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Journal articles on the topic 'Gene and Molecular Therapy'

To see the other types of publications on this topic, follow the link: Gene and Molecular Therapy.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

M. Gordon, Erlinda, Joshua R. Ravicz, Sant P. Chawla, Christopher W. Szeto, Sant P. Chawla, Michael A. Morse, Frederick L. Hall, and Erlinda M. Gordon. "CCNG1 oncogene: a novel biomarker for cancer therapy /gene therapy." Cancer Research and Cellular Therapeutics 5, no. 4 (August 30, 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.

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2

Chung, Hesson, Ick Chan Kwon, and Seo Young Jeong. "Gene Therapy and Molecular Imaging." Journal of the Korean Medical Association 47, no. 2 (2004): 139. http://dx.doi.org/10.5124/jkma.2004.47.2.139.

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3

Das, Dipak K., Richard M. Engelman, Nilanjana Maulik, John A. Rousou, Joseph E. Flack, and David W. Deaton. "Molecular targets of gene therapy." Annals of Thoracic Surgery 68, no. 5 (November 1999): 1929–33. http://dx.doi.org/10.1016/s0003-4975(99)01015-2.

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4

Escobar Fernandez, H., A. Zhogov, E. Metzler, R. Kühn, and S. Spuler. "GENE EDITING AND MOLECULAR THERAPY." Neuromuscular Disorders 29 (October 2019): S150. http://dx.doi.org/10.1016/j.nmd.2019.06.399.

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5

Robbins, Jeffrey. "Gene Therapy and Molecular Toxicology." Cardiovascular Toxicology 1, no. 1 (2001): 03–06. http://dx.doi.org/10.1385/ct:1:1:03.

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6

Pálffy, R., R. Gardlík, J. Hodosy, M. Behuliak, P. Reško, J. Radvánský, and P. Celec. "Bacteria in gene therapy: bactofection versus alternative gene therapy." Gene Therapy 13, no. 2 (September 15, 2005): 101–5. http://dx.doi.org/10.1038/sj.gt.3302635.

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7

Tanaka, N., N. Matsubara, M. Ikeda, H. Takashima, T. Fujiwara, J. Shao, M. Ogawa, T. Fukazawa, and A. Hizuta. "Molecular colorectal tumorigenesis and gene therapy." Nippon Daicho Komonbyo Gakkai Zasshi 51, no. 9 (1998): 686–686. http://dx.doi.org/10.3862/jcoloproctology.51.686.

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8

Cehajic Kapetanovic, McClements, Martinez-Fernandez de la Camara, and MacLaren. "Molecular Strategies for RPGR Gene Therapy." Genes 10, no. 9 (September 4, 2019): 674. http://dx.doi.org/10.3390/genes10090674.

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Mutations affecting the Retinitis Pigmentosa GTPase Regulator (RPGR) gene are the commonest cause of X-linked and recessive retinitis pigmentosa (RP), accounting for 10%–20% of all cases of RP. The phenotype is one of the most severe amongst all causes of RP, characteristic for its early onset and rapid progression to blindness in young people. At present there is no cure for RPGR-related retinal disease. Recently, however, there have been important advances in RPGR research from bench to bedside that increased our understanding of RPGR function and led to the development of potential therapies, including the progress of adeno-associated viral (AAV)-mediated gene replacement therapy into clinical trials. This manuscript discusses the advances in molecular research, which have connected the RPGR protein with an important post-translational modification, known as glutamylation, that is essential for its optimal function as a key regulator of photoreceptor ciliary transport. In addition, we review key pre-clinical research that addressed challenges encountered during development of therapeutic vectors caused by high infidelity of the RPGR genomic sequence. Finally, we discuss the structure of three current phase I/II clinical trials based on three AAV vectors and RPGR sequences and link the rationale behind the use of the different vectors back to the bench research that led to their development.

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9

Glode, L. Michael. "The molecular bridge to gene therapy." Urology 44, no. 6 (December 1994): 81–88. http://dx.doi.org/10.1016/s0090-4295(94)80249-1.

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10

Orkin, Stuart H. "Molecular genetics and potential gene therapy." Clinical Immunology and Immunopathology 40, no. 1 (July 1986): 151–56. http://dx.doi.org/10.1016/0090-1229(86)90080-2.

