Relevant bibliographies by topics / GD2

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Academic literature on the topic 'GD2'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 April 2022

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Journal articles on the topic "GD2"

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Rai, Seema, Gurmeet Kaur Sethi, Rama Kumari, and Varun Kaul. "Gaucher disease: masquerading as chronic malaria." International Journal of Contemporary Pediatrics 5, no. 4 (June 22, 2018): 1688. http://dx.doi.org/10.18203/2349-3291.ijcp20182588.

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Gaucher disorder s rare lysosomal disorder characterized by glycolipid laden lysosomes leading to hepatosplenomegaly, bone marrow involvement. Three types of Gaucher disease have been described based on the clinical features, ethnicity and the natural history of the disease. Gaucher disease Type 1 (GD1) occurs mainly in infancy to adulthood and is the commonest lysosomal storage disorder. Gaucher Disease Type II (GD2) and Gaucher disease type III (GD3) patients have onset at less than 1 year, and 2-20 years, respectively.1 GD1 patients do not have neurological involvement. GD2 is the acute neuronopathic and GD3 is the chronic neuronopathic type.
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Awasthi, Sita, Gregory G. Mahairas, Carolyn E. Shaw, Meei-Li Huang, David M. Koelle, Christine Posavad, Lawrence Corey, and Harvey M. Friedman. "A Dual-Modality Herpes Simplex Virus 2 Vaccine for Preventing Genital Herpes by Using Glycoprotein C and D Subunit Antigens To Induce Potent Antibody Responses and Adenovirus Vectors Containing Capsid and Tegument Proteins as T Cell Immunogens." Journal of Virology 89, no. 16 (June 3, 2015): 8497–509. http://dx.doi.org/10.1128/jvi.01089-15.

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ABSTRACTWe evaluated a genital herpes prophylactic vaccine containing herpes simplex virus 2 (HSV-2) glycoproteins C (gC2) and D (gD2) to stimulate humoral immunity and UL19 (capsid protein VP5) and UL47 (tegument protein VP13/14) as T cell immunogens. The HSV-2 gC2 and gD2 proteins were expressed in baculovirus, while the UL19 and UL47 genes were expressed from replication-defective adenovirus vectors. Adenovirus vectors containing UL19 and UL47 stimulated human and murine CD4+and CD8+T cell responses. Guinea pigs were either (i) mock immunized; (ii) immunized with gC2/gD2, with CpG and alum as adjuvants; (iii) immunized with the UL19/UL47 adenovirus vectors; or (iv) immunized with the combination of gC2/gD2-CpG/alum and the UL19/UL47 adenovirus vectors. Immunization with gC2/gD2 produced potent neutralizing antibodies, while UL19 and UL47 also stimulated antibody responses. After intravaginal HSV-2 challenge, the mock and UL19/UL47 adenovirus groups developed severe acute disease, while 2/8 animals in the gC2/gD2-only group and none in the combined group developed acute disease. No animals in the gC2/gD2 or combined group developed recurrent disease; however, 5/8 animals in each group had subclinical shedding of HSV-2 DNA, on 15/168 days for the gC2/gD2 group and 13/168 days for the combined group. Lumbosacral dorsal root ganglia were positive for HSV-2 DNA and latency-associated transcripts for 5/8 animals in the gC2/gD2 group and 2/8 animals in the combined group. None of the differences comparing the gC2/gD2-only group and the combined group were statistically significant. Therefore, adding the T cell immunogens UL19 and UL47 to the gC2/gD2 vaccine did not significantly reduce genital disease and vaginal HSV-2 DNA shedding compared with the excellent protection provided by gC2/gD2 in the guinea pig model.IMPORTANCEHSV-2 infection is a common cause of genital ulcer disease and a significant public health concern. Genital herpes increases the risk of transmission and acquisition of HIV-1 infection 3- to 4-fold. A herpes vaccine that prevents genital lesions and asymptomatic genital shedding will have a substantial impact on two epidemics, i.e., both the HSV-2 and HIV-1 epidemics. We previously reported that a vaccine containing HSV-2 glycoprotein C (gC2) and glycoprotein D (gD2) reduced genital lesions and asymptomatic HSV-2 genital shedding in guinea pigs, yet the protection was not complete. We evaluated whether adding the T cell immunogens UL19 (capsid protein VP5) and UL47 (tegument protein VP13/14) would enhance the protection provided by the gC2/gD2 vaccine, which produces potent antibody responses. Here we report the efficacy of a combination vaccine containing gC2/gD2 and UL19/UL47 for prevention of genital disease, vaginal shedding of HSV-2 DNA, and latent infection of dorsal root ganglia in guinea pigs.
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Vladimirova, Liubov Yu, Natalya A. Abramova, and Oleg Ivanovich Kit. "Treatment for RAS wild-type (wt) metastatic colorectal cancer (mCRC): Continuation of anti-EGFR therapy while switching chemotherapy regimen." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 744. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.744.

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744 Background: The purpose of the study was to assess the effeciency and safety of continuing of EGFR-inhibition while switching the chemotherapy (CT) from FOLFOX+Cetuximab (C) as the 1st-line to FOLFIRI+С as the 2nd-line treatment for pts with RAS wt mCRC. Methods: Pts with RAS wt mCRC were enrolled to the pilot study according to inclusion criteria: ECOG≤2, normal bone marrow, liver and kidney functions, no brain metastases, measurable metastatic lesions. The therapy included: the 1st-line with FOLFOX-6+C until progression, then FOLFIRI+C as the 2nd-line therapy. The treatment continued until progression or unacceptable toxicity. Response rate (RR), PFS after the 1st and the 2ndlines of treatment as well as toxicity were evaluated. Results: 20 pts (11 men, 9 women), 38-58 years old, mean age 48.3±1.3 years, were recruited. All pts had multiple visceral metastases: to the liver –30.0%(6), lungs and pleura – 20.0%(4), liver and lungs – 50.0%(10), including the bone metastases – 15.0%(3). The RR was 85.0 %(17), including PR - 4(20.0%) and SD - 13(65.5%). Median PFS after the 1st-line therapy was 12.3±2.6 months, median PFS after the 2nd-line therapy - 6.5±2.8 months. Median OS was not reached yet. Adverse events included: neutropenia Gd2 – 30.0%(6), Gd3 – 20.0%(4), anemia Gd2 – 10.0%(2), stomatitis Gd2-3 – 20.0%(4), diarrhea Gd2 - 55.0%(11), thrombophlebitis – 10.0%(2). C-associated dermatologic toxicity: acneiform rash Gd2-3 – 85.0%(17), skin itching Gd2 - 30.0%(6), panaritium Gd1-2 -30.0%(6), blepharitis Gd1-2 – 10.0%(2), hypertrichosis – 20.0%(4). Conclusions: Continuing EGFR-inhibition with C while switching CT regimens beyond progression provided significant tumor control and was not accompanied by unacceptable toxicity. This strategy deserves futher evaluation in randomized studies in EGFR-dependent mCRC pts.
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Anya, D. K., and K. I. Eghianruwa. "Concurrent administration of methanolic extract of Zingiber officinale Roscoe (Zingiberales: Zingiberaceae) and diminazene aceturate enhanced survival rate and reduced parasitaemia in experimental murine Trypanosoma brucei Plimmer & Bradford, 1899 (Kinetoplastea: Trypanosomatida) infection." Brazilian Journal of Biological Sciences 5, no. 9 (2018): 95–104. http://dx.doi.org/10.21472/bjbs.050910.

