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Thematische Bibliographien / Gene therapy

Auswahl der wissenschaftlichen Literatur zum Thema „Gene therapy“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 25. Mai 2024

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Dissertationen
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Buchteile
Konferenzberichte
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Zeitschriftenartikel zum Thema "Gene therapy":

1

Goyal, Anjana, Reena Doomra, Aayushi Garg und Kruthiventi Hemalata. „CRISPR Gene Therapy in Dentistry“. Asian Pacific Journal of Health Sciences 6, Nr. 2 (Juni 2019): 182–83. http://dx.doi.org/10.21276/apjhs.2019.6.2.26.

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Gawthorpe, Paula. „Gene Therapy Gene Therapy“. Nursing Standard 17, Nr. 33 (30.04.2003): 29. http://dx.doi.org/10.7748/ns2003.04.17.33.29.b25.

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M. Gordon, Erlinda, Joshua R. Ravicz, Sant P. Chawla, Christopher W. Szeto, Sant P. Chawla, Michael A. Morse, Frederick L. Hall und Erlinda M. Gordon. „CCNG1 oncogene: a novel biomarker for cancer therapy /gene therapy“. Cancer Research and Cellular Therapeutics 5, Nr. 4 (30.08.2021): 01–09. http://dx.doi.org/10.31579/2640-1053/090.

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Background: Metastatic cancer is associated with an invariably fatal outcome. However, DeltaRex-G, a tumor-targeted retrovector encoding a gene-edited dominant-negative CCNG1 inhibitor gene, has induced long term (>10 years) survival of patients with chemo-resistant metastatic pancreatic adenocarcinoma, malignant peripheral nerve sheath tumor, osteosarcoma, B-cell lymphoma, and breast carcinoma. Objective: To evaluate the level of CCNG1 expression in tumors as a potential biomarker for CCNG1 (Cyclin G1-blocking) inhibitor therapy. Methods: CCNG1 RNA expression levels that were previously measured as part of whole genome molecular profiling of tumors (TCGA, N=9161), adjacent “tissues” (TCGA, N=678) and GTEx normal tissues (N=7187) across 22 organ sites were analyzed. Differential expression of CCNG1 and Ki-67 in primary (N= 9161) vs metastatic (N= 393) tumors were also compared in primary (N=103) vs. metastatic (N=367) skin cancers (i.e., melanoma). Statistical Analysis: To detect systematically differential expression of CCNG1 and Ki-67 expression between populations (e.g. tumor vs. normal), unpaired Student's t-tests were performed. Results: Enhanced CCNG1 RNA and Cyclin G1 protein expression were noted in tumors compared to normal analogous counterparts, and CCNG1 expression correlated significantly with that of Ki-67. Moreover, CCNG1 expression tended to be higher than that of Ki-67 in metastatic vs primary tumors. Conclusions: Taken together with the emerging Cyclin G1 / Cdk / Myc / Mdm2 / p53 Axis governing Cancer Stem Cell Competence, this supportive data indicates: (1) CCNG1 expression is frequently enhanced in tumors when compared to their normal analogous counterparts, (2) CCNG1 and Ki-67 expressions are higher in metastatic vs primary tumors, (3) CCNG1 expression is significantly correlated with that of Ki-67, and (4) CCNG1 may actually be a stronger prognostic marker of stem cell competence, chemo-refractoriness, and EMT/metastasis than Ki-67. Phase 2 studies are planned to identify patients most likely to respond favorably to CCNG1 inhibitor therapy.

4

Sose, Mr Aadesh S., und Mr Pramod M. Bhosale. „A Review on Gene Therapy for Cancer“. International Journal of Research Publication and Reviews 4, Nr. 4 (April 2023): 3058–63. http://dx.doi.org/10.55248/gengpi.4.423.36713.

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5

&NA;. „Gene therapy“. Inpharma Weekly &NA;, Nr. 1161 (Oktober 1998): 12. http://dx.doi.org/10.2165/00128413-199811610-00018.

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&NA;. „Gene therapy“. Inpharma Weekly &NA;, Nr. 1184 (April 1999): 8. http://dx.doi.org/10.2165/00128413-199911840-00015.

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Peroutka, Christina, und Joann Bodurtha. „Gene Therapy“. Pediatrics in Review 41, Nr. 11 (November 2020): 606–8. http://dx.doi.org/10.1542/pir.2019-0224.

