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Статті в журналах з теми "COMBINATORIAL THERAPY"
Stritzker, J., and A. A. Szalay. "Single-agent combinatorial cancer therapy." Proceedings of the National Academy of Sciences 110, no. 21 (May 10, 2013): 8325–26. http://dx.doi.org/10.1073/pnas.1305832110.
Повний текст джерелаBaust, J. G. "Cryoablation: An Emergent Combinatorial Therapy." Cryobiology 92 (February 2020): 272. http://dx.doi.org/10.1016/j.cryobiol.2019.11.010.
Повний текст джерелаKoh, Yoon Woo. "Combinatorial Targeted Therapy in Thyroid Cancer." Korean Journal of Otorhinolaryngology-Head and Neck Surgery 53, no. 4 (2010): 203. http://dx.doi.org/10.3342/kjorl-hns.2010.53.4.203.
Повний текст джерелаMittra, Arjun, and Debu Tripathy. "Looking ahead to rational combinatorial therapy." Community Oncology 9, no. 2 (February 2012): 40–41. http://dx.doi.org/10.1016/j.cmonc.2012.02.002.
Повний текст джерелаSabbatino, Francesco, Yangyang Wang, Ravin Poudel, Matteo Ligorio, Elvira Favoino, Xinhui Wang, Jennifer Wargo, Soldano Ferrone, Keith D. Lillemoe, and Cristina R. Ferrone. "Novel combinatorial therapy for pancreatic adenocarcinoma." Journal of the American College of Surgeons 217, no. 3 (September 2013): S137. http://dx.doi.org/10.1016/j.jamcollsurg.2013.07.319.
Повний текст джерелаAnitha, A., S. Maya, Amal J. Sivaram, U. Mony, and R. Jayakumar. "Combinatorial nanomedicines for colon cancer therapy." Wiley Interdisciplinary Reviews: Nanomedicine and Nanobiotechnology 8, no. 1 (June 10, 2015): 151–59. http://dx.doi.org/10.1002/wnan.1353.
Повний текст джерелаVojvodic, Sladjana, Gabor Katona, and Miroslav Sarac. "Combinatorial pharmacogenomic test for successful antidepressant treatment of a major depressive disorder." Medical review 74, no. 3-4 (2021): 117–22. http://dx.doi.org/10.2298/mpns2104117v.
Повний текст джерелаSabei, Fahad Y., Olena Taratula, Hassan A. Albarqi, Adel M. Al-Fatease, Abraham S. Moses, Ananiya A. Demessie, Youngrong Park, et al. "A targeted combinatorial therapy for Ewing's sarcoma." Nanomedicine: Nanotechnology, Biology and Medicine 37 (October 2021): 102446. http://dx.doi.org/10.1016/j.nano.2021.102446.
Повний текст джерелаKwong, L. N., and M. A. Davies. "Targeted therapy for melanoma: rational combinatorial approaches." Oncogene 33, no. 1 (February 18, 2013): 1–9. http://dx.doi.org/10.1038/onc.2013.34.
Повний текст джерелаMukerjee, A., A. P. Ranjan, and J. K. Vishwanatha. "Combinatorial Nanoparticles for Cancer Diagnosis and Therapy." Current Medicinal Chemistry 19, no. 22 (June 1, 2012): 3714–21. http://dx.doi.org/10.2174/092986712801661176.
Повний текст джерелаДисертації з теми "COMBINATORIAL THERAPY"
CATTANEO, STEFANO. "Combinatorial gene therapy for epilepsy." Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/128275.