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The efficacy of concurrent diminazene and Zingiber officinale Roscoe (Zingiberales: Zingiberaceae) extract in murine Trypanosoma brucei Plimmer & Bradford, 1899 (Kinetoplastea: Trypanosomatida) infection was evaluated. Two infected groups were treated with extract at 400 mg.kg-1 (G1) and 800 mg.kg-1 (G2) alone while another two groups received 400 mg.kg-1 (GD1) and 800 mg.kg-1 (GD2) of extract concurrently with diminazene 3.5 mg.kg-1 intraperitoneally. One infected group received diminazene 3.5 mg.kg-1 only (D) while another received 1 mg.kg-1 Tween 80 (C1) orally. The seventh group was uninfected and untreated (C2). Survival rate, parasitemia, liver weight, spleen weight, haematological indices were evaluated. Survival rates were 0% in C1, G1 and G2, 20% in D, 40% in GD2, 60% in GD1 and 100% in C2. Animals in groups G1, G2 and C1 died between 6 and 8 days pt. Parasitemia levels were significantly (P < 0.05) higher in D1 than in GD1 and GD2 by day 16 post treatment. PCV and RBC counts were significantly (P < 0.05) lower in GD1, GD2 and D than in C2. Liver and spleen weights increased significantly (P < 0.05) due to infection and never fully recovered in all treatment options. Ginger (Z. officinale) extract enhanced diminazene efficacy by increasing survival rates and lowering parasitemia.
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Kasprowicz, Angelina, Groux-Degroote Sophie, Chann Lagadec, and Philippe Delannoy. "Role of GD3 Synthase ST8Sia I in Cancers." Cancers 14, no. 5 (March 3, 2022): 1299. http://dx.doi.org/10.3390/cancers14051299.

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GD3 synthase controls the biosynthesis of complex gangliosides, bearing two or more sialic acid residues. Disialylated gangliosides GD3 and GD2 are tumor-associated carbohydrate antigens (TACA) in neuro–ectoderm-derived cancers, and are directly involved in cell malignant properties, i.e., migration, invasion, stemness, and epithelial–mesenchymal transition. Since GD3 and GD2 levels are directly linked to GD3 synthase expression and activity, targeting GD3 synthase appears to be a promising strategy through which to interfere with ganglioside-associated malignant properties. We review here the current knowledge on GD3 synthase expression and regulation in cancers, and the consequences of complex ganglioside expression on cancer cell signaling and properties, highlighting the relationships between GD3 synthase expression and epithelial–mesenchymal transition and stemness. Different strategies were used to modulate GD3 synthase expression in cancer cells in vitro and in animal models, such as inhibitors or siRNA/lncRNA, which efficiently reduced cancer cell malignant properties and the proportion of GD2 positive cancer stem cells, which are associated with high metastatic properties, resistance to therapy, and cancer relapse. These data show the relevance of targeting GD3 synthase in association with conventional therapies, to decrease the number of cancer stem cells in tumors.
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Cheresh, D. A., M. D. Pierschbacher, M. A. Herzig, and K. Mujoo. "Disialogangliosides GD2 and GD3 are involved in the attachment of human melanoma and neuroblastoma cells to extracellular matrix proteins." Journal of Cell Biology 102, no. 3 (March 1, 1986): 688–96. http://dx.doi.org/10.1083/jcb.102.3.688.

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Human melanoma cells express relatively large amounts of the disialogangliosides GD3 and GD2 on their surface whereas neuroblastoma cells express GD2 as a major ganglioside. Monoclonal antibodies (Mabs) directed specifically to the carbohydrate moiety of GD3 and GD2 inhibit melanoma and neuroblastoma cell attachment to various substrate adhesive proteins, e.g. collagen, vitronectin, laminin, fibronectin, and a heptapeptide, glycyl-L-arginyl-glycyl-L-aspartyl-L-seryl-L-prolyl-L-cysteine, which constitutes the cell attachment site of fibronectin. Cells that are preattached to a fibronectin substrate can also be induced to detach and round up in the presence of purified anti-ganglioside Mab. Moreover, when melanoma cells that contain both GD2 and GD3 are incubated with Mabs directed to both of these molecules an additive inhibition is observed. The specificity of this inhibition is demonstrated since Mabs of various isotypes directed to either protein or carbohydrate epitopes on a number of other major melanoma or neuroblastoma cell surface antigens have no effect on cell attachment. A study of the kinetics involved in this inhibition indicates that significant effects occur during the first 5 min of cell attachment, suggesting an important role for GD2 and GD3 in the initial events of cell-substrate interactions. The role of gangliosides in cell attachment apparently does not directly involve a strong interaction with fibronectin since we could not observe any binding of radiolabeled fibronectin or fragments of the molecule known to contain the cell attachment site to melanoma gangliosides separated on thin-layer chromatograms. An alternative explanation would be that gangliosides may play a role in the electrostatic requirements for cell-substrate interactions. In this regard, controlled periodate oxidation of terminal, unsubstituted sialic acid residues on the cell surface not only specifically destroys the antigenic epitopes on GD2 and GD3 recognized by specific Mabs but also inhibits melanoma cell and neuroblastoma cell attachment. In fact, the periodate-induced ganglioside oxidation and the inhibition of cell attachment are equally dose dependent. These data suggest that cell-substratum interactions may depend in part on the electrostatic environment provided by terminal sialic acid residues of cell surface gangliosides and possibly other anionic glycoconjugates.
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Zhao, X. J., and N. K. Cheung. "GD2 oligosaccharide: target for cytotoxic T lymphocytes." Journal of Experimental Medicine 182, no. 1 (July 1, 1995): 67–74. http://dx.doi.org/10.1084/jem.182.1.67.