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&NA;. „Gene therapy“. Inpharma Weekly &NA;, Nr. 1120 (Januar 1998): 4. http://dx.doi.org/10.2165/00128413-199811200-00004.

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9

Whartenby, Katharine A., Aizen J. Marrogi und Scott M. Freeman. „Gene Therapy“. Drugs 50, Nr. 6 (Dezember 1995): 951–58. http://dx.doi.org/10.2165/00003495-199550060-00003.

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Williamson, Robert. „Gene therapy“. Australian Prescriber 20, Nr. 3 (01.07.1997): 72–73. http://dx.doi.org/10.18773/austprescr.1997.062.

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Dissertationen zum Thema "Gene therapy":

1

Vasanwala, Farha Huseini. „Gene manipulations for cancer gene therapy“. Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/289776.

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Tumor cells can be modified with cytokine genes such as the Interleukin-2 (IL-2) gene. The levels of IL-2 expressed are critical for successful treatment. We have tried to achieve higher levels of IL-2 than those currently available by conventional plasmids. Use of a transcriptional activator, e.g; the tat gene along with the HIV promoter driving the IL-2 gene, greatly increased IL-2 levels compared to widely used cytomegalovirus (CMV) driven plasmids. Control of the tat gene with an inducible promoter, i.e; the human HSP70B promoter, permitted control of gene expression. The inducibility of the HSP70B promoter by heat, γ-radiation and geldanamycin (a chemotherapeutic drug) allowed for a combinatorial approach to cancer treatment with hyperthermia, radiation therapy and chemotherapy. Also a brief heat treatment of 10 min at 42°C of target cells increased plasmid uptake, and higher levels of gene expression could be achieved. Another arm of immunotherapy is adoptive therapy with Tumor Infiltrating Lymphocytes (TILs). Insufficient numbers of tumor-specific T-cells limit the success of TIL therapy. An alternative approach to overcome this limitation is to transfer tumor-specific T cell receptor (TCR) into peripheral T-cells, redirecting their specificity to the tumor cell. To prove the feasibility of this technique, T-cell receptors were identified and cloned from hybridomas specific for the tumor cell line, MO5. A three domain single chain T-cell receptor was also constructed from the tumor-specific TCR genes to investigate the ability of a single chain T-cell receptor to activate T-cells. The CD3ζ chain was linked to the single chain to allow signal transduction upon antigen recognition by the TCR. The full length and the single chain TCR were cloned into a retroviral vector and transfected into mouse and human T cell lines. Cell surface expression of the chains were detected by flow cytometry. Functionality of the transfected TCR chains was assessed by IL-2 secretion on co-culture of the tumor cell line MO5 and the transfected T-cells. The two different approaches described here, i.e; higher levels of IL-2 for IL-2 gene therapy and specific redirection of T-cells can potentially greatly enhance the success rate of cancer treatment.

2

Santos, João Miguel Almeida. „Gene therapy: development of a new nanocarrier system for mitochondrial gene therapy“. Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1627.

