journal of Nursing Sciences 12, nr 2 (2020): 272–79. http://dx.doi.org/10.5336/nurses.2019-72274.

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Hosen, Naoki. "2) CAR T Cell Therapy". Nihon Naika Gakkai Zasshi 108, nr 3 (10.03.2019): 438–42. http://dx.doi.org/10.2169/naika.108.438.

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Rozprawy doktorskie na temat "CAR-T therapy"

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Bourbon, Estelle. "Developing logic-gated CAR T cells for saferT-cell lymphoma therapy". Electronic Thesis or Diss., université Paris-Saclay, 2025. http://www.theses.fr/2025UPASL006.

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La thérapie par cellules T à récepteur antigénique chimérique (CAR) est apparue comme l'une des percées les plus convaincantes dans le traitement du cancer au cours de la dernière décennie. Cependant, les résultats remarquables obtenus dans les hémopathies B ne se sont pas encore étendus aux lymphomes T (LT) où l'éventuelle toxicité « on-target off-tumor » a limité le développement d'approches similaires.Dans ce travail, nous avons développé une plateforme NOT-gate, tirant parti de la perte d'expression du CD7 dans les LT pour distinguer les cellules T tumorales des cellules T normales. Cette plateforme associe un CAR 4-28^1 XX activateur ciblant le CD4, un antigène T fortement exprimé dans les LT, à un CAR 7PD1 inhibiteur ciblant le CD7. Les nouvelles cellules CAR T 4-28(1XX, éditées CD4 pour limiter le fratricide, ont démontré une activité antitumorale robuste contre les cellules tumorales CD4-positives in vitro et in vivo dans des modèles murins de LT disséminé. Cependant, la perte du CD4 a démasqué un phenotype hyperproliferatif reponsable d'une infiltration tissulaire létale, dont les mécanismes exacts restent à élucider. L'ajout d'un CAR inhibiteur 7PD1 a permis de réduire la sécrétion de cytokines et la dégranulation des cellules T CAR4-28C1XX, mais il a été plus difficile d'obtenir une inhibition de la cytotoxicité globale. De nombreux paramètres doivent être optimisés pour une plateforme NOT- gate plus efficace, comprenant principalement le rapport stoechiométrique CAR/cible et l'intensité du signal médié par chaque CAR
Chimeric antigen receptor (CAR) T cell therapy has emerged as one of the most compelling breakthroughs in cancer treatment in the past decade. However, the remarkable results achieved in B-cell malignancies hâve not yet translated in T-cell lymphomas (TCL) where concerns over potential "on- target off-tumor" toxicity hâve hindered the development of similar approaches. In this work, we sought to developp a NOT-gate platform, leveraging CD7 loss in mature T-cell malignancies to distinguish tumor from normal T- cells. This platform intergates an activating 4-28£1XX CARtargeting CD4, a T-cell antigen highly expressed in TCL, paired with an inhibitory 7PD1 CAR targeting CD7. The novel 4-28(1XX CAR T cells, CD4-edited to prevent fratricide, demonstrated robust antitumor activity against CD4-positive tumor cells in vitro and in vivo in disseminated TCL murine models. However, CD4-disruption unleashed léthal hyperproliferative CAR T cell infiltration, whose exact mechanisms remains to be elucidated. The addition of a 7PD1 inhibitory CAR allowed for decreased sécrétion of cytokine and degranulation of the 4-28(1XX CAR T cells, but overall killing inhibition was more difficult to achieve. Numerous parameters are to be optimized for a more efficient NOT-gate platform, including mainly CAR/target stoechiometry ratio and the signaling strenght of each CAR
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Ringwelski, Beth Anne. "Label-Free CD8+ T-cell Purification and Electroporation in Relation to CAR T-cell Therapy". Thesis, North Dakota State University, 2020. https://hdl.handle.net/10365/31881.

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Immunotherapy is becoming recognized as a superior treatment for cancer. In recent years, chimeric antigen receptor (CAR) therapy is among the immunotherapies that has had growing success rates. CAR T-cell therapy takes patient’s T-cells and encodes them with a CAR expressing gene, which can then target their cancer cells. However, there are some dangers associated with this therapy. If a cancer cell is mistakenly transfected with the CAR molecule, it can become resistant to the therapy. Using the electric properties of the cells, we have created a technique that can purify the T-cells from the remaining cancer cells using microfluidics and dielectrophoresis (DEP). Then, to further improve the therapy, the sample is electroporated following being patterned using DEP forces, which transfects the cells without using viral vectors and provides longer CD19 expression.
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Agliardi, Giulia. "Development of a Chimeric Antigen Receptor (CAR)-based T cell therapy for glioblastoma". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10025011/.