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Carbohydrate antigens rarely provide target epitopes for cytotoxic T lymphocytes (CTL). Disialoganglioside GD2 is a glycolipid expressed at high levels in human tumors and a small group of murine lymphomas (EL4, RBL5, RMA, RMA-S, A13, and BALBRVE). Immunization of C57B1/6 mice with irradiated EL4 cells stimulated a specific CTL response and protected these animals from engraftment of EL4 lymphoma. The CTL activity resided in the CD4-CD8+ population, was dependent on T cell receptor alpha/beta, and was not removed by anti-natural killer cell immunoabsorption, but was restricted to GD2 and H-2b bearing targets. CTL activity could be completely inhibited by GD2-oligosaccharide-specific monoclonal antibodies and their F(ab')2 fragments, but not by immunoglobulin G3 myelomas or antibodies against GD3 or GM2. Soluble GD2 did not inhibit specific tumor lysis. RMA-S lymphoma cells (GD2+H-2b-TAP2 deficient) were resistant to GD2-specific CTL. Sialic acid-containing peptides eluted from EL4 lymphoma cells could (a) stabilize H-2 molecules on RMA-S cells and (b) sensitize them for GD2-specific CTL. Control peptides (derived from vesicular stomatitis virus nucleoprotein peptide and GD2-negative lymphomas) could also stabilize H-2 on RMA-S, but were resistant to GD2-specific CTL. These H-2-binding peptides could be purified by anti-GD2 affinity chromatography. We postulate a new class of naturally occurring epitopes for T cells where branched-chain oligosaccharides are linked to peptides with anchoring motifs for the major histocompatibility complex class I pocket. While analogous to the haptens trinitrophenyl and O-beta-linked acetyl-glucosamine, the potential implications of natural carbohydrates as antigenic epitopes for CTL in biology are considerable.
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Chan, Godfrey Chi-Fung, and Carol Matias Chan. "Anti-GD2 Directed Immunotherapy for High-Risk and Metastatic Neuroblastoma." Biomolecules 12, no. 3 (February 24, 2022): 358. http://dx.doi.org/10.3390/biom12030358.

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Neuroblastoma is one of the few childhood cancers that carries a tumor-specific antigen in the form of a glycolipid antigen known as GD2. It has restricted expression in normal tissue, such as peripheral afferent nerves. Monoclonal antibodies targeting GD2 have been applied clinically to high-risk neuroblastoma with significant success. However, there are different anti-GD2 products and administration regimens. For example, anti-GD2 has been used in combination with chemotherapy during the induction phase or with retinoic acid during the maintenance stage. Regimens also vary in the choice of whether to add cytokines (i.e., IL-2, GMCSF, or both). Furthermore, the addition of an immune enhancer, such as β-glucan, or allogeneic natural killer cells also becomes a confounder in the interpretation. The question concerning which product or method of administration is superior remains to be determined. So far, most studies agree that adding anti-GD2 to the conventional treatment protocol can achieve better short- to intermediate-term event-free and overall survival, but the long-term efficacy remains to be verified. How to improve its efficacy is another challenge. Late relapse and central nervous system metastasis have emerged as new problems. The methods to overcome the mechanisms related to immune evasion or resistance to immunotherapy represent new challenges to be resolved. The newer anti-GD2 strategies, such as bispecific antibody linking of anti-GD2 with activated T cells or chimeric antigen receptor T cells, are currently under clinical trials, and they may become promising alternatives. The use of anti-GD2/GD3 tumor vaccine is a novel and potential approach to minimizing late relapse. How to induce GD2 expression from tumor cells using the epigenetic approach is a hot topic nowadays. We expect that anti-GD2 treatment can serve as a model for the use of monoclonal antibody immunotherapy against cancers in the future.
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Wei, Jianshe, Yoshiki Takamatsu, Ryoko Wada, Masayo Fujita, Gilbert Ho, Eliezer Masliah, and Makoto Hashimoto. "Therapeutic Potential of αS Evolvability for Neuropathic Gaucher Disease." Biomolecules 11, no. 2 (February 15, 2021): 289. http://dx.doi.org/10.3390/biom11020289.

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Gaucher disease (GD), the most common lysosomal storage disorder (LSD), is caused by autosomal recessive mutations of the glucocerebrosidase gene, GBA1. In the majority of cases, GD has a non-neuropathic chronic form with adult onset (GD1), while other cases are more acute and severer neuropathic forms with early onset (GD2/3). Currently, no radical therapies are established for GD2/3. Notably, GD1, but not GD2/3, is associated with increased risk of Parkinson’s disease (PD), the elucidation of which might provide a clue for novel therapeutic strategies. In this context, the objective of the present study is to discuss that the evolvability of α-synuclein (αS) might be differentially involved in GD subtypes. Hypothetically, aging-associated PD features with accumulation of αS, and the autophagy-lysosomal dysfunction might be an antagonistic pleiotropy phenomenon derived from αS evolvability in the development in GD1, without which neuropathies like GD2/3 might be manifested due to the autophagy-lysosomal dysfunction. Supposing that the increased severity of GD2/3 might be attributed to the decreased activity of αS evolvability, suppressing the expression of β-synuclein (βS), a potential buffer against αS evolvability, might be therapeutically efficient. Of interest, a similar view might be applicable to Niemann-Pick type C (NPC), another LSD, given that the adult type of NPC, which is comorbid with Alzheimer’s disease, exhibits milder medical symptoms compared with those of infantile NPC. Thus, it is predicted that the evolvability of amyloid β and tau, might be beneficial for the adult type of NPC. Collectively, a better understanding of amyloidogenic evolvability in the pathogenesis of LSD may inform rational therapy development.
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Li, Yuexi, Sumei Li, Yong Qi, Tingting Xu, Jiameng Li, Ying Pan, and Suqin Li. "Eucaryotic expression of HSV glycoproteins gC2, gD1, gD2 and immunogenicity analysis." New Biotechnology 33 (July 2016): S75. http://dx.doi.org/10.1016/j.nbt.2016.06.977.

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Dissertations / Theses on the topic "GD2"

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Cerato, Evelyne. "Repertoire d'anticorps murins diriges contre les gangliosides gd2 et gd3 : production et caracterisation d'un fragment d'anticorps recombinant colorimetrique anti-gd2." Nantes, 1997. http://www.theses.fr/1997NANT02VS.

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Faraj, Sébastien. "Immunochimiothérapie du neuroblastome : nouvelle thérapeutique améliorée ciblant le ganglioside GD2 O-acétylé pour le traitement des neuroblastomes chez l'enfant." Thesis, Nantes, 2018. http://www.theses.fr/2018NANT1037.