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Mitochondria are unique organelles that have their own genome, the mitochondrial DNA (mtDNA). Although quite small compared to nuclear DNA (nDNA), mutations in mtDNA are quite frequent due to the lack of protection and repair mechanisms. Per consequence, cytopathies and diseases are quite common and mostly associated with high energy demanding tissues such as muscles and the brain. Therefore, the development of a new and efficient mitochondrial gene therapy protocol is seen as a promising approach. During this MSc thesis we try to bring together a new nanocarrier system with the ability to deliver plasmid DNA into the mitochondria, for future application in mitochondrial gene therapy (MGT). Hence, the development of this research project can be divided itself into three main stages: 1. Isolation and purification of three plasmid DNAs (pUC19, pVAX1-LacZ and pcDNA3-myc-FLNa S2152A); 2. Synthesis and characterization of nanoparticles with mitochondria affinity; 3. In vitro study of mitochondrial transfection ability. The newly developed nanoparticles, created through a co precipitation method, offer us unique features such as: biocompatibility, plasmid DNA (pDNA) encapsulation efficiency and low manufacturing cost. We were able to successfully achieve transfection into the mitochondria which may result in a huge step in the correction of mitochondrial defects, offering new therapeutic strategies for a variety of pathologies ranging from cancer to Parkinson and Alzheimer´s diseases.
As mitocôndrias são organelos únicos pois possuem o seu próprio genoma, o ADN mitocondrial (ADNmt). Apesar de bastante pequeno quando comparado com o ADN nuclear (ADNn), mutações ao nível do ADNmt são bastante frequentes devido à falta de mecanismos de protecção e de reparação. Como consequência, citopatias e doenças associadas à mitocôndria são bastante frequentes afectando essencialmente órgãos e tecidos onde existe muito dispêndio de energia como é o caso dos músculos e do cérbero. Logo, o desenvolvimento de um novo e eficiente protocolo para terapia génica mitocondrial (MGT) é visto como uma proposta aliciante. Durante esta tese de Mestrado, tentamos criar um novo nanosistema que consiga entregar eficazmente ADN plasmídico (pDNA) à mitocôndria para que no futuro possa ser usado em terapia génica mitocondrial (MGT). Assim, este projecto de investigação pode ser dividido em três etapas principais: 1. O isolamento e purificação de três plasmídeos (pUC19, pVAX1-LacZ e pcDNA3-myc-FLNa S2152A); 2. A síntese e caracterização de nanopartículas com afinidade para a mitocôndria; 3. O estudo da capacidade das nanopartículas efectuarem transfecção celular e dirigirem-se à mitocôndria; As nanopartículas desenvolvidas, através do método de co-precipitação oferecem-nos qualidades únicas como a sua biocompatibilidade, alta eficiência de encapsulamento de ADN e baixo custo de produção. A transfecção celular foi alcançada com sucesso sendo que, tais resultados, podem contribuir em grandes avanços na correcção de defeitos mitocondriais, oferecendo-nos uma nova estratégia terapêutica no combate a diversas patologias desde o cancro, às doenças de Parkinson e Alzheimer.

3

Nanda, Dharminderkoemar. „Gene therapy for gliomas“. [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13140.

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4

Hayes, E. A. L. „Anti-angiogenic gene therapy“. Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603877.

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The aim of this project was to assess a novel anti-angiogenic gene therapy in which a therapeutic gene is activated exclusively in proliferating endothelial cells using tissue-specific promoters and the Cre/IoxP recombination system. Adenoviruses and transgenic mice were generated in parallel to test individual components of the targeting system. One of the therapeutic effector strategies investigated was the herpes simplex virus-1 thymidine kinase (HSV-1TK)/ganciclovir (GCV)-mediated suicide system, which is reported to kill proliferating cells selectively. Administration of GCV to pTie2-TK transgenic mice expressing HSV-1 TK under the control of the endothelial cell-specific Tie2 promoter and to mice treated systemically with a pTie2-TK adenovirus was lethal, demonstrating that additional control was required to target exclusively proliferating endothelial cells. Intra-tumoural (i.t.) injection of pTie2-TK adenovirus resulted in tumour-restricted expression of HSV-1 TK and preliminary data demonstrated a trend towards a decrease in primary tumour growth following treatment of mice with i.t. pTie2 adenovirus and GCV. The tet Off system was investigated as a method to obtain conditional control of Cre recombinase expression. Despite showing tight regulation in vitro, this system did not result in complete silencing of transgene expression in vivo. Transgenic mice expressing tamoxifen (TMX)-regulated Cre recombinase under the control of the cell-cycle dependent Cyclin A promoter were also generated, but problems with TMX administration precluded determination of whether Cre recombinase was activated by TMX in these mice. However, conditional transgene activation was achieved in vivo by generating a pCycA-Cre adenovirus in which the Cyclin A promoter was used to drive expression of Cre recombinase. A pTie2-stuffer-TK transgenic mouse line was generated which expressed a Cre-activatable form of HSV-1 TK under the control of the Tie2 promoter. To target proliferating endothelial cells specifically, the pCycA-Cre adenovirus was used to activate HSV-1 TK in these transgenic mice. Preliminary data showed that there was a trend towards a decrease in primary tumour growth following treatment of pTie2-stuffer-TK transgenic mice with i.t. pCycA-Cre adenovirus and GCV. Transgenic mice expressing an alternative Cre-activated therapeutic gene, the pro-apoptotic gene Bax, under the control of the Tie2 promoter were generated by direct pronuclear injection and by site-specific transgene insertion into the hprt locus. pTie2-stuffer-Bax mice generated using the latter technique showed higher levels of Tie2 promoter-driven transgene expression than those made by pronuclear injection.

5

Bilsland, Alan. „Telomerase directed gene therapy“. Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272871.