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11

Stasiak, Andrzej. "Gene therapy." EMBO reports 2, no. 3 (March 2001): 180. http://dx.doi.org/10.1093/embo-reports/kve059.

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12

Culver, Kenneth W., W. French Anderson, and R. Michael Blaese. "Lymphocyte Gene Therapy." Human Gene Therapy 2, no. 2 (July 1991): 107–9. http://dx.doi.org/10.1089/hum.1991.2.2-107.

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13

VandenDriessche, Thierry. "Gene Therapy Delivers." Human Gene Therapy 20, no. 11 (November 2009): 1222–23. http://dx.doi.org/10.1089/hum.2009.1007.

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14

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 24, no. 5 (May 2013): 467–69. http://dx.doi.org/10.1089/hum.2013.2506.

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15

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 24, no. 6 (June 2013): 565–67. http://dx.doi.org/10.1089/hum.2013.2507.

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16

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 24, no. 7 (July 2013): 641–43. http://dx.doi.org/10.1089/hum.2013.2508.

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17

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 24, no. 12 (December 2013): 965–67. http://dx.doi.org/10.1089/hum.2013.2521.

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18

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 25, no. 2 (February 2014): 92–95. http://dx.doi.org/10.1089/hum.2014.2502.

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19

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 25, no. 4 (April 2014): 262–64. http://dx.doi.org/10.1089/hum.2014.2507.

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20

Philippidis, Alex. "Gene Therapy Briefs." Human Gene Therapy 25, no. 6 (June 2014): 482–85. http://dx.doi.org/10.1089/hum.2014.2526.

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21

Walsh MD PhD, Christopher E. "Fetal gene therapy." Gene Therapy 6, no. 7 (July 1999): 1200–1201. http://dx.doi.org/10.1038/sj.gt.3300991.

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22

Evans, CH, JN Gouze, E. Gouze, PD Robbins, and SC Ghivizzani. "Osteoarthritis gene therapy." Gene Therapy 11, no. 4 (January 15, 2004): 379–89. http://dx.doi.org/10.1038/sj.gt.3302196.

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23

Bagley, J., and J. Iacomini. "Gene Therapy Progress and Prospects: Gene therapy in organ transplantation." Gene Therapy 10, no. 8 (April 2003): 605–11. http://dx.doi.org/10.1038/sj.gt.3302020.

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24

Walsh, Christopher E. "Gene therapy Progress and Prospects: Gene therapy for the hemophilias." Gene Therapy 10, no. 12 (May 30, 2003): 999–1003. http://dx.doi.org/10.1038/sj.gt.3302024.

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25

Yechoor, V., and L. Chan. "Gene Therapy Progress and Prospects: Gene therapy for diabetes mellitus." Gene Therapy 12, no. 2 (October 21, 2004): 101–7. http://dx.doi.org/10.1038/sj.gt.3302412.

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26

Woo, Savio LC. "From “Gene Therapy” to “Gene and Cell Therapy”: Why?" Molecular Therapy 16, no. 12 (December 2008): 1899–900. http://dx.doi.org/10.1038/mt.2008.246.

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27

de Jesus, Marcelo Bispo. "Gene Therapy & Cell Therapy." Current Gene Therapy 21, no. 5 (December 23, 2021): 361. http://dx.doi.org/10.2174/156652322105211223141951.

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28

Douglas, Joanne T. "Cancer Gene Therapy." Technology in Cancer Research & Treatment 2, no. 1 (February 2003): 51–63. http://dx.doi.org/10.1177/153303460300200107.

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Cancer gene therapy is the transfer of genetic material to the cells of an individual with the goal of eradicating cancer cells, both in the primary tumor and metastases. Cancer gene therapy strategies exploit our expanding knowledge of the genetic basis of cancer, thereby allowing rationally targeted interventions at the molecular level. The successful implementation of cancer gene therapy in the clinic awaits the development of vectors capable of specific and efficient gene delivery to cancer cells. The first clinical applications of cancer gene therapy are likely to be in combination with conventional therapies, such as radiotherapy and immunotherapy.

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29

Baranov, V. S. "Molecular medicine: Molecular diagnostics, preventive medicine, and gene therapy." Molecular Biology 34, no. 4 (July 2000): 590–600. http://dx.doi.org/10.1007/bf02759567.