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Malgré les récentes avancées dans la prise en charge des neuroblastomes de haut risque, le pronostic des patients qui en sont atteints reste péjoratif. Les modalités thérapeutiques sont agressives et de nombreux enfants souffrent des effets secondaires de celles-ci, dégradant de ce fait leur qualité de vie. L’immunothérapie anti-GD2 offre dans ce contexte une alternative thérapeutique, permettant d’améliorer le pronostic de ces tumeurs, mais leur utilisation est néanmoins limitée par la présence d’une toxicité des molécules existantes. Le GD2 O-acétylé n’étant pas exprimé à la surface des fibres nerveuses périphériques, le choisir comme cible thérapeutique peut s’avérer efficace tout en diminuant la toxicité de l’immunothérapie. Nous avons vérifié l’expression du GD2 O-acétylé à la surface des cellules de 4 lignées cellulaires de neuroblastome (LAN1, LAN5, IMR5, NXS2). Cette expression n’est pas modifiée par les traitements par chimiothérapie utilisés dans les traitements des neuroblastomes de haut grade (cisplatine, doxorubicine et topotecan). Nous montrons que l’anticorps murin 8B6 spécifique du GD2 O-acétylé a une relation synergique in vitro avec les molécules de chimiothérapie testées (cisplatine, doxorubicine et topotecan). Nous montrons par la suite que cet anticorps augmente l’efficacité de la doxorubicine et du topotecan in vivo chez la souris sans diminuer la tolérance globale du traitement multimodal. Nos résultats montrent qu’un traitement combinant chimiothérapie et immunothérapie peut augmenter l’efficacité et la tolérance cliniques des chimiothérapies dans le traitement des neuroblastomes de haut grade
Despite recent advances in high-risk neuroblastoma therapy, the prognosis for patients remains poor. In addition, many patients suffer from complications related to available therapies that are highly detrimental to their quality of life. New treatment modalities are, thus, urgently needed to further improve the efficacy and reduce the toxicity of existing therapies. Since antibodies specific for Oacetyl GD2 ganglioside display pro-apoptotic activity against neuroblastoma cells, we hypothesized that combination of immunotherapy could enhance tumor efficacy of neuroblastoma chemotherapy. We demonstrate here that combination of anti-Oacetyl GD2 monoclonal antibody 8B6 with topotecan synergistically inhibited neuroblastoma cell proliferation, as shown by the combination index values. Mechanistically, we evidence that mAb 8B6 induced plasma cell membrane lesions, consistent with oncosis. Neuroblastoma tumour cells treated with mAb 8B6 indeed showed an increased uptake of topotecan by the tumor cells and a more profound tumor cell death evidenced by increased caspase-3 activation. We also found that the combination with topotecan plus monoclonal antibody 8B6 showed a more potent anti-tumor efficacy in vivo than either agent alone. Importantly, we used low-doses of topotecan with no noticeable side effect. Our data suggest that chemoimmunotherapy combinations may improve the clinical efficacy and safety profile of current chemotherapeutic modalities of neuroblastoma
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Tong, Wenyong. "Chemistry and biology of tumor-associated ganglioside GD2." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107647.

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Effective therapies typically target diseased tissues without significantly affecting healthy tissues. A tumor-related glycosphingolipid (GSL), such as ganglioside GD2, distinguishes neuroectoderm tumors from their healthy counterparts and is a validated tumor target. GD2 is clinically targeted for diagnosis and immunotherapy. GD2 plays an important functional role in tumor progression and in chemoresistance. It also plays an important functional role in pain; however, the mechanisms that make GD2 important in such phenomena remain unknown.Thus, understanding the structure-activity relationship of GD2, a GSL with two sialic acids, would be helpful. However, such studies on glycolipids are challenging. We employed a chemical biology approach to elucidate the structure and function of GD2 and to further direct the rational design of GD2 ligands and vaccines for GD2-related cancer treatment.The combined use of STD NMR spectroscopy, transferred NOE experiments, and molecular modeling furnished details on the molecular recognition of the ganglioside GD2 by the clinically used anti-GD2 monoclonal antibody 3F8 that can induce apoptosis of GD2 expressing tumours. A binding model that provided the basis for a rational development of GD2 ligands and vaccines was then established. Based on the structural information of GD2-3F8 interactions, small molecule monomeric peptide ligands binding to GD2 were developed. ELISA and NMR experiments demonstrated that peptides selectively bound to GD2 via an induced-fit mechanism. Furthermore, peptidic GD2 ligands, including 3F8, mediated similar biological functions in cell-based assays of activation of NMDA receptor via Src family kinase, calcium fluxe and cAMP. These can explain at least some of the mechanisms associated with tumor progression and pain, where GD2 plays a role. However, current GD2 peptide ligands did not demonstrate any treatment effect in vivo. Hence, we turned to the design of GD2 vaccines as a therapeutic approach. The rigid nature of GD2-oligosaccharides, discovered in our structural study, makes it perfectly suited to drive a structurally convergent immune response. A novel and homogenous tetra-GD2 dendrimer was designed to mimic a clustered GD2 lipid raft. Immunization of mice with tetra-GD2 dendrimer elicited a potent anti-GD2 humoral response. The antibodies (sera or mAbs) thus generated can kill GD2-expressing cells in culture, in the absence of a complement. Tumor growth was significantly delayed in vivo in prophylactic and in therapeutic paradigms. Our research strategy may be expanded to other clinically relevant glycolipids.
Typiquement, les thérapies efficaces agissent sur les tissus malades sans toutefois nuire considérablement aux tissus en santé. Un glycosphingolipide (GSL) associé à une tumeur, tel que le ganglioside GD2, peut reconnaître selectivement les tumeurs neuroectodermes malignes et est ainsi validé comme une cible tumorale. Sur le plan clinique, on utilise le GD2 à des fins de diagnostic et d'immunothérapie. D'une part, le GD2 joue un rôle fonctionnel important dans la progression tumorale et la chimiorésistance. D'autre part, le GD2 joue un rôle fonctionnel important dans la douleur, mais les mécanismes qui expliqueraient l'importance du GD2 lors de tels phénomènes demeurent encore inconnus. C'est pourquoi il serait utile de mieux comprendre la relation structure-activité du GD2, un GSL constitué de 2 acides sialiques. Toutefois, entreprendre de telles études sur les glycolipides représente un défi de taille. Nous avons alors utilisé une approche basée sur la biologie chimique pour élucider la structure et la fonction des GD2 et pour mieux concevoir rationnellement des ligands GD2 et des vaccins pour le traitement contre le cancer lié au GD2. En combinant l'utilisation de la spectroscopie RMN DTS, des expériences NOE transférées et des modèles moléculaires, il est possible d'obtenir plus de détails sur la reconnaissance moléculaire du ganglioside GD2 au moyen du 3F8, un anticorps monoclonal anti-GD2 utilisé médicalement et qui peut induire l'apoptose de cellues cancereuses exprimant GD2. Comme point de départ pour le développement rationnel des ligands GD2 et des vaccins, nous avons établi un modèle contraignant. En nous appuyant sur l'information structurelle des interactions GD2-3F8, nous avons développé des petits ligands monomériques peptidiques liés au GD2. Des expériences RMN et ELISA ont démontré que les peptides se lient sélectivement au GD2 via un mécanisme d'ajustement induit. Par ailleurs, les ligands peptidiques GD2, dont le 3F8, deviennent médiateurs de fonctions biologiques similaires dans les essais cellulaires de l'activation des récepteurs NMDA via les kinases de la famille Src, les flux de calcium et cAMP. Ces derniers peuvent au moins expliquer certains des mécanismes associés avec la progression tumorale et la douleur, dans lesquels le GD2 jour un rôle prépondérant. Cependant, les ligands peptidiques GD2 actuels n'ont pas démontré les effets désirés au cours des traitements in vivo. C'est pourquoi nous nous sommes tournés vers le développement de nouveaux vaccins GD2 comme une approche thérapeutique. La nature rigide des oligosaccharides GD2, que nous avons découverte par le biais de notre étude structurale, devient une caractéristique parfaitement adaptée pour favoriser une réponse immunitaire structurellement convergente. Un nouveau dendrimère tetra-GD2 homogène a été conçu de manière à reproduire un radeau lipidique GD2 regroupé. L'immunisation des souris par le dendrimère tetra-GD2 a engendré une puissante réponse humorale anti-GD2. En l'absence d'un complément, les anticorps (sera ou mAbs) ainsi générés peuvent tuer les cellules exprimant le GD2 en culture. La croissance tumorale a été considérablement retardée in vivo dans les paradigmes thérapeutiques et prophylactiques. Notre stratégie de recherche pourrait ainsi être élargie pour inclure d'autres glycolipides pertinents sur le plan clinique.
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Leprieur, Truet Stéphanie Birkle Stéphane. "Production et évaluation chez l'animal d'anticorps thérapeutiques anti-ganglioside GD2." [S.l.] : [s.n.], 2007. http://castore.univ-nantes.fr/castore/GetOAIRef?idDoc=16881.