Повний текст джерелаL'epilessia è una malattia neurologica caratterizzata da una persistente predisposizione a generare crisi, che colpisce circa l'1% della popolazione mondiale. Circa il 30% dei pazienti epilettici sono resistenti ai farmaci, quindi refrattari ai farmaci antiepilettici attualmente disponibili (AED). Meno del 10% di questi pazienti resistenti ai farmaci sono eleggibili per la chirurgia, spesso a causa di foci epilettici generalizzati o multipli, o a causa della vicinanza del focus epilettico alle aree cerebrali eloquenti. Pertanto, la terapia genica può rappresentare un approccio fattibile. Il neuropeptide Y (NPY) può agire come un anticonvulsivo endogeno. L'espressione di NPY è aumentata sia nelle sezioni ippocampali di roditori che in quelle di campioni chirurgici umani di epilessia del lobo temporale, nonostante la forte perdita di interneuroni GABAergici a livello dell’ilo. Pertanto, la terapia genica basata su NPY può rappresentare un nuovo approccio per il trattamento delle epilessie focali. Idealmente, tuttavia, tali vettori dovrebbero contenere più elementi (almeno NPY e Y2R guidati da promotori appropriati). In passato, il nostro laboratorio ha fatto grandi progressi nel campo dei vettori virali basati su HSV-1. Abbiamo quindi mirato a combinare il potenziale dei vettori HSV di ospitare DNA di grandi dimensioni, e la complessità del sistema NPY, per creare una cassetta terapeutica combinatoria "ideale". Tuttavia, le preoccupazioni residue in merito alla sicurezza della nostra nuova generazione di vettori basati su HSV-1 (chiamati J∆NI8) ci hanno spinto a valutare i profili di sicurezza ed efficacia in vitro per valutare l’effetto dell’infezione sulle proprietà elettrofisiologiche in neuroni primari. Sorprendentemente e in maniera deludente, abbiamo dimostrato che mutazioni nella glicoproteina B dell'involucro (gB), che è responsabile dell'entrata virale e della fusione cellulare, potrebbero sorgere durante la produzione del vettore virale. A livello elettrofisiologico, abbiamo inoltre visto che la gB mutata può aumentare la frequenza di potenziali d’azione e contemporaneamente ridurre sia la resistenza di ingresso che il potenziale di riposo neuroni trasdotti. Complessivamente, questi dati suggeriscono che un'attenta valutazione delle glicoproteine dell'involucro è necessaria per sviluppare vettori sicuri non replicativi basati su HSV-1 per il trattamento dei disturbi del SNC. Abbiamo quindi deciso di passare ai vettori Lentivirali (LV), una piattaforma più robusta e caratterizzata nonostante una capacità di carico più limitata rispetto ai vettori HSV. Per potenziare l'effetto protettivo di NPY, abbiamo sviluppato un approccio combinatorio di terapia genica basato sull'espressione di NPY insieme al suo recettore (Y2). Poiché i recettori Y2 agiscono principalmente a livello pre-sinaptico per diminuire il rilascio di glutammato riducendo l’ingresso di Ca2+, l'espressione dei transgeni è stata guidata dal promotore minimal CamKII, orientando così la loro espressione selettivamente nei neuroni eccitatori. Abbiamo successivamente caratterizzato la capacità dei nostri vettori LV di esprimere NPY e il suo recettore funzionale Y2 nei neuroni ippocampali e nel cervello dei topi. In seguito, abbiamo utilizzato un sistema di monitoraggio video-EEG mediante telemetria per valutare l'effetto dei geni terapeutici sul fenotipo epilettico in un modello genetico di epilessia. Abbiamo scoperto che l'espressione combinata di NPY e Y2 è sufficiente a ridurre sia la frequenza che la durata delle crisi nel modello di epilessia Synapsin triple-KO. Questi dati rafforzano ulteriormente l'ipotesi che le strategie mirate all’utilizzo di NPY e Y2 possono avere successo per il trattamento dell'epilessia, in particolare per le forme resistenti ai farmaci ma anche per forme genetiche della malattia.
Pace, Emily A. "Investigating combinatorial ligand addiction provides insights into rational drug combinations in cancer therapy." Thesis, Boston University, 2012. https://hdl.handle.net/2144/34647.