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Katabi, Maha M. „Transcriptional targeting of suicide genes in cancer gene therapy“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/NQ55345.pdf.

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Morin, Kevin Wayne. „Scintigraphic imaging during gene therapy“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21605.pdf.

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Singwi, Sanjeev. „HIV gene therapy using nucleases“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0001/MQ46100.pdf.

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9

Horst, Maarten ter. „Gene therapy of malignant gliomas“. [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/10864.

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Lau, Cara Jean. „Gene therapy for malignant gliomas“. Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18478.

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Gliomas are the most common primary brain tumours found in adults. The median survival of patients diagnosed with the most malignant form, glioblastoma multiforme (GBM), is 9-12 months and has changed little over the years despite advances in medical technology. Gene therapy may offer new solutions to treat this resistant disease. Hence, we tested three different gene therapy strategies. In our first study, we tested the efficacy of targeted therapy to correct common aberrations found in gliomas including amplification/mutation of receptor tyrosine kinases (RTK) and loss of PTEN, which result in an overactive PI3K/Akt pathway. Without PTEN, FOXO transcription factors are inactivated, and the cell becomes resistant to apoptosis and cell cycle arrest. By using an adenoviral vector (AdV) expressing an activated FOXO1 mutant (AdFOXO1;AAA), we restored apoptosis and cell cycle arrest, reduced tumour volume and prolonged survival in an intracerebral xenograft model. Secondly, we examined the therapeutic capacity of a novel replicating/non-disseminating AdV expressing the fusion protein of cytosine deaminase and uracil phosphoribosyltransferase (CU). CU can convert the non-toxic pro-drug, 5-fluorocytosine (5-FC) to the tissue diffusible chemotherapeutic drug, 5-fluorouracil (5-FU) to target dividing cells. In vitro, the replicating vectors were superior to the non-replicating vectors, but the fully replicating/disseminating vector did not perform considerably better than the replicating/non-disseminating vector suggesting that dissemination may not be advantageous. In vivo, the replicating/non-disseminating vector administered in conjunction with 5-FC prolonged survival in both an athymic and an immunocompetent mouse model. Moreover, an immune bystander effect in vivo was mediated by macrophages and T cells. Lastly, we investigated a method to harness a tool of the immune system, IFN-ß; this cytokine is known to have anti-angiogenic, anti-proliferative, and immunomo
Les gliomes sont des tumeurs primaires de cerveau les plus communes retrouvées dans les adultes. La survie médiane des patients diagnostiqués avec la forme la plus maligne, le glioblastome multiforme (GBM), est de 9 à 12 mois et a peu changé au cours des années en dépit des avances en technologie médicale. La thérapie génique peut offrir de nouvelles solutions pour traiter cette maladie résistante. Durant nos travaux, nous avons examiné trois stratégies différentes de thérapie génique Dans notre première étude, nous avons examiné l'efficacité de la thérapie visée à corriger des anomalies communes retrouvées dans les gliomes, comprenant l'amplification/mutation de récepteurs de type tyrosine kinase (RTK) et la perte de PTEN, qui mènent en conséquence à une voie activée de PI3K/Akt. Sans PTEN, les facteurs de transcription FOXO sont inactivés, et la cellule devient résistante à l'arrêt du cycle cellulaire et à l'apoptose. En utilisant un vecteur adénoviral (AdV) exprimant une protéine activée du mutant FOXO1 (AdFOXO1;AAA.), nous avons reconstitué les signaux pour l'arrêt du cycle cellulaire et l'apoptose in vitro ainsi que in vivo. Deuxièmement, nous avons examiné la capacité thérapeutique d'un nouveau vecteur adénovirale qui a la capacité de se répliquer sans provoquer de lyse cellulaire et qui exprime en plus la protéine de fusion uracile phosphoribosyltransférase/cytosine déaminase (CU). La protéine CU peut convertir le promédicament non-toxique, le 5-fluorocytosine (5-FC) à la drogue chimiothérapeutique diffusible, le 5-fluorouracile (5-FU) qui a comme cible des cellules en division cellulaire. In vitro, les vecteurs à capacité de répliquation étaient meilleurs que ceux qui ne pouvaient pas se répliquer. In vivo, le vecteur en présence du 5-FC a prolongé la survie de deux modès animaux (avec et sans sytèmes immunitaires). Dans un dernier temps, nous avons étudié une méthode pour exprimer l'IF

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Bücher zum Thema "Gene therapy":

1

Xanthopoulos, Kleanthis G., Hrsg. Gene Therapy. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72160-1.