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MARQUES, Maria Danielle Rodrigues. "Caracterização estrutural, microestrutural e magnética de amostras tipo Gd2-xHoxRu2O7." Universidade Federal de Pernambuco, 2010. https://repositorio.ufpe.br/handle/123456789/1439.

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Materiais que apresentam estrutura tipo pirocloro tem sido objeto de estudos intensivos nos anos recentes. Estes materiais possuem fórmula geral A2B2O6O, onde A é uma terra rara e B é geralmente um metal de transição. Estudos anteriores mostraram que estes compostos têm muitas propriedades interessantes tais como condução iônica, condução elétrica, fluorescência, supercondutividade e atividade catalítica. O presente trabalho descreve os estudos realizados para a síntese e caracterização dos pirocloros Gd2−xHoxRu2O7, com x = 0,0 , 0,1 , 0,2 , 1,0 e 2,0 . As amostras foram preparadas pelo método de reação de estado sólido, onde quantidades dos óxidos Gd2O3, RuO2 e Ho2O3 foram pesados nas proporções estequiométricas, misturados, homogeneizados em ácido nítrico concentrado e submetidas a tratamento térmico. Em seguida, foram caracterizadas estruturalmente por difração de raios X e morfologicamente por microscopia eletrônica de varredura. Os difratogramas de raios X foram analisados pelo método de Rietveld, que possibilitou a identificação da estrutura e a determinação do parâmetro de rede. O refinamento indicou que as amostras cristalizam em uma rede cúbica de face centrada, onde o parâmetro de rede sofre uma contração com o aumento da dopagem, de acordo com a lei de Vegard. As micrografias obtidas por microscopia eletrônica de varredura revelaram uma morfologia com tamanhos de grãos mais uniformes e homogêneos. Esse resultado foi atribuído ao fato de se ter diluído os grãos em ácido nítrico antes de submetê-los ao tratamento térmico. Um estudo das propriedades magnéticas dos compostos foi realizado mediante medidas de susceptibilidade dc, onde o momento magnético foi obtido. A dependência da susceptibilidade com a temperatura apresentou um comportamento em acordo com a lei de Curie-Weiss no intervalo de 35 K a 300 K, para todas as amostras estudadas, Entretanto, dependendo da quantidade do dopante, foram observados desvios desse comportamento. Os resultados das diferentes caracterizações são discutidos em detalhes
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Cavdarli, Sumeyye. "Deciphering biosynthesis mechanisms of O-acetylated GD2 in breast cancer." Thesis, Lille 1, 2020. http://www.theses.fr/2020LIL1S100.

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Le ganglioside GD2, ré-exprimé dans les cancers d’origine neuro-ectodermique, a été caractérisé comme un antigène oncofetal constituant une cible pour l’immunothérapie. L’anticorps anti-GD2 dinutuximab (Unitixin, TM) a récemment obtenu l’agrément de la Food Drug Administration et de l’Agence Européenne du Médicament pour le traitement des neuroblastomes pédiatriques. Cependant, l’utilisation de cet anticorps se heurte à de forts problèmes de toxicité due à l’expression du GD2 dans les nerfs périphériques sains. La forme O-acétylée du GD2 (OAcGD2) n’est exprimé que dans les tissus cancéreux représentant ainsi une cible thérapeutique moins toxique que le GD2. Les activités de la société OGD2 Pharma, partenaire de ce projet, sont axées sur le développement d’anticorps thérapeutiques dirigés contre le GD2 O-acetylé. L’anticorps développé cible spécifiquement au GD2 O-acetylé sans réaction croisée avec GD2. Dans le cancer du sein, les gangliosides complexes, notamment le GD2 et sa forme O-acetylé sont ré-exprimés. Cette expression est corrélée à un mauvais pronostic chez les patientes atteintes de cancer du sein. L’objectif principale de ma thèse est d’identifier les mécanismes moléculaires régissant l’O-acétylation du GD2 dans le cancer du sein afin de mettre en évidence l’intérêt thérapeutique et diagnostique du ciblage de cet antigène
O-Acetylated GD2 (OAcGD2) ganglioside is neo-expressed in neuroectodermal derived tumors as neuroblastoma and breast cancer. This oncofetal marker is an essential target for immunotherapy. Dinutuximab (Unitixin TM), a therapeutic antibody targeting GD2 has recently obtained Food Drug Administration and European Medicines Agency approval for neuroblastoma treatment. Nevertheless, Dinutuximab causes toxicity due to the expression of GD2 on peripheral nerve fibers. In that way, targeting OAcGD2 seems more beneficial because of absence of this antigen in normal tissues. The activities of OGD2 Pharma Company, partner of this project, are focused on therapeutic antibody development against OAcGD2. OGD2 Pharma developed an antibody specifically targeting OAcGD2 with no cross reaction with GD2. Absent from the normal mammary gland, complex gangliosides especially GD2 and its O-acetylated form have been detected in breast cancer. This expression is correlated with poor patient outcome. The aim of this thesis project was to decipher the molecular mechanisms of OAcGD2 biosynthesis, expression and its role in breast cancer, in order to highlight the therapeutic and diagnostic value of targeting OAcGD2 in breast cancer
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Fleurence, Julien. "Ciblage du GD2-O-acétylé par un anticorps monoclonal dans le glioblastome multiforme." Thesis, Nantes, 2017. http://www.theses.fr/2017NANT1007.