Повний текст джерелаPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Cancer, the second most common cause of death in the United States, is a collection of diseases caused by uncontrolled cell growth and metastasis. The main treatment for cancer is chemotherapy, which generally kills fast growing cells nonspecifically and has many side effects. A different type of cancer treatment, called targeted therapy, aims to avoid general toxicity by using drugs that block the activity of specific gene products, usually encoded by oncogenes, which have been shown to drive tumor growth. To date, targeted therapies, alone or in combination with chemotherapies, have mainly been successful in rare subsets of patients with tumors addicted to single oncogenes. This has created a rationale to mainly treat patients with an oncogene-addiction (such as those carrying mutated or overexpressed kinases) with targeted therapies like erlotinib and trastuzumab, which inhibit human epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2/ErbB2), respectively. Here, evidence is provided that targeted therapies are also effective in tumors that are dependent on multiple growth factors - a phenomenon that is called combinatorial ligand addiction. Specifically, it is shown that ligands that bind the EGFR family and the hepatocyte growth factor receptor (HGFR/MET) can activate protein kinase B (PKB/ AKT) across a broad set of cancer cell lines, suggesting that ligand signaling is redundant and widespread. It is also shown that ErbB ligands have distinct signaling dynamics and strengths, which provides a rationale for investigating each component of the ErbB signaling network. Using a systematic approach, we found that ErbB3 is an imp01tant therapeutic target even though it is not overexpressed and lacks kinase activity. Furthermore, it is shown that cell lines with and without known oncogene-addiction express autocrine ligands and have improved growth inhibition with drug combinations that include autocrine ligand-blocking antibodies. This research demonstrates that combinatorial ligand addiction creates a new rationale for therapeutic combinations to improve efficacy and prevent resistance in cancer cells that are treated with current targeted drugs.
2031-01-01
Tavallai, Mehrad. "INTRODUCING NOVEL COMBINATORIAL TARGETED THERAPIES IN MULTIPLE TYPES OF CANCER." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4088.
Повний текст джерелаValencia, Pedro M. (Pedro Miguel). "A microfluidic platform for combinatorial synthesis and optimization of targeted polymeric nanoparticles for cancer therapy." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/79197.
Повний текст джерела"November 2012." Cataloged from PDF version of thesis.
Includes bibliographical references.
The use of nanotechnology to engineer drug delivery vehicles comprised of controlled release polymers with targeting molecules has the potential to revolutionize cancer therapy, among other diseases. Although a myriad of nanotherapeutics have been developed at the bench side, many of them stay at the research stage due to their complexity and difficulty in their optimization. A key challenge for optimization of nanoparticles (NPs) for drug delivery is the ability to systematically and combinatorially create and screen libraries of NPs with distinct physicochemical properties, from which promising formulations can be moved forward to preclinical and clinical studies. In this work, the development of a controlled method to synthesize libraries of NPs with distinct properties is described. The procedure uses a microfluidic platform that rapidly mixes reagents and provides homogeneous reaction environments, resulting in the reproducible, single-step synthesis of NPs with well-defined properties and narrow size distributions. The microfluidic system is composed of a mixing unit and a NP assembly unit. The mixing unit consists of a multi-inlet, 2-layer mixer where different precursors such as polymers of different MW and charge, ligand- and drug-conjugated polymers, free drugs, and solvents are mixed at different ratios into a homogenous solution. In the assembly unit, the precursor solution is quickly mixed with an anti-solvent (i.e. water) using 3D hydrodynamic flow focusing where NPs self-assemble after complete mixing. With the microfluidic platform, a library of 100 NPs with different sizes (15-200nm), charge (-30 to +30mV), surface chemistry (i.e. PEG coverage), surface ligand density (0-2.510⁵ ligands/[mu]m²), and drug loading (0-5 w/w%) was producedd in a high-throughput manner by simply varying the flow ratios of precursors entering the system. This library was implemented for (i) screening for formulations (in vitro and in vivo) with optimal clinical properties for cancer treatment and (ii) deepening the understanding of how NP properties affect their biological behavior. The platform developed in this work would likely lead to better understanding of the design parameters for polymeric NPs and their smoother transition to the clinic.
by Pedro M. Valencia.
Ph.D.
MAROCCHI, FEDERICA. "FUNCTIONAL DROP-OUT SCREENINGS IDENTIFY ACTIONABLE VULNERABILITIES TO HALT MELANOMA GROWTH AND METASTASIS FORMATION." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/820408.
Повний текст джерелаMary, Bareford. "Sorafenib enhances pemetrexed-induced cytotoxicity through and autophagy-dependent mechanism in cancer cells." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2870.
Повний текст джерелаKUMAR, SUNIL. "COMBINATORIAL THERAPY FOR TUMOR TREATMENT." Thesis, 2023. http://dspace.dtu.ac.in:8080/jspui/handle/repository/20430.
Повний текст джерелаRhee, Younghwa. "Efficacy of losartan and growth hormone combinatorial therapy in DyW mice." Thesis, 2015. https://hdl.handle.net/2144/16344.