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High grade gliomas are aggressive brain tumours for which treatment is highly challenging due to the location within the central nervous system (CNS), which may reduce access of cytotoxic chemotherapy, and their infiltrative growth, which precludes complete surgical resection. Current treatment includes surgical removal – wherever possible - followed by radiotherapy and chemotherapy. However, recurrence is common, resulting in a survival of only 12 to 15 months after diagnosis. This highlights the need for new therapies. Chimeric antigen receptors (CARs) are synthetic molecules which combine the specificity of an antibody to the signalling domains of a T cell receptor (TCR), allowing T cells to directly recognise tumour antigens with no need for co-stimulation. CAR-T cells have shown promising responses in the treatment of haematological malignancies, inducing complete and durable responses in patients with chemo-refractory disease treated with CD19-redirected T cells. This therapeutic approach may be highly suitable for high grade gliomas as T cells have the ability to track to distant tumour sites. However, translation of this technology to solid tumours is proving more difficult, due to several challenges, including: requirement for an effective infiltration of CAR-T cells within the tumour and the immunosuppressive environment provided by solid malignancies. In this work, we developed an immunocompetent animal model of glioma, to study kinetics of migration and infiltration of CAR-T cells and the interplay between CAR-T cells, the tumour and the endogenous immune system to inform the design of T cell immunotherapy for this brain tumours. The tumour specific variant III of the epidermal growth factor receptor (EGFRvIII) – a mutation found in 30% of glioblastomas – was used as model antigen. A murine CAR was constructed based on the single chain fragment variant (ScFv) of EGFRvIII-specific antibody MR1.1 linked with a CD8 stalk to CD28-CD3ζ activation domains. A murine marker gene (truncated CD34) was co-expressed to allow for ex vivo analysis as well as firefly luciferase for in vivo tracking of CAR T-cells. The mouse glioma cell line GL261 was modified to express the mouse version of EGFRvIII and used to establish orthotopic tumours. After validation of function and specificity in vitro, efficacy of CAR-T cells was tested in vivo. Both bioluminescence imaging (BLI) and flow cytometry demonstrated that CAR T cells accumulated within the tumour in an antigen-dependent manner. MRI demonstrated that CAR T cells delayed tumour growth and increased survival. However, tumours were not consistently eradicated. Both immunohistochemistry and BLI indicated lack of long term persistence of T cells within the tumour. Analysis of tumour infiltrating lymphocytes (TILs) phenotype suggested that decreased functionality of CAR-T cells could be a result of their exhaustion in situ. We hypothesised that additional strategies were required to improve efficacy and persistence of CAR-T cells. We postulated that CAR-T cell fitness may be prolonged by: - Incorporation of 41BB as additional co-stimulatory domain in the CAR to provide a pro-survival signal. - Combination therapy with PD1 blockade to overcome T cell exhaustion (both on CAR and endogenous T cells) in situ. While the employment of third-generation CAR did not significantly improve survival and showed increased toxicity, combination therapy of CAR-T cells and PD-1 blockade promoted complete clearance of tumours resulting in long term survival. Immunohistochemistry and flow cytometry analysis suggested that combination therapy may increase persistence of CAR-T cells, leading to a more rapid and consistent tumour eradication compared to CAR-T cell administration alone. However, data presented here did not demonstrate a synergistic effect of CAR-T cell therapy and PD1 blockade, as an effect of PD1 blockade alone was also observed. Therefore, additional experiments are required to examine this further.
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Xie, Yushu Joy. "Engineering VHH-based chimeric antigen receptor (CAR) T cell therapy for solid tumor treatment". Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/123070.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2019
Cataloged from PDF version of thesis.
Includes bibliographical references.
Chimeric antigen receptor (CAR) T cells are a promising cancer therapeutic, as they can specifically redirect the cytotoxic function of a T cell to a chosen target of interest. CAR T cells have been successful in clinical trials against hematological cancers, but have experienced low efficacy against solid tumors for a number of reasons, including a paucity of tumor-specific antigens to target and a highly immunosuppressive solid tumor microenvironment. In chapter 2 of this thesis, we develop a strategy to target multiple solid tumor types through markers in their microenvironment. The use of single domain antibody (VHH)-based CAR T cells that recognize these markers circumvents the need for tumor-specific targets. Chapter 3 will describe methods to overcome the immunosuppressive microenvironment of solid tumors. Here, we have developed VHH-secreting CAR T cells that can modulate additional aspects of the tumor microenvironment, including the engagement of the innate immune system through secretion of a VHH against an inhibitor of phagocytosis. We show that this strategy of VHH-secretion by CAR T cells can lead to significant benefits in outcome. We also demonstrate that delivery of therapeutics by CAR T cells can improve the safety profile of the therapeutic. Chapter 4 of this thesis explores strategies to increase the targeting capacity of CAR T cells by building logic-gated CARs. Finally, chapter 5 will describe work in imaging CAR T cells specifically, longitudinally, and non-invasively through PET imaging. Our results demonstrate the flexibility of VHHs in CAR T cell engineering and the potential of VHH-based CAR T cells to target the tumor microenvironment, modulate the tumor microenvironment, and treat solid tumors.
by Yushu Joy Xie.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biological Engineering
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Bento, Rui Pedro Garcia de Oliveira. "CAR-modified T cells targeted to CD19 antigen for lymphocytic leukemia". Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13445.

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Mestrado em Biomedicina Farmacêutica
Cellular immunotherapies, or Advanced Therapy Medicinal Products (ATMPs), are emerging as novel and specific therapeutic approaches to treat diseases, such as certain types of leukemias, which are difficult or impossible to treat with today’s biopharmaceutical products. Breakthroughs in basic, preclinical, and clinical science spanning cellular immunology, and cellprocessing technologies has allowed clinical applications of chimeric antigen receptor–based therapies. A recent example is CTL019, a lentivirus-based gene therapy for autologous T cells, acquired by Novartis in 2012 through a global alliance with the University of Pennsylvania. Although this technology is still in its infancy, clinical trials have already shown clinically significant antitumor activity in chronic lymphocytic leukemia and acute lymphocytic leukemia. Trials targeting a variety of other adult and pediatric malignancies are under way. The potential to target essentially any tumor-associated cell-surface antigen for which a monoclonal antibody can be made opens up an entirely new arena for targeted therapy of cancer. The regulatory environment for these Advanced Therapies Medicinal Products is complex and in constant evolution. Many challenges lie ahead in terms of manufacturing process, non-conventional supply chain logistics, business models, intellectual property, funding and patient access.
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Pfeilschifter, Janina Marie. "Targeting B non-Hodgkin lymphoma and tumor-supportive follicular helper T cells with anti-CXCR5 CAR T cells". Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/23169.