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Le glioblastome multiforme (GBM) est la tumeur cérébrale maligne la plus fréquente et la plus agressive chez l’adulte. Malgré l’utilisation concomitante de la chirurgie avec la radiothérapie et la chimiothérapie (protocole de Stupp), le pronostic des patients reste sombre avec un taux de survie à 5 ans inférieur à 10 %. La présence de cellules souches cancéreuses (CSC) favorise le maintien de la tumeur puis l’échappement tumoral responsable de la rechute des patients. Il est donc nécessaire d’identifier de nouvelles cibles thérapeutiques pour améliorer la prise en charge de ces patients. Dans ce contexte, l’immunothérapie, stratégie utilisant le système immunitaire pour traiter le cancer, représente une voie prometteuse.Nous identifions ici le OAcGD2 comme un nouvel antigène tumoral du GBM et a partir de biopsie tumorale provenant d’une cohorte de 37 patients. L’utilisation de primoculture de GBM nous permet de plus de démontrer que ce marqueur est également exprimé par les cellules souches de GBM. Nous apportons la preuve de concept de l’immunothérapie du GBM à l’aide d’anticorps monoclonaux anti-OAcGD2 in vitro et in vivo. A côté de la cytotoxicté immunologique, nous identifions un nouveau mécanisme de mort programmé, l’oncose, mis en jeu par les AcM anti-OAcGD2 permettant de sensibiliser ces cellules aux agents de chimiothérapie comme le témolozomide. L’utilisation de l’immunothérapie ciblant le marqueur gangliosidique tumoral OAcGD2 pourrait ainsi permettre d’améliorer l’efficacité de la thérapeutique actuelle (protocole de Stupp) du GBM
Glioblastoma multiforme (GBM) is the most common and agressive primary brain tumors in adults. Despite the concomitant use of surgery with radiotherapy and chemotherapy, the prognosis of patients remains extremely low. The presence of cancer stem cells (CSC) promotes the maintenance of the tumor and then the tumor escape responsible for the relapse of the patients. Therefore it is necessary to identify new therapeutic targets to improve the management of these patients. In the past few decades, immunotherapy represents an important part of treating certain type of cancer. It uses the immune system to treat cancer. Here, we found that O-acetyl GD2 (OAcGD2) is expressed in surgically resected human glioblastoma tissue. In addition, we demonstrated that 8B6 monoclonal antibody specific for OAcGD2 could effectively inhibit glioblastoma cell proliferation in vitro and in vivo. Mostly, we found that OAcGD2 was expressed on the GBM stem cells. We also observed that mAb 8B6 promoted the elimination of GBM via a oncosis-like mechanism. Moreover, this mechanism of programmed cell death induced by anti-OAcGD2 mAbs, sensitizes GBM cells and CSCs to chemotherapy agents such as temolozomide (TMZ). Taken together, these results indicate that O-acetylated GD2 represents a novel antigen for immunotherapeutic-based treatment of high-grade gliomas, and that anti-OAcGD2 mAbs combined with TMZ could enhance therapeutic response in GBM
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Seidel, Diana. "Mechanism and efficacy of a GD2-specific immunotherapy using NK cells." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17151.

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Das Neuroblastom (NB) ist ein solider, extrakranieller Tumor neuroektodermalen Ursprungs, der sich im Kleinkindalter manifestiert. Ein etabliertes Zielantigen für die passive Immuntherapie beim NB ist das Disialogangliosid GD2. Aufgrund der geringen oder fehlenden Expression von MHC Klasse I Molekülen sowie der Tatsache, dass die Lyse von NB-Zellen durch verschiedene Mechanismen der natürlichen Zytotoxizität von NK-Zellen vermittelt werden kann, stellt eine auf NK-Zellen basierende Therapie einen vielversprechenden Ansatz zur Behandlung dieser Erkrankung dar. Auf dieser Grundlage wurde eine NK-Zelllinie generiert, die einen GD2-spezifischen chimären Antigenrezeptor (CAR) exprimiert (NK-92-scFv(ch14.18)-zeta). Die Hauptbestandteile dieses CARs sind ein Einzelkettenantikörper, welcher die variablen Regionen des GD2-spezifischen Antikörpers ch14.18 enthält, und die CD3ζ-Kette als signaltransduzierende Komponente. Im Rahmen dieser Arbeit konnte gezeigt werden, dass NK-92-scFv(ch14.18)-zeta in der Lage sind, auch Chemotherapie-resistente GD2-positive NB-Zelllinien effektiv abzutöten und dass dabei die Interaktion des CARs mit GD2 den Hauptmechanismus darstellt. Die anti-tumorale Wirkung von NK-92-scFv(ch14.18)-zeta in vivo wurde in einem Chemotherapie-resistenten GD2-positiven Xenograft-Mausmodell gezeigt. Die wiederholte Applikation von NK-92-scFv(ch14.18)-zeta in Kombination mit IL-2 resultierte in einem signifikant verlangsamten Tumorwachstum und einem verbesserten Überleben. Die Ergebnisse dieser Arbeit belegen, dass GD2-spezifische NK-92 das Potential für eine zukünftige klinische Anwendung besitzen. Demnach stellt der Einsatz einer solchen GD2-spezifischen NK-Zelllinie, die unter GMP-Bedingungen expandiert werden kann und zu jeder Zeit in einer standardisierten Qualität verfügbar wäre, eine vielversprechende Alternative zur Behandlung von Hochrisikopatienten dar, deren Erkrankung nicht mehr auf die Standardtherapie anspricht.
Neuroblastoma (NB) is a solid extracranial childhood malignancy of neuroectodermal origin. The Disialoganglioside GD2 is an established antigen for passive immunotherapy of NB. Cellular therapy of NB with natural killer (NK) cells is especially appealing because MHC class I expression is absent or low in most NB, rendering this tumor sensitive to NK cell recognition. Additionally, natural cytotoxicity of NK cells, mediated by interaction of activating NK cell receptors and their respective ligands on tumor cells, has been shown to play a role in lysis of NB cells. It is therefore tempting to assume that a combination of passive immunotherapy with GD2-specific antibodies and adoptive transfer of NK effector cells would result in an improved NB therapy. To achieve this goal an NK cell line expressing a GD2-specific chimeric antigen receptor (CAR) was engineered: NK-92-scFv(ch14.18)-zeta. This CAR consists of a GD2-specific scFv-fragment, which was generated from ch14.18, and the CD3ζ-chain as intracellular signal-transducing domain. Within this thesis, GD2-specificity of NK-92-scFv(ch14.18)-zeta as well as efficacy towards GD2-expressing NB cell lines, including relapse cell lines that exhibit partial or multidrug resistance were demonstrated. Blocking the interaction between the CAR and GD2 resulted in almost complete abrogation of NK-92-scFv(ch14.18)-zeta-mediated lysis of GD2-positive NB cell lines in vitro, indicating that this interaction is the main mechanism of activation of NK-92-scFv(ch14.18)-zeta. Importantly, repeated application of NK-92-scFv(ch14.18)-zeta in combination with IL-2 significantly decreased tumor growth and prolonged survival of mice in an aggressively growing drug-resistant xenograft NB mouse model. These findings suggest that GD2-specific NK-92 has potential for a future clinical application as NB-specific effector cells that would be ready on demand in a standardized quality.
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Bahri, Meriem. "Anticorps thérapeutiques du marqueur gangliosidique tumoral GD2 O-acétylé : nouvelles stratégies d'optimisation." Thesis, Nantes, 2020. http://www.theses.fr/2020NANT1009.