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Blankenstein, Thomas, Hrsg. Gene Therapy. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-7011-5.

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3

Sobol, R. E., K. J. Scanlon und E. Nestaas, Hrsg. Gene Therapy. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03577-1.

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Giacca, Mauro. Gene Therapy. Milano: Springer Milan, 2010. http://dx.doi.org/10.1007/978-88-470-1643-9.

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Kelly, Evelyn B. Gene therapy. Westport, Conn: Greenwood Press, 2007.

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NATO, Study Institute "Gene Therapy" (1997 Spetsai Greece). Gene therapy. Berlin: Springer, 1998.

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Giacca, Mauro. Gene therapy. Dordrecht: Springer, 2010.

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1952-, Sobol Robert E., Hrsg. Gene therapy. Berlin: Springer-Verlag, 1998.

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Dr, Cooper David N., und Lemoine Nicholas R, Hrsg. Gene therapy. Oxford, UK: Bios Scientific Publishers, 1996.

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Naff, Clay Farris. Gene therapy. Herausgegeben von Naff Clay Farris. Detroit: Thomson/Gale, 2005.

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Buchteile zum Thema "Gene therapy":

1

Lee, Thomas F. „Gene Therapy“. In Gene Future, 127–63. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4899-2760-6_6.

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Cornetta, Kenneth. „Gene Therapy“. In Molecular Genetic Pathology, 717–29. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-405-6_29.

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Douglas, Joanne T., und David T. Curiel. „Gene Therapy“. In Molecular Biology of the Lung, 1–20. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8784-7_1.

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Choi, Vivian W., und R. Jude Samulski. „Gene Therapy“. In Vogel and Motulsky's Human Genetics, 867–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-37654-5_40.

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Rohini, K. „Gene Therapy“. In Advances in Biotechnology, 41–54. New Delhi: Springer India, 2013. http://dx.doi.org/10.1007/978-81-322-1554-7_4.

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Khan, Manzoor M. „Gene Therapy“. In Immunopharmacology, 363–96. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30273-7_11.

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Tanabe, Kenneth K., und James C. Cusack. „Gene Therapy“. In Surgery, 1881–900. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-57282-1_86.

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Huh, Warner K., Mack N. Barnes, F. Joseph Kelly und Ronald D. Alvarez. „Gene Therapy“. In Ovarian Cancer, 133–57. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3587-1_6.

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Swazo, Norman K. „Gene Therapy“. In Encyclopedia of Global Bioethics, 1–9. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05544-2_213-1.

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Taura, Akiko. „Gene Therapy“. In Regenerative Medicine for the Inner Ear, 215–21. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54862-1_23.

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Konferenzberichte zum Thema "Gene therapy":

1

„Advances in Gene Therapy“. In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916417.

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. Shcherbakova, S. A., P. E. Karitskaya, A. S. Chesnokova, I. O. Karpets, I. V. Evgenov und D. V. Tseylikman. „DIFFERENTIALLY EXPRESSED GENES PREDICTING RESPONSE TO TAMOXIFEN THERAPY IN BREAST CANCER PATIENTS“. In OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-40.

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The study is aimed at finding genes mediating the response to tamoxifen therapy. Meta-analysis of the articles and the construction of gene networks revealed 7 genes that make a significant contribution to survival rates. For the purpose of validation, the approach of analysis of differential gene expression was chosen. The validation results revealed a high occurrence of the desired genes. The pattern of deviation of their expression from the reference values was combined with that indicated by other authors.

3

Salimova, A. A., V. D. Drozd, D. S. Rybalko, A. A. Eldeeb, A. A. Dedovskayav und D. M. Kolpashchikov. „ANTISENSE OLIGONUCLEOTIDES RELEASING CASSETTE FOR CANCER THERAPY“. In OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-49.

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Cancer gene therapy is a challenging area of research. Cancer therapy aims to target mutated genes that play crucial roles in tumorigenesis. However, this approach often encounters challenges such as low efficiency and off-target effects. Consequently, the number of drugs approved for clinical use remains limited. Here, we suggest a novel approach in cancer therapy — a DNA construct that is able to target vital housekeeping genes in a cancer-marker dependent manner.