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CAR-T-Zell-Therapie ist eine vielversprechende neuartige Behandlungsform für Patienten mit aggressiven B-Zell Non-Hodgkin-Lymphomen (B-NHL). In dieser Arbeit wurde die anti-CXCR5 CAR-T-Zell-Therapie als Alternative zur anti-CD19 CAR-T-Zell-Therapie für die Behandlung von reifen B-NHLs untersucht. CXCR5 ist ein B-Zell-homing Rezeptor, der von reifen B Zellen und follikulären T-Helferzellen (TFH Zellen) exprimiert wird. TFH Zellen wurden als tumor-unterstützend in chronisch lymphatischer Leukämie (CLL) und im follikulären Lymphom (FL) beschrieben. Dieses Expressionsmuster erlaubt es, auf einzigartige Weise zeitgleich die malignen Zellen und die tumorunterstützende Mikroumgebung mithilfe von CAR-T-Zell-Therapie gerichtet gegen einen Chemokinrezeptor anzugreifen. Die wichtigsten Ergebnisse dieser Arbeit waren, dass (1) die anti-CXCR5 CAR T-Zellen zielgerichtet CXCR5 positive reife B-NHL Zelllinien und Patientenproben in vitro eliminierten und eine starke anti-Tumor Reaktivität in einem immundefizienten Xenotransplantationsmausmodell zeigten, (2) die anti-CXCR5 CAR T-Zellen zielgerichtet die tumorunterstützenden TFH Zellen in CLL und FL Patientenproben in vitro erkannten und dass (3) CXCR5 ein sicheres Expressionsprofil zeigte. CXCR5 war stark und häufig auf B-NHL exprimiert und die Expression auf gesundem Gewebe war auf lymphoide Zellen beschränkt. Zusammenfassend lässt sich sagen, dass die anti-CXCR5 CAR-T-Zell-Therapie eine neue Behandlungsmöglichkeit für Patienten mit reifen B-NHL darstellt, indem durch die anti-CXCR5 CAR-T Zellen sowohl der Tumor als auch ein Anteil der tumorunterstützende Mikroumgebung eliminiert werden. Im zweiten Teil der Arbeit wurde das Eμ-Tcl1 murine CLL Lymphommodell genutzt um die Auswirkung der Lymphomentwicklung auf die CXCR5+ T Zellen zu untersuchen. Mittels RNA-Einzelzell-Sequenzierung konnte ein profunder Einfluss des Lymphomwachstums auf das T Zell-Kompartiment der Mäuse, denen Eμ-Tcl1 Zellen gespritzt wurden, gezeigt werden.
CAR T cell therapy is a promising new treatment option for patients suffering from aggressive B non-Hodgkin lymphomas (NHLs). In CAR T cell therapy, patient-derived T cells are genetically modified to express a chimeric receptor commonly directed towards a surface antigen expressed by neoplastic cells. In this thesis, anti-CXCR5 CAR T cell therapy was investigated as an alternative to anti-CD19 CAR T cell therapy for the treatment of mature B-NHLs. CXCR5 is a B cell homing receptor expressed by mature B cells and follicular helper T (TFH) cells. TFH cells were described to support the tumor cells in chronic lymphocytic leukemia (CLL) and follicular lymphoma (FL). This expression pattern allows simultaneous targeting of the malignant cells and the tumor-supporting microenvironment by CAR T cell therapy against a chemokine receptor in an unprecedented manner. Main findings included that (1) anti-CXCR5 CAR T cells targeted specifically CXCR5 expressing mature B-NHL cell lines and patient samples in vitro and showed strong in vivo anti-tumor reactivity in an immunodeficient xenograft mouse model, (2) anti-CXCR5 CAR T cells targeted tumor-supportive TFH cells derived from CLL and FL patient samples in vitro and (3) CXCR5 showed a safe expression profile. CXCR5 was strongly and frequently expressed by B-NHLs and its expression on healthy tissue was restricted to lymphoid cells. In summary, anti-CXCR5 CAR T cell therapy presents a novel treatment option for patients suffering from mature B-NHLs by eliminating the tumor and part of the tumor-supportive microenvironment. The second part of the project, the Eμ-Tcl1 murine lymphoma model, which mimics human CLL, was used to study the impact of lymphomagenesis on CXCR5+ T cells. Using single cell RNA sequencing, a profound influence of lymphoma growth on the T cell compartment in Eμ-Tcl1 tumor-challenged mice could be shown.
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Karlsson, Hannah. "CD19-targeting CAR T Cells for Treatment of B Cell Malignancies : From Bench to Bedside". Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-232638.