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30

Gaspar, H. B., S. Howe, and A. J. Thrasher. "Gene therapy progress and prospects: gene therapy for severe combined immunodeficiency." Gene Therapy 10, no. 24 (October 20, 2003): 1999–2004. http://dx.doi.org/10.1038/sj.gt.3302150.

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31

Griesenbach, U., D. M. Geddes, and E. W. F. W. Alton. "Gene therapy for cystic fibrosis: an example for lung gene therapy." Gene Therapy 11, S1 (September 29, 2004): S43—S50. http://dx.doi.org/10.1038/sj.gt.3302368.

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32

Wolkowicz, R., and G. P. Nolan. "Gene therapy progress and prospects: Novel gene therapy approaches for AIDS." Gene Therapy 12, no. 6 (February 10, 2005): 467–76. http://dx.doi.org/10.1038/sj.gt.3302488.

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33

Greenberger, J., M. Epperly, J. Gretton, M. Jefferson, S. Nie, M. Bernarding, V. Kagan, and H. Guo. "Radioprotective Gene Therapy." Current Gene Therapy 3, no. 3 (June 1, 2003): 183–95. http://dx.doi.org/10.2174/1566523034578384.

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34

Shah, K., A. Jacobs, X. O. Breakefield, and R. Weissleder. "Molecular imaging of gene therapy for cancer." Gene Therapy 11, no. 15 (May 13, 2004): 1175–87. http://dx.doi.org/10.1038/sj.gt.3302278.

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35

R. Weichselbaum, Donald W. Kufe, Su, Ralph. "Molecular Targeting of Gene Therapy and Radiotherapy." Acta Oncologica 40, no. 6 (January 2001): 735–38. http://dx.doi.org/10.1080/02841860152619151.

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36

Wivel, Nelson A. "Gene Therapy: Molecular Medicine of the 1990s." International Journal of Technology Assessment in Health Care 10, no. 4 (1994): 655–63. http://dx.doi.org/10.1017/s0266462300008230.

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AbstractIn less than four years, the techniques of gene transfer have been taken from the laboratory and translated into numerous clinical trials. Although gene therapy was initially designed for the molecular repair of monogenic deficiency diseases, most of the current studies of gene therapy are targeting cancer.

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37

Lewin, Alfred S., and William W. Hauswirth. "Ribozyme gene therapy: applications for molecular medicine." Trends in Molecular Medicine 7, no. 5 (May 2001): 221–28. http://dx.doi.org/10.1016/s1471-4914(01)01965-7.

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38

Larkin, Marilynn. "Molecular imaging boosts effectiveness of gene therapy." Lancet Oncology 4, no. 8 (August 2003): 455. http://dx.doi.org/10.1016/s1470-2045(03)01182-3.

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39

Wold, William, and Karoly Toth. "Adenovirus Vectors for Gene Therapy, Vaccination and Cancer Gene Therapy." Current Gene Therapy 13, no. 6 (January 31, 2014): 421–33. http://dx.doi.org/10.2174/1566523213666131125095046.

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40

Brower, Vicki. "Gene therapy revisited." EMBO reports 2, no. 12 (December 2001): 1064–65. http://dx.doi.org/10.1093/embo-reports/kve260.

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41

Robbins, P. D., C. H. Evans, and Y. Chernajovsky. "Gene therapy for arthritis." Gene Therapy 10, no. 10 (May 2003): 902–11. http://dx.doi.org/10.1038/sj.gt.3302040.

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42

Kohrman, D. C., and Y. Raphael. "Gene therapy for deafness." Gene Therapy 20, no. 12 (July 18, 2013): 1119–23. http://dx.doi.org/10.1038/gt.2013.39.

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43

Vile, Richard G. "Gene therapy." Current Biology 8, no. 3 (January 1998): R73—R75. http://dx.doi.org/10.1016/s0960-9822(98)70049-1.

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44

Pederson, Thoru. "Gene Therapy Now?" FASEB Journal 32, no. 4 (March 29, 2018): 1731–32. http://dx.doi.org/10.1096/fj.180401ufm.

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45

Olsen, R. J., S. R. Tarantolo, and S. H. Hinrichs. "Molecular Approaches to Sarcoma Therapy." Sarcoma 6, no. 1 (2002): 27–42. http://dx.doi.org/10.1080/13577140220127530.