4

Jiang, Xingyu. „Nanocluster-enabled Gene Therapy“. In The 7th International Multidisciplinary Conference on Optofluidics 2017. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/optofluidics2017-04542.

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Sakr, N. „DEVELOPMENT OF GENE THERAPY FOR CAH“. In Конференция «Перспективы применения генной терапии и биомедицинского клеточного продукта» с блоком летней школы для молодых ученых. Федеральное государственное бюджетное учреждение «Национальный медицинский исследовательский центр эндокринологии» Министерства здравоохранения Российской Федерации, 2022. http://dx.doi.org/10.14341/gnct-2022-51.

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6

Morgan, Jeffrey R. „Genetic Strategies for Tissue Engineering“. In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1165.

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Annotation:

Abstract Recent advances in molecular genetics have resulted in the development of new technologies for the introduction and expression of genes in human somatic cells. These gene transfer technologies have given rise to a potentially new field of medical treatment known as gene therapy. Gene therapy is broadly defined as the transfer of genetic material to cells or tissues in order to achieve a therapeutic effect for inherited as well as acquired diseases. We are exploring the potential application of gene transfer technologies to the field of tissue engineering and are interested in determining if genetic modification can be used to enhance the function and/or performance of cells used as or part of biological substitutes for the restoration, maintenance or improvement of tissue function. We believe that gene transfer technologies will be an important addition to the field of tissue engineering.

7

Vahedi, Golnaz, Babak Faryabi, Jean-Francois Chamberland, Aniruddha Datta und Edward Dougherty. „Modeling cyclic therapy in gene regulatory networks“. In 2008 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2008. http://dx.doi.org/10.1109/gensips.2008.4555670.

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8

Sirsi, Shashank R., Darrell Yamashiro, Jessica Kandel und Mark Borden. „Polyplex-microbubbles for ultrasound-mediated gene therapy“. In ICA 2013 Montreal. ASA, 2013. http://dx.doi.org/10.1121/1.4801416.

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9

Atsumi, N., A. Pilou, I. Pringle, RC Ashworth, C. Meng, M. Chan, DR Gill et al. „S120 Gene therapy for pulmonary alveolar proteinosis“. In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.126.

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10

Mokkapati, Sharada, Jon Duplisea, Michael Metcalfe, Amy Lim, Vikram Narayan, Devin Plote, Debashish Sundi et al. „Abstract IA21: Intravesical gene therapy for NMIBC“. In Abstracts: AACR Special Conference on Bladder Cancer: Transforming the Field; May 18-21, 2019; Denver, CO. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.bladder19-ia21.

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Berichte der Organisationen zum Thema "Gene therapy":

1

Higgins, Paul J. Inducible Anti-Angiogenic Gene Therapy. Fort Belvoir, VA: Defense Technical Information Center, Mai 2005. http://dx.doi.org/10.21236/ada437209.

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2

Agarwal, Nitin, Jorgen Magnus, John Kerwin, Charlotte Holmes, Sy Gebrekidan, Don Powers, Emily Moran et al. Gene therapy process manufacturing maps. BioPhorum, September 2020. http://dx.doi.org/10.46220/2020cgt003.

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3

Hayward, Simon W. Therapy Selection by Gene Profiling. Fort Belvoir, VA: Defense Technical Information Center, Mai 2008. http://dx.doi.org/10.21236/ada491350.

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4

Hayward, Simon W. Therapy Selection by Gene Profiling. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada454306.

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5

Hayward, Simon W. Therapy Selection by Gene Profiling. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada426169.

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6

Higgins, Paul J. Inducible Anti-Angiogenic Gene Therapy. Fort Belvoir, VA: Defense Technical Information Center, Mai 2004. http://dx.doi.org/10.21236/ada427186.

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7

Baylink, David J. Gene Therapy for Fracture Repair. Fort Belvoir, VA: Defense Technical Information Center, Dezember 2003. http://dx.doi.org/10.21236/ada431895.

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8

Segal, David J. Gene Therapy for Childhood Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, Mai 2014. http://dx.doi.org/10.21236/ada609751.

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9

Buchsbaum, Donald J. Radiopharmaceutical and Gene Therapy Program. Office of Scientific and Technical Information (OSTI), Februar 2006. http://dx.doi.org/10.2172/875908.

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10

Lau, William. Gene Therapy for Fracture Repair. Fort Belvoir, VA: Defense Technical Information Center, Mai 2007. http://dx.doi.org/10.21236/ada474569.

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