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Immunotherapy for cancer is a young research field progressing at high speed. The first chimera of an antibody and a signaling chain was designed by Zelig Eshhar and was later further developed to enhance existing T cell therapy by combining a single-chain fragment of an antibody with the CD3 zeta chain of the TCR complex. T cells expressing these chimeric antigen receptors (CARs) could recognize and specifically kill tumor cells. However the T cells, lacked in persistence and tumor rejection did not occur. Thus, the CAR constructs have been improved by providing the T cell with costimulatory signals promoting activation. The focus of this thesis has been to evaluate second and third generation αCD19-CAR T cells for the treatment of B cell leukemia and lymphoma. B cell tumors commonly upregulate anti-apoptotic proteins such as Bcl-2, which generates therapy resistance. In the first paper a second generation (2G) αCD19-CD28-CAR T cell was combined with the Bcl-2 family inhibitor ABT-737. ABT-737 sensitized tumor cells to CAR T cell therapy and may be an interesting clinical combination treatment. In paper II, the phenotype and function of a third generation (3G) αCD19-CD28-4-1BB-CAR T cell were evaluated. B cell-stimulated CAR T cells showed increased proliferation and an antigen-driven accumulation of CAR+ T cells. 3G CAR T cells had equal cytotoxic capacity, similar lineage, memory and exhaustion profile phenotype compared to 2G CARs. However, 3G CAR T cells proliferated better and had increased activation of intracellular signaling pathways compared to 2G CAR T cells. In paper III, αCD19-CD28-4-1BB-CAR T cells were used to stimulate immature dendritic cells leading to an upregulation of maturation markers on co-cultured dendritic cells. Hence, CAR T cells may not only directly kill the tumor cells, but may induce bystander immunity that indirectly aids tumor control. This thesis also include supplementary information about the development and implementation of protocols for GMP production of CAR T cell batches for a phase I/IIa clinical trial currently ongoing for patients with refractory B cell leukemia and lymphoma. So far, two patients have safely been treated on the lowest dose.
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Wang, Valentine. "Improving Allogeneic CAR-T cells : HLA class I KO Virus Specific T cells to limit GvHD and graft rejection". Electronic Thesis or Diss., Université de Lorraine, 2024. https://docnum.univ-lorraine.fr/ulprive/DDOC_T_2024_0235_WANG.pdf.

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La thérapie CAR-T a transformé le traitement du cancer en modifiant les lymphocytes T pour cibler spécifiquement les antigènes tumoraux. Bien que cette approche ait montré un succès remarquable dans les hémopathies malignes à cellules B, le processus reste coûteux et long, car il nécessite la collecte et la modification des cellules du patient, ce qui peut retarder le traitement. De plus, certains patients, en raison de traitements antérieurs ou de maladies avancées, ne disposent pas de cellules viables, limitant l'accès à cette thérapie.Les cellules CAR-T allogéniques provenant de donneurs offrent une solution plus rapide et évolutive, réduisant le temps de production et les coûts. Cependant, elles présentent des risques, notamment la maladie du greffon contre l'hôte (GvHD), où les cellules du donneur attaquent les tissus du patient. Notre étude a exploré une approche innovante, combinant la technologie CAR avec des lymphocytes T spécifiques aux virus (Virus Specific T cells, VST), connus pour leurs propriétés antivirales et antitumorales, afin de générer des CAR-VST. Ces CAR-VST à double spécificité représentent une alternative prometteuse, particulièrement pour les patients à risque de rechute tumorale ou de réactivation virale.Dans notre étude, nous avons généré des CAR-T et des CAR-VST à partir des mêmes donneurs, obtenant respectivement 40,28%±9,30% et 35,96%±11,40% d'expression de CD19.CAR au jour 7 (N=3). Les CAR-VST ont montré in vitro une clairance tumorale similaire à celle des CAR-T, avec 74,13%±22,06% de lyse des cellules CD19+. Dans un modèle murin, un contrôle de la croissance tumorale ainsi qu'une amélioration de la survie similaires ont été observés dans les deux groupes. De plus, les CAR-VST ont conservé leur activité antivirale, lysant 62,32%±13,84% des cellules chargées en peptides viraux. Concernant l'alloréactivité, les CAR-VST ont montré une prolifération CD3+ inférieure (28,27%±21,64%) par rapport aux CAR-T (88,3%±24,48%, p=0,0285, N=4), suggérant un risque réduit de GvHD.En collaboration avec l'Université de Caroline du Nord, nous avons également exploré la suppression des molécules HLA de classe I via la B-2-microglobuline (B2M) pour réduire le risque de rejet immunitaire. Une expression de HLA-ABC de 15,1±14,6% (N=11) a été obtenue après knockout par CRISPR/Cas9. Nous travaillons également sur la surexpression de HLA-E et HLA-G pour prévenir la lyse médiée par les cellules NK, nécessitant des optimisations supplémentaires.En conclusion, générer des HLA-E+ ou G+/B2M-/CAR-VST offre une alternative prometteuse pour créer des cellules entièrement allogéniques. Ces CAR-VST modifiés conservent leurs fonctions antivirales et antitumorales, ce qui en fait des candidats prometteurs pour les immunothérapies prêtes à l'emploi qui pourraient réduire les risques de rejet immunitaire et de GvHD
CAR-T cell therapy have revolutionized cancer treatment by modifying a patient's T cells to target specific tumor antigens. This personalized approach has shown remarkable success in treating B-cell malignancies like leukemia and lymphoma. However, the process is costly and time-consuming, as it involves collecting and modifying the patient's own cells, which delays treatment. Moreover, some patients may not have sufficient or viable T cells due to prior treatments or advanced disease stages, limiting the availability of CAR-T therapies for all patients.To address these challenges, allogeneic CAR-T cells from healthy donors provide a faster and more scalable solution, reducing production time and costs. However, these off-the-shelf therapies face risks like graft-versus-host disease (GvHD), where donor cells might attack the patient's tissues. Our study explored combining CAR technology with Virus Specific T cells (VSTs), known for their antiviral and antitumor properties, to generate CAR-VSTs. These dual-specific CAR-VSTs present a promising alternative, especially for patients prone to both tumor relapse and viral reactivation.In our study, we generated CAR-Ts and CAR-VSTs from same donors obtaining 40.28%±9.30% and 35.96%±11.40% CD19.CAR expression on day 7 (N=3), respectively. In vitro, CAR-VSTs showed robust tumor clearance similar to CAR-Ts, achieving 74.13%±22.06% lysis of CD19+ tumor cells. In a murine lymphoma model, both CAR-VSTs and CAR-Ts demonstrated comparable antitumor efficacy, successfully controlling tumor growth and improving survival. Moreover, CAR-VSTs maintained their antiviral function, efficiently lysing 62.32%±13.84% virus-peptide-pulsed cells, similar to native VSTs. We assessed the alloreactivity of CAR-VSTs and found that they exhibited significantly lower CD3 proliferation rates (28.27%±21.64%) compared to CAR-T cells (88.3%±24.48%, p=0.0285, N=4), indicating a reduced risk of GvHD. CAR-VSTs' dual-specificity for both tumor and viral antigens makes them a powerful tool to address cancer relapse and viral complications in patients.In collaboration with the University of North Carolina, we explored strategies to delete HLA class I molecules in CAR-VSTs by targeting B-2-microglobulin (B2M), aiming to reduce immune rejection. In addition, we worked on overexpressing tolerogenic molecules such as HLA-E and HLA-G to prevent NK cell-mediated lysis. Our results showed an HLA-ABC expression of 15.1±14.6% (N=11) after CRISPR/Cas9 knockout, which indicates successful deletion, though further optimization is necessary to prevent NK-lysis by re-expressing HLA-E or HLA-G.In conclusion, generating HLA-E+ or G+/B2M-/CAR-VSTs offers a promising alternative for creating fully allogeneic cells. These modified CAR-VSTs retain their dual antiviral and antitumor functions, making them a promising candidate for "off-the-shelf" immunotherapies that could reduce the risks of immune rejection and graft-versus-host disease
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ALBERTI, GAIA. "Evaluation of a Tandem CD33-CD146 Chimeric Antigen Receptor (CAR) for the simultaneous targeting of Acute Myeloid Leukemia (AML) blasts and stromal cells in the niche". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/382304.