Повний текст джерелаJAIN, SHALEEN. "PREPARATION OF TUMOR TARGETING COMBINATORIAL THERAPY USING NANOPARTICLE CONJUGATED NATURAL COMPOUNDS." Thesis, 2020. http://dspace.dtu.ac.in:8080/jspui/handle/repository/18150.
Повний текст джерелаBao, Xuhui. "Immunotoxin Monotherapy and Combinatorial Therapy With Immune Checkpoint Inhibitors for Malignant Brain Tumors." Diss., 2016. http://hdl.handle.net/10161/13365.
Повний текст джерелаGlioblastoma is the most common and aggressive malignant brain tumor among all primary brain and central nervous system (CNS) tumors. The median survival time for glioblastoma patients given the current standard of care treatment (surgery, radiation, and chemotherapy) is less than 15 months. Medulloblastoma is another major malignant brain tumor that most frequently occurs in children. Although recent advances in surgery, radiotherapy, and chemotherapy have led to an increase in 5-year survival rates of medulloblastoma patients, treatment-related toxicity often has a major impact on long-term quality of survival.
As a result, there is an urgent need to develop more efficient and novel therapeutic approaches that specifically target tumor cells while preserving the surrounding normal CNS to improve the poor survival and quality of life of patients with malignant brain tumors. To address this need, we have developed two novel targeted immunotoxins (ITs), D2C7-(scdsFv)-PE38KDEL (D2C7-IT) and NZ-1-(scdsFv)-PE38KDEL (NZ-1-IT). D2C7-IT was developed by fusing the single-chain variable fragment (scFv) of the D2C7 monoclonal antibody (mAb) with domains II and III of Pseudomonas exotoxin A (PE38KDEL), and NZ-1-IT was developed by fusing the scFv of the NZ-1 mAb with PE38KDEL. D2C7-IT reacts with both the wild-type epidermal growth factor receptor (EGFRwt) and the EGFR variant III (EGFRvIII), two overexpressed proteins in glioblastomas. NZ-1-IT reacts with podoplanin (PDPN), a protein that has a high expression in glioblastomas and medulloblastomas.
In vitro cytotoxicity data shows that both ITs effectively inhibited protein synthesis in a variety of epitope-expressing glioblastoma and medulloblastoma xenograft cells and human tumor cell lines. Furthermore, the direct anti-tumor efficacy of D2C7-IT was examined in orthotopic glioma models in immunocompromised mice, while the direct anti-tumor efficacy of NZ-1-IT was observed in medulloblastoma xenograft-bearing immunocompromised mice. Both immunotoxins showed a robust anti-tumor efficacy in the preclinical brain tumor models. D2C7-IT was first investigated in the subsequent studies to accelerate its translation to the clinic. The preclinical toxicity of intracerebral D2C7-IT infusion was subsequently determined in normal Sprague-Dawley (SD) rats. The maximum tolerated dose (MTD) of D2C7-IT was determined to be between a total dose of 0.10 and 0.35 μg, and the no-observed-adverse-effect level (NOAEL) of D2C7-IT was a total dose of 0.05 μg in SD rats. Both the MTD and NOAEL were utilized as references for the D2C7-IT clinical trial design.
In addition to direct tumor cell killing, immunotoxin monotherapy has been shown to induce a secondary anti-tumor immune response through the engagement of T cells. Therefore, the D2C7-IT-induced secondary anti-tumor immune response was investigated using syngeneic mouse glioma models in immunocompetent mice. Moreover, previous studies have demonstrated that immune checkpoint inhibitors have a robust anti-tumor efficacy by augmenting the T cell response to the tumor cells. Thus, immune checkpoint inhibitors were combined with D2C7-IT in order to enhance the immunotoxin-induced anti-tumor immune response to eliminate residual tumor cells and prevent tumor recurrence in the long term. Meanwhile, studies with NZ-1-IT remain preliminary; thus, this IT will not be as robustly discussed as D2C7-IT throughout this text.
Dissertation
Книги з теми "COMBINATORIAL THERAPY"
Ganai, Shabir Ahmad. Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3.
Повний текст джерела1966-, Seeberger Peter H., ed. Solid support oligosaccharide synthesis and combinatorial carbohydrate libraries. New York: Wiley, 2001.