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Soft tissue sarcomas comprise a heterogeneous group of aggressive tumors that have a relatively poor prognosis. Although conventional therapeutic regimens can effectively cytoreduce the overall tumor mass, they fail to consistently achieve a curative outcome. Alternative gene-based approaches that counteract the underlying neoplastic process by eliminating the clonal aberrations that potentiate malignant behavior have been proposed. As compared to the accumulation of gene alterations associated with epithelial carcinomas, sarcomas are frequently characterized by the unique presence of a single chromosomal translocation in each histological subtype. Similar to the Philadelphia chromosome associated with CML, these clonal abnormalities result in the fusion of two independent unrelated genes to generate a unique chimeric protein that displays aberrant activity believed to initiate cellular transformation. Secondary gene mutations may provide an additional growth advantage that further contributes to malignant progression. The recent clinical success of the tyrosine kinase inhibitor, STI571, suggests that therapeutic approaches specifically directed against essential survival factors in sarcoma cells may be effective. This review summarizes published approaches targeting a specific molecular mechanism associated with sarcomagenesis. The strategy and significance of published translational studies in six distinct areas are presented. These include: (1) the disruption of chimeric transcription factor activity; (2) inhibition of growth stimulatory post-translational modifications; (3) restoration of tumor suppressor function; (4) interference with angiogenesis; (5) induction of apoptotic pathways; and (6) introduction of toxic gene products. The potential for improving outcomes in sarcoma patients and the conceptual obstacles to be overcome are discussed.

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46

Denny, William A. "Prodrugs for Gene-Directed Enzyme-Prodrug Therapy (Suicide Gene Therapy)." Journal of Biomedicine and Biotechnology 2003, no. 1 (2003): 48–70. http://dx.doi.org/10.1155/s1110724303209098.

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This review focuses on the prodrugs used in suicide gene therapy. These prodrugs need to satisfy a number of criteria. They must be efficient and selective substrates for the activating enzyme, and be metabolized to potent cytotoxins preferably able to kill cells at all stages of the cell cycle. Both prodrugs and their activated species should have good distributive properties, so that the resulting bystander effects can maximize the effectiveness of the therapy, since gene transduction efficiencies are generally low. A total of 42 prodrugs explored for use in suicide gene therapy with 12 different enzymes are discussed, particularly in terms of their physiocochemical properties. An important parameter in determining bystander effects generated by passive diffusion is the lipophilicity of the activated form, a property conveniently compared by diffusion coefficients (log Pfor nonionizable compounds andlog D7for compounds containing an ionizable centre). Many of the early antimetabolite-based prodrugs provide very polar activated forms that have limited abilities to diffuse across cell membranes, and rely on gap junctions between cells for their bystander effects. Several later studies have shown that more lipophilic, neutral compounds have superior diffusion-based bystander effects. Prodrugs of DNA alkylating agents, that are less cell cycle-specific than antimetabolites and more effective against noncycling tumor cells, appear in general to be more active prodrugs, requiring less prolonged dosing schedules to be effective. It is expected that continued studies to optimize the bystander effects and other properties of prodrugs and the activated species they generate will contribute to improvements in the effectiveness of suicide gene therapy.

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47

Everett, W. H., and D. T. Curiel. "Gene therapy for radioprotection." Cancer Gene Therapy 22, no. 4 (February 27, 2015): 172–80. http://dx.doi.org/10.1038/cgt.2015.8.

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48

Wirth, Thomas, Florian Kuhnel, and Stefan Kubicka. "Telomerase-Dependent Gene Therapy." Current Molecular Medicine 5, no. 2 (March 1, 2005): 243–51. http://dx.doi.org/10.2174/1566524053586536.

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49

Amalfitano, A. "Molecular Therapy: The Journal of the American Society of Gene Therapy;Gene Function and Disease." JAMA: The Journal of the American Medical Association 289, no. 5 (February 5, 2003): 622. http://dx.doi.org/10.1001/jama.289.5.622-a.

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50

Scanlon, Ian, Panos Lehouritis, Ion Niculescu-Duvaz, Richard Marais, and Caroline J. Springer. "Gene Regulation in Cancer Gene Therapy Strategies." Current Medicinal Chemistry 10, no. 20 (October 1, 2003): 2175–84. http://dx.doi.org/10.2174/0929867033456837.

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