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La leucemia mieloide acuta (LMA) è la neoplasia ematologica maggiormente diagnosticata nei pazienti adulti (25%) e mentre rappresenta il 15-20% dei casi nei pazienti pediatrici. La chemioterapia convenzionale, che impiega antraciclina e citarabina, rappresenta il trattamento standard per l’LMA, con tassi di remissione completa dal 60% all'80% nei bambini e dal 40% al 60% negli adulti (>60 anni). Sfortunatamente, la ricaduta dopo tale terapia è comune e la sopravvivenza dei pazienti stimata a 5 anni è ancora inferiore al 30%. Risulta quindi di primaria importanza trovare alternative terapeutiche per i pazienti recidivanti e refrattari. Il recente successo clinico, ottenuto nelle leucemie di tipo B, dell'immunoterapia con cellule CAR (chimeric antigen receptor) T ha portato allo sviluppo di nuove strategie terapeutiche nell’ambito dell’LMA. Tuttavia, lo sviluppo del trattamento con cellule CAR T nel contesto dell'LMA è ancora agli albori a causa dell'eterogeneità della malattia, della mancanza di un antigene bersaglio adatto e del ruolo protettivo del microambiente tumorale (TME). Infatti, non esiste ancora un protocollo clinico approvato per il trattamento della leucemia mieloide. Per creare le cellule CAR T abbiamo scelto di utilizzare la piattaforma non virale Sleeping-Beauty (SB) per ingegnerizzare le cellule CIK (cytokine-induced killer). In primo luogo, abbiamo scelto di utilizzare come potenziale strumento per il targeting del TME le cellule CIK ingegnerizzate con anti-CD146.CAR. Di conseguenza, abbiamo ottimizzato 6 diverse molecole CAR aventi un design differente, ottenendo un'espressione ottimale di CD146 nella variante VLVH Long. Abbiamo quindi testato le cellule CD146.CAR-CIK in vitro, ottenendo l’attivazione specifica delle funzioni effettrici (in termini di capacità di killing, produzione di citochine e proliferazione) contro cellule target CD146+. In seguito, abbiamo progettato un Tandem CAR bispecifico (CD33xCD146.CAR-CIKs) che ha mostrato una significativa attività antileucemica in vitro. È stato ampiamente dimostrato che la nicchia midollare contribuisce al supporto e alla protezione delle cellule staminali leucemiche (CSLs). Quindi, per mimare al meglio l’azione del CAR nella nicchia midollare umana, abbiamo testato le cellule CD33xCD146.CAR-CIK contro le linee cellulari stromali CD146+ e le cellule mesenchimali (MSC) primarie sane (HD-) e di derivazione mieloide (LMA-). I dati mostrano una inibizione delle funzioni effettrici delle cellule CAR-CIK e una drastica diminuzione della produzione di citochine e della proliferazione. Inoltre, l'equilibrio tra citochine pro e antinfiammatorie è risultato alterato, infatti la produzione di citochine Th1/Tc1 da parte delle cellule CD146.CAR-CIK è stata inibita dalla co-coltura con cellule stromali, mentre è stato rilevato un aumento delle citochine Th2/Tc2. Questi risultati suggeriscono un potenziale ruolo immunosoppressivo del compartimento stromale nei confronti delle cellule CAR-CIK. Sulla base dell’ effetto immunomodulatorio delle MSC sui linfociti T, abbiamo ipotizzato che la nicchia midollare possa influenzare le funzioni effettrici delle cellule CAR T. Di conseguenza, il targeting del CD146 rappresenta una "proof-of-principles" del fatto che aggredire il microambiente leucemico possa migliorare la terapia CAR T nell’ambito dell’LMA. Per ridurre al minimo la tossicità "off-target ", stiamo cercando di selezionare un antigene bersaglio specifico ed overespresso sulle cellule stromali dell'LMA, che abbia un'espressione minima nello stroma sano e che sia coinvolto nelle interazioni leucemia/nicchia. Il nuovo marker di interesse sarà accoppiato al CD33.CAR nella creazione di un CAR bispecifico, che verrà confrontato con il costrutto CD33xCD146.CAR, valutandone i profili di efficacia e sicurezza sia in vitro che in vivo.
Acute myeloid leukemia (AML) is the most frequently diagnosed leukemia in adults (25%) and accounts for 15-20% cases in pediatric patients. Conventional chemotherapy employing anthracycline and cytarabine represents the gold standard treatment for AML, with rates of complete remission from 60% to 80% in children and from 40% to 60% in adults (>60 years). Despite these high rates, relapse after conventional therapy is common and the estimated five-year survival of AML patients is still below 30%. Indeed, there is an urgency to find alternative therapeutic strategies for relapsed and refractory patients. The recent clinical success of chimeric antigen receptor (CAR) T cell immunotherapy in the context of B-cell malignancies has opened a new route of investigation also towards AML. However, the development of CAR T cell therapy in the context of AML is still in its infancy due to heterogeneity of the disease, the lack of a suitable target antigen and the leukemia protective role of the tumor microenvironment (TME) and no approved CAR T cells study exists for AML treatment yet. Non-viral Sleeping-Beauty (SB) transposon platform was employed to redirect cytokine-induce killer (CIK) cell. In this scenario, we firstly characterize non-viral SB engineered CIK cells with anti-CD146.CAR as a potential tool for the targeting of the bone marrow (BM) microenvironment. We optimized the CAR design structure by testing 6 different CAR molecules, achieving a specific and efficient CD146 expression in the VLVH Long variant. CD146.CAR-CIK cells were subsequently tested in vitro, showing an optimal activation of effector functions (in terms of killing activity, cytokines production and proliferation) when they were engaged against CD146+ target cells. Consequently, we developed a bispecific Tandem CAR (CD33xCD146.CAR-CIKs), which displayed anti-leukemic activity in vitro. It has been extensively proven that BM niche contribute to establish a sanctuary in which leukemic stem cells (LSCs) are able to acquire drug-resistant phenotype, therefore, to better mimicking the human BM niche we tested CD33xCD146.CAR-CIK cells against CD146+ stromal cell lines (HS-27A and HS-5) and primary derived healthy (HD-) and patient-derived (AML-) mesenchymal stromal cells (MSCs). Results showed inhibition of the redirected CAR-CIK cells effector functions, resulting in a drastic decrease of cytokines production and proliferation. The balance between pro- and anti- inflammatory cytokines showed that Th1/Tc1 cytokines production by CD146.CAR-CIK cells was inhibited by the co-culture with stromal cells, while increase Th2/Tc2 cytokines was detected when CD146.CAR-CIK cells were co-cultured with stromal target cells. These results suggest a potential immunosuppressive role of the stromal compartment against CAR-CIK cells. According to these results, we hypothesized that BM stromal cells can potentially exert an immunomodulatory effect on T cells, suggesting that the niche microenvironment may be involved in the regulation of CAR T cells therapy effectiveness. Indeed, the targeting of CD146 on stroma represents a “proof-of-principle” that stromal components of leukemic microenvironment may be attractive targets for CAR T based immunotherapy. To minimize “off-tumor” toxicity, we are looking for a specific surface target antigen selectively overexpressed on AML stromal cells, with minimal expression in healthy stroma and possibly involved in leukemia/niche interactions. The newly marker of interest will be coupled to the CD33.CAR and this bispecific CAR will be compared with CD33xCD146.CAR construct, evaluating their efficacy and safety profiles both in vitro and in vivo.
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Aichelin, Katharina [Verfasser], i Peter [Akademischer Betreuer] Angel. "Development of a CD22-specific chimeric antigen receptor (CAR) for the adoptive T cell therapy of leukemia and lymphoma / Katharina Aichelin ; Betreuer: Peter Angel". Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1211090434/34.