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Les anticorps thérapeutiques spécifiques d’antigènes tumoraux permettent d’améliorer le pronostic des patients atteints de cancers. Leur utilisation se heurte toutefois à des mécanismes d’échappement tumoraux variés. L’identification de ces mécanismes permet aujourd’hui d’envisager différentes stratégies d’optimisation basée sur l’utilisation d’association thérapeutique. Ces aspects ont été étudié ici dans le cadre du ciblage immunologique du marqueur gangliosidique tumorale GD2 O-acétylé dans le cadre du neuroblastome chez l’enfant et du glioblastome chez l’adulte. Nous montrons que les propriétés proapoptotiques des anticorps du GD2 O-acétylé permettent de sensibiliser les cellules tumorales aux agents de chimiothérapie et ainsi un meilleur contrôle du développement tumoral. Plus particulièrement, ce mécanisme s’applique également aux cellules souches cancéreuses, population cellulaire particulièrement résistante aux agents cytotoxiques qui est impliquée dans les échecs thérapeutiques et les rechutes. Cette association soulève toutefois des incertitudes atour des bénéfices sur le long terme car nous montrons qu’elle induit la surexpression tumorale du point de contrôle phagocytaire CD47 et inhibe l’activité phagocytaire dépendante des anticorps anti- GD2 O-acétylé. Ces mécanismes d’échappement tumoraux peuvent être contrôlé par l’utilisation combiné d’inhibiteur de point de contrôle immunologique. Ensemble, ces travaux montrent l’intérêt d’associer les anticorps thérapeutiques du GD2 O-acétylé à la chimiothérapie et à des inhibiteurs de point de contrôle immunologique. Cet intérêt pourrait conduire à la réalisation d’un essai clinique de phase I de la prise en charge des neuroblastomes
Therapeutic antibodies specific for tumor antigens improve the prognosis of cancer patients. Tumor cells, however, develop various escape mechanisms. The identification of these mechanisms allows different optimization strategies based on therapeutic combinations to achieve long term response in patients with cancer. We studied here some of these aspects in the context neuroblastoma and glioblastoma using O-acetylated GD2- specific monoclonal antibodies. We show that the pro-apoptotic activity of O-acetylated GD2- specific antibodies sensitizes tumor cells to chemotherapeutic agents, allowing thereby a more potent tumor control. Mostly, this mechanism also applies to glioma cancer stem cells, a tumor cell subset particularly resistant to cytotoxic agents which is involved in therapeutic failures and relapses. However, this therapeutic combination might not be able to provide long-term benefits because we show that it further induces the CD47 phagocytic checkpoint in tumor cells. This innate immune checkpoint inhibits the phagocytic activity induced by O-acetylated-specific antibodies against opsonized tumor cells. Yet, this tumor escape mechanism can be controlled by immunological checkpoint inhibitors. Together, we provided the proof of concept of tri-therapy approach to achieve long lasting response in patient with neuroblastoma
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Vogel, Anna [Verfasser]. "Herstellung chimärer Antikörper gegen das Tumorantigen GD2 unter Verwendung einer transgenen Mauslinie / Anna Vogel." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1042336393/34.

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Books on the topic "GD2"

1

Dick, Claésson, ed. GDH. Göteborg: Litterär gestaltning, Göteborgs universitet, 2010.

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Dragunskiĭ, V. Gde ėto vidano, gde ėto slykhano--. Moskva: "Samovar", 1999.

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Proceedings, of the Third International Symposium on the Gerasimov-Drell-Hearn Sum Rule and Its Extensions (. GDH 2004. Singapore: World Scientific Publishing, 2005.

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Nordqvist, Sven. Gde Petson? [Moskva?]: Al'bus Corvus, 2017.

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Heun, Matthew Kuperus, Michael Carbajales-Dale, and Becky Roselius Haney. Beyond GDP. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12820-7.

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Kuzne︠t︡sova, ︠I︡Uli︠i︡a. Gde papa ? Moskva: Izd. Dom Meshcher︠i︡akovoĭ, 2013.

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orner, Thomas K. Das Grab des Novalis: Dramatisierter Essay. Fragment von der Weltanschauung. Frankfurt a. M., Germany: Edition Büchergilde GmbH, 2007.

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Clark, Mary Higgins. Gde ty teperʹ? Moskva: ĖKSMO, 2011.

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Gde my zhivem? Moskva: OGI, 2005.

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Shtilʹmark, F. R. Lukomorʹe, gde ono? Moskva: "Myslʹ", 1993.

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Book chapters on the topic "GD2"

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Suski, W., and T. Palewski. "Gd2/3Cr2S4." In Pnictides and Chalcogenides II, 205–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_52.

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Holze, Rudolf. "Ionic conductance of Gd2(SO4)3." In Electrochemistry, 895. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49251-2_842.

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Hartard, C., M. Jakisch, and K. Kunze. "Immunhistochemische Darstellung der Ganglioside GM1, GD2 und GD1b im peripheren Nerv." In Verhandlungen der Deutschen Gesellschaft für Neurologie, 949–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83771-5_221.

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Moon, P. K., and H. L. Tuller. "Fast ion conduction in the Gd2(ZrxTi1−x) 2O7 pyrochlore system." In NATO ASI Series, 307–12. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0509-5_14.

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Devanathan, R., and W. J. Weber. "Computational and Experimental Studies of the Radiation Response of Gd2 Ti2 O7 Pyrochlore." In Ceramic Transactions Series, 41–54. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118407950.ch5.