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Książki na temat "CAR-T therapy"

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Furniss, Tilman. The multi-professional handbook of child sexual abuse: Integrated management, therapy, and legal intervention. London: Routledge, 1991.

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Tejirian, Edward J. Sexuality andthe devil: Symbols of love, power, and fear in male psychology. London: Routledge, 1990.

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InfoNet, BMT. Apr 2020 CAR T-Cell Therapy. Before, During and After. BMT InfoNet, 2020.

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InfoNet, BMT. Jan 2021 CAR T-Cell Therapy. Before, During and After. BMT InfoNet, 2021.

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InfoNet, BMT. Aug 2022 CAR T-Cell Therapy: Before, During and after - English. BMT InfoNet, 2022.

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Buka, Richard J., i Ankit J. Kansagra. Fast Facts : CAR T-Cell Therapy: Insight into Current and Future Applications. Karger AG, S., 2021.

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NCCN Guidelines for Patients® Immunotherapy Side Effects CAR T-Cell Therapy. National Comprehensive Cancer Network® (NCCN®), 2024.

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Fast Facts : CAR T-Cell Therapy: Insight into Current and Future Applications. Karger AG, S., 2021.

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National Comprehensive Cancer Network® (NCCN®). NCCN Guidelines for Patients® Immunotherapy Side Effects: CAR T-Cell Therapy. National Comprehensive Cancer Network® (NCCN®), 2022.

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Young, Ken, Zheming Lu i Wenbin Qian, red. The Novel Engineering Strategies and Clinical Progress of Solid Tumor in CAR-T Cell Therapy. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-791-5.

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Części książek na temat "CAR-T therapy"

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Irizarry Gatell, Vivian M., Jeffrey Huang i Omar A. Castaneda Puglianini. "CAR T-Cell Therapy". W Anesthesia for Oncological Surgery, 35–44. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-50977-3_5.

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Friedman, Mark T., Kamille A. West, Peyman Bizargity, Kyle Annen, H. Deniz Gur i Timothy Hilbert. "“CAR T”-esian Thinking". W Immunohematology, Transfusion Medicine, Hemostasis, and Cellular Therapy, 693–97. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-14638-1_95.

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Samal, Priyanka, i Sasmita Das. "Patients on CAR T Cell Therapy". W Critical Care Hematology, 321–40. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-97-5565-3_26.

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Gutierrez, Cristina, Oren Pasvolsky i Partow Kebriaei. "CAR T-Cell Therapy and Critical Care Considerations". W Pulmonary and Critical Care Considerations of Hematopoietic Stem Cell Transplantation, 427–35. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-28797-8_32.

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Rasche, Leo, Luca Vago i Tuna Mutis. "Tumour Escape from CAR-T Cells". W The EBMT/EHA CAR-T Cell Handbook, 15–22. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_4.

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AbstractOver the past decade, CAR-T cells have emerged as one of the most powerful cellular immune therapy approaches in the battle against haematological malignancies. Nonetheless, similar to other immunotherapeutic approaches, tumour cells develop strategies to evade CAR-T cell therapy, often with the support of a highly immunosuppressive and protective tumour microenvironment. To date, antigen loss, immune dysfunction, exhaustion and (microenvironment-mediated) upregulation of antiapoptotic pathways have been identified as major modes of tumour escape from CAR-T cell therapy. This chapter will focus on our current understanding of these modes of immune escape from CAR-T cells.
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Hu, Jinqiao. "CAR-NK Cell Therapy: A Promising Alternative to CAR-T Cell Therapy". W Proceedings of the 2022 6th International Seminar on Education, Management and Social Sciences (ISEMSS 2022), 372–81. Paris: Atlantis Press SARL, 2022. http://dx.doi.org/10.2991/978-2-494069-31-2_48.

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Zhao, Jingyu. "Research Progress of CAR-T Therapy in Tumor Therapy". W Proceedings of the 2022 6th International Seminar on Education, Management and Social Sciences (ISEMSS 2022), 49–58. Paris: Atlantis Press SARL, 2022. http://dx.doi.org/10.2991/978-2-494069-31-2_7.

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Delgado, Julio, Claire Roddie i Michael Schmitt. "Point-of-Care Production of CAR-T Cells". W The EBMT/EHA CAR-T Cell Handbook, 45–49. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_8.

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AbstractCAR-T cells for clinical application are classified as advanced therapy medicinal products (ATMPs), and their manufacture is subject to laws and regulations governed by the European Medicines Agency (EMA) and by federal and regional authorities. CAR-T cells must be manufactured to achieve good manufacturing practice (GMP) compliance and are defined as potent products manufactured safely according to standardized methods under closely controlled, reproducible, and auditable conditions. BioPharma supplies the vast majority of CAR-T products for patients, but some academic centres have developed point-of-care cGMP CAR-T manufacturing capability, striving to uphold the same stringency of product quality while improving patient access to CAR-T cells and streamlining the costs of therapy. Point-of-care CAR-T manufacturing can only be performed in facilities with the appropriate regulatory approvals in place.
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Adada, Mohamad M., Elizabeth L. Siegler i Saad S. Kenderian. "Combination Therapeutics with CAR-T Cell Therapy". W Cancer Drug Discovery and Development, 69–90. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87849-8_5.

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Manier, Salomon, Artur Jurczyszyn i David H. Vesole. "Bridging Chemotherapy: Multiple Myeloma". W The EBMT/EHA CAR-T Cell Handbook, 127–29. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_24.

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AbstractIn the phase 2 KarMMa study, 88% of the patients received bridging therapy with only a 5% response (Munshi et al. 2021). In the CARTITUDE 1 trial, 75% of the patients received bridging therapy, with a reduction in tumour burden observed in 34% of the patients prior to cilta-cel infusion, but no patients achieved a CR or better while on bridging therapy (Madduri et al. 2019). Bridging therapy is recommended for virtually all patients. An exception can be discussed for patients with slowly progressive disease, who may not need to receive bridging therapy after leukapheresis; however, this strategy exposes them to a risk of rapid progression later during the manufacturing period. In the future, with allogeneic CAR-T cells, bridging therapy will likely not be necessary because the time between patient inclusion and CAR-T cell infusion is much reduced.
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Streszczenia konferencji na temat "CAR-T therapy"

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Gupta, Aarya Kapil, i Gaurav Sharma. "Graph Neural Network and Molecular Docking Simulations of Aptamer-Mediated CAR T-Cell Therapy". W 2024 IEEE MIT Undergraduate Research Technology Conference (URTC), 1–4. IEEE, 2024. https://doi.org/10.1109/urtc65039.2024.10937542.

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Caoimh, Russell, Stanila Raluca, Bacon Larry, Doherty Colin i Langan Yvonne. "EEG in CAR-T Therapy". W Association of British Neurologists: Annual Meeting Abstracts 2023. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jnnp-2023-abn.48.

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Padmanabhan Menon, D., Y. T. Debella, J. A. Marin-Acevedo, S. Fernandez-Bussy i I. C. Mira-Avendano. "CAR-T Therapy Complicated by Cavitary CMV". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5202.

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Gui, Yuyin. "The bottleneck of CAR-T cell therapy". W International Conference on Biological Engineering and Medical Science (ICBIOMed2022), redaktorzy Gary Royle i Steven M. Lipkin. SPIE, 2023. http://dx.doi.org/10.1117/12.2669935.