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Reid, D. P., M. C. Stennett, and N. C. Hyatt. "Synthesis and Structures of Gd2(Zr2-xCex)O7: A Model Ceramic System for Plutonium Disposition." In Ceramic Transactions Series, 11–20. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470930991.ch2.

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Galik, Elizabeth, Shin Fukudo, Yukari Tanaka, Yori Gidron, Tavis S. Campbell, Jillian A. Johnson, Kristin A. Zernicke, et al. "GDS." In Encyclopedia of Behavioral Medicine, 835. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100680.

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Timson, David J., Richard J. Reece, James B. Thoden, Hazel M. Holden, Andrea L. Utz, Beverly M. K. Biller, Eugen-Matthias Strehle, et al. "GDM." In Encyclopedia of Molecular Mechanisms of Disease, 692. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8580.

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Charles, Steindel. "GDP." In Economic Indicators for Professionals, 11–50. 1 Edition. | New York : Routledge, 2018.: Routledge, 2018. http://dx.doi.org/10.4324/9780203712955-2.

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Davis, Adam L. "GDK." In Learning Groovy, 17–22. Berkeley, CA: Apress, 2016. http://dx.doi.org/10.1007/978-1-4842-2117-4_4.

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Conference papers on the topic "GD2"

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Battula, Venkata Lokesh, Yuexi Shi, Kurt Evans, Rui-Yu Wang, Erika L. Speath, Rodrigo Jacamo, Rudy Guerra, et al. "Abstract LB-193: Ganglioside GD2 identifies cancer stem cells and inhibition of GD2 biosynthesis by targeting GD3 synthase exerts antitumor effects." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-193.

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Spreckelmeyer, S., J. Rogasch, K. Schönbeck, N. Beindorff, HN Lode, J. Schulte, P. Hundsdörfer, and H. Amthauer. "A Novel Tracer for GD2-Positive Neuroblastoma." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683563.

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SAID, M. R., I. ABU-ALJARAYESH, and A. AL-SHARIF. "MAGNETIC AND STRUCTURAL PROPERTIES OF Gd2−xYxNi17." In Proceedings of the First Regional Conference. World Scientific Publishing Company, 2000. http://dx.doi.org/10.1142/9789812793676_0099.

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Yaglioglu, Gul, Robinson Pino, Roger Dorsinville, J. Z. Liu, and Ming Yan. "Nonlinear optical response of Gd2@C80 thin films." In SPIE's International Symposium on Optical Science, Engineering, and Instrumentation, edited by Manfred Eich and Mark G. Kuzyk. SPIE, 1999. http://dx.doi.org/10.1117/12.368294.

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Liang, X. F., Q. Y. Zhang, D. D. Chen, X. H. Ji, and J. W. Zhai. "Cooperative energy transfer in Gd2(MoO4)3:Tb,Yb nanophosphors." In 2008 2nd IEEE International Nanoelectronics Conference. IEEE, 2008. http://dx.doi.org/10.1109/inec.2008.4585447.

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Erber, R., S. Kailayangiri, H. Hübner, M. Rübner, A. Hartmann, L. Häberle, J. Meyer, et al. "Disialogangliosids GD2 beim Mammakarzinom und dessen Einfluss auf die Prognose." In 94. Kongress der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e. V. (BGGF). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1713987.

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Tarim, John, Rebecca S. Sowers, Sajida Piperdi, Chand Khanna, and Richard G. Gorlick. "Abstract 5332: Evaluation of GD2 expression in patients with osteosarcoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5332.

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Gaß, P., S. Kailayangiri, H. Huebner, M. Ruebner, A. Hartmann, L. Häberle, J. Meyer, et al. "Expression of disialoganglioside GD2 and prognosis in breast cancer subtypes." In Wissenschaftliche Abstracts zur 40. Jahrestagung der Deutschen Gesellschaft für Senologie e.V. (DGS) Interdisziplinär. Kommunikativ. Digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730159.

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Nouso, Hiroshi, Hiroshi Tazawa, Terutaka Tanimoto, Morimichi Tani, Takanori Oyama, Hiroaki Sato, Kazuhiro Noma, et al. "Abstract 3831: Development of near-infrared photoimmunotherapy targeting GD2-positive neuroblastoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3831.

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Sujjitjoon, Jatuporn, La-ong Sri Atchaneeyasakul, Shih-Ting Tsao, Elias Sayour, Pa-thai Yenchitsomanus, and Lung-Ji Chang. "Abstract 3150: GD2-specific chimeric antigen receptor T cells targeting retinoblastoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3150.

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Reports on the topic "GD2"

1

Cheung, Nai-Kong. Single Chain FV Constructs of Anti-Ganglioside GD2 Antibodies for Radioimaging and Radioimmunotherapy. Office of Scientific and Technical Information (OSTI), March 2003. http://dx.doi.org/10.2172/900755.

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Cheung, N. K. V., and S. M. Larson. Single chain FV constructs of anti-ganglioside GD2 antibodies for radioimaging and radioimmumotheraphy. Progress report. Office of Scientific and Technical Information (OSTI), November 1993. http://dx.doi.org/10.2172/10105853.

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Archambault, Mark, Douglas Talley, and Oshin Peroomian. Computational Analysis of a Single-Element, Shear-Coaxial, GH2/GO2 Engine. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada410952.

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Archambault, Mark, Richard Cohn, Doug Talley, and Oshin Peroomian. Computational Analysis of a Single-Element, Shear-Coaxial, GH2/GO2 Engine. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada412802.

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5

Bobkov, Konstantin. Scanning the Fluxless G_2 Landscape. Office of Scientific and Technical Information (OSTI), July 2009. http://dx.doi.org/10.2172/958575.

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6

Clark, Hunter, Maxim Pinkovskiy, and Xavier Sala-i-Martin. China's GDP Growth May be Understated. Cambridge, MA: National Bureau of Economic Research, April 2017. http://dx.doi.org/10.3386/w23323.

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7

Herman, D., W. Summers, and E. Danko. FINAL REPORT ON GDE GAP CELL. Office of Scientific and Technical Information (OSTI), September 2009. http://dx.doi.org/10.2172/964999.

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8

Talbot, C. Conover, Jr. GDB - Human Genome Database final report. Office of Scientific and Technical Information (OSTI), January 2002. http://dx.doi.org/10.2172/771354.

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9

Bhandari, Pranjul, and Jeffrey Frankel. Nominal GDP Targeting for Developing Countries. Cambridge, MA: National Bureau of Economic Research, January 2015. http://dx.doi.org/10.3386/w20898.

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10

Susnjak, Teo, and Christoph Schumacher. Nowcasting: Towards Real-time GDP Prediction. Knowledge Exchange Hub, December 2018. http://dx.doi.org/10.33217/keh/gdplive/001/12.2018.

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