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Zijia, Cheng. "Chimeric-antigen Receptor T (CAR-T) Cell Therapy for Leukemia". W ICBET 2020: 2020 10th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3397391.3397451.

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Tent, Michiel. "CAR-T cell therapy results in sustained lupus remission". W ACR Convergence 2023. Baarn, the Netherlands: Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/00470d55.

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Li, Yumeng. "Existing problems and improving methods of CAR-T therapy". W Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), redaktor Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3012990.

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Wang, Clara, Haoyang Guo, Hanqin Yang i Beibo Kang. "Developing CAR-T Therapy for Treating B Cell Malignancies". W International Conference on Biotechnology and Biomedicine. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0012015100003633.

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Roddie, Claire. "23 Origins of CAR-T cell therapy: hematologic perspective". W 13th Annual Meeting of the Lupus Academy, Hybrid Annual Meeting (Amsterdam), September 6–8, 2024, A14.1—A14. Lupus Foundation of America, 2024. http://dx.doi.org/10.1136/lupus-2024-la.24.

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Jing, Ran, Mohamad Najia, Eleanor Meader, Luca Hensch, Edroaldo Lummertz da Rocha, R. Grant Rowe, Thorsten Schlaeger, Marcela Maus, Trista North i George Daley. "950 Epigenetic reprogramming of iPSC-derived T cells for CAR T cell therapy". W SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0950.

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Raporty organizacyjne na temat "CAR-T therapy"

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Bonnett, Megan. CAR T Cell Therapy. Ames (Iowa): Iowa State University, styczeń 2019. http://dx.doi.org/10.31274/cc-20240624-337.

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Gilkeson, Kyle. CAR T-Cell Therapy: A New Road to Treat Cancer. Ames (Iowa): Iowa State University, styczeń 2020. http://dx.doi.org/10.31274/cc-20240624-339.

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Parris, Austin. CAR T-Cell Therapy for Solid Tumors: How Far Are We from Reality? Ames (Iowa): Iowa State University, styczeń 2019. http://dx.doi.org/10.31274/cc-20240624-338.

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Kumar, Tarun, i Sauvit S. Patil. Reimagining Clioblastoma Multiforme Treatment with the Emerging Role of CAR-T Cell Therapy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, październik 2024. http://dx.doi.org/10.37766/inplasy2024.10.0040.

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Zhao, Kangjia, Jiwen Sun, Nanping Shen, Mengxue He, Haishan Ruan, Geng Lin, Jiali Ma i Yanhua Xu. Treatment-Related Adverse Events of Chimeric Antigen receptor T-Cell (CAR-T) Cell Therapy in B-cell hematological malignancies in the Pediatric and Young Adult Population: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, lipiec 2022. http://dx.doi.org/10.37766/inplasy2022.7.0034.

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Tzfira, Tzvi, Michael Elbaum i Sharon Wolf. DNA transfer by Agrobacterium: a cooperative interaction of ssDNA, virulence proteins, and plant host factors. United States Department of Agriculture, grudzień 2005. http://dx.doi.org/10.32747/2005.7695881.bard.

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Agrobacteriumtumefaciensmediates genetic transformation of plants. The possibility of exchanging the natural genes for other DNA has led to Agrobacterium’s emergence as the primary vector for genetic modification of plants. The similarity among eukaryotic mechanisms of nuclear import also suggests use of its active elements as media for non-viral genetic therapy in animals. These considerations motivate the present study of the process that carries DNA of bacterial origin into the host nucleus. The infective pathway of Agrobacterium involves excision of a single-stranded DNA molecule (T-strand) from the bacterial tumor-inducing plasmid. This transferred DNA (T-DNA) travels to the host cell cytoplasm along with two virulence proteins, VirD2 and VirE2, through a specific bacteriumplant channel(s). Little is known about the precise structure and composition of the resulting complex within the host cell and even less is known about the mechanism of its nuclear import and integration into the host cell genome. In the present proposal we combined the expertise of the US and Israeli labs and revealed many of the biophysical and biological properties of the genetic transformation process, thus enhancing our understanding of the processes leading to nuclear import and integration of the Agrobacterium T-DNA. Specifically, we sought to: I. Elucidate the interaction of the T-strand with its chaperones. II. Analyzing the three-dimensional structure of the T-complex and its chaperones in vitro. III. Analyze kinetics of T-complex formation and T-complex nuclear import. During the past three years we accomplished our goals and made the following major discoveries: (1) Resolved the VirE2-ssDNA three-dimensional structure. (2) Characterized VirE2-ssDNA assembly and aggregation, along with regulation by VirE1. (3) Studied VirE2-ssDNA nuclear import by electron tomography. (4) Showed that T-DNA integrates via double-stranded (ds) intermediates. (5) Identified that Arabidopsis Ku80 interacts with dsT-DNA intermediates and is essential for T-DNA integration. (6) Found a role of targeted proteolysis in T-DNA uncoating. Our research provide significant physical, molecular, and structural insights into the Tcomplex structure and composition, the effect of host receptors on its nuclear import, the mechanism of T-DNA nuclear import, proteolysis and integration in host cells. Understanding the mechanical and molecular basis for T-DNA nuclear import and integration is an essential key for the development of new strategies for genetic transformation of recalcitrant plant species. Thus, the knowledge gained in this study can potentially be applied to enhance the transformation process by interfering with key steps of the transformation process (i.e. nuclear import, proteolysis and integration). Finally, in addition to the study of Agrobacterium-host interaction, our research also revealed some fundamental insights into basic cellular mechanisms of nuclear import, targeted proteolysis, protein-DNA interactions and DNA repair.
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