Знайти повний текст джерелаGanai, Shabir Ahmad. Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy. Springer Singapore Pte. Limited, 2021.
Знайти повний текст джерелаGanai, Shabir Ahmad. Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy. Springer Singapore Pte. Limited, 2020.
Знайти повний текст джерелаAndersson, Patrik, and Christian Ostheimer, eds. Combinatorial Approaches to Enhance Anti-Tumor Immunity: Focus on Immune Checkpoint Blockade Therapy. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-161-2.
Повний текст джерелаAtta-ur-Rahman and M. Iqbal Choudhary, eds. Frontiers in Cardiovascular Drug Discovery: Volume 4. BENTHAM SCIENCE PUBLISHERS, 2019. http://dx.doi.org/10.2174/97816810839951180401.
Повний текст джерелаKahn, Michael. High Throughput Screening for Novel Anti-Inflammatories (Progress in Inflammation Research). Birkhauser, 2000.
Знайти повний текст джерелаЧастини книг з теми "COMBINATORIAL THERAPY"
Dalasanur Nagaprashantha, Lokesh. "Combinatorial Cancer Therapy." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7158-7.
Повний текст джерелаNagaprashantha, Lokesh Dalasanur. "Combinatorial Cancer Therapy." In Encyclopedia of Cancer, 1180–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_7158.
Повний текст джерелаWinbanks, Catherine E., and Paul Gregorevic. "Combinatorial Gene Therapy Strategies for Treating Muscular Dystrophies." In Muscle Gene Therapy, 117–39. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1207-7_8.
Повний текст джерелаRothenberg, S. Michael, Joan Fisher, David Zapol, David Anderson, Yasumichi Hitoshi, Philip Achacoso, and Gany P. Nolan. "Intracellular Combinatorial Chemistry with Peptides in Selection of Caspase-like Inhibitors." In Gene Therapy, 171–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72160-1_18.
Повний текст джерелаBanerjee, Ena Ray. "Novel Combinatorial Probiotics in Therapy and Prophylaxis." In Perspectives in Translational Research in Life Sciences and Biomedicine, 89–98. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5870-7_3.
Повний текст джерелаMangla, Bharti, Pankaj Kumar, Kamya Goyal, Kanchan Kohli, and Shammy Jindal. "Breast Cancer Therapy by Combinatorial Herbo-Synthetic Nanocarrier." In Bioactive-Loaded Nanomedicine for the Management of Health and Disease, 61–85. New York: Apple Academic Press, 2022. http://dx.doi.org/10.1201/9781003277101-5.
Повний текст джерелаGanai, Shabir Ahmad. "Overview of Epigenetic Signatures and Their Regulation by Epigenetic Modification Enzymes." In Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 1–33. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_1.
Повний текст джерелаGanai, Shabir Ahmad. "Combining Histone Deacetylase Inhibitors with Other Anticancer Agents as a Novel Strategy for Circumventing Limited Therapeutic Efficacy and Mitigating Toxicity." In Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 203–39. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_10.
Повний текст джерелаGanai, Shabir Ahmad. "Futuristic Approaches Towards Designing of Isozyme-Selective Histone Deacetylase Inhibitors Against Zinc-Dependent Histone Deacetylases." In Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 241–58. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_11.
Повний текст джерелаGanai, Shabir Ahmad. "Epigenetic Regulator Enzymes and Their Implications in Distinct Malignancies." In Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 35–65. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_2.
Повний текст джерелаТези доповідей конференцій з теми "COMBINATORIAL THERAPY"
Amiji, Mansoor M. "Multifunctional combinatorial-designed nanoparticles for nucleic acid therapy." In SPIE Defense + Security, edited by Thomas George, Achyut K. Dutta, and M. Saif Islam. SPIE, 2016. http://dx.doi.org/10.1117/12.2224764.
Повний текст джерелаLam, Kit S., and Ruiwu Liu. "From Combinatorial Chemistry to Nanotechnology to Cancer Therapy." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.014.
Повний текст джерелаWang, Yangyang, Shalin S. Patel, Juan Cong, Nan Zhang, Yuan Qi, Francesco Sabbatino, Steven Isakoff, Albert B. DeLeo, Soldano Ferrone, and Xinhui Wang. "Abstract 3639: Combinatorial therapy for triple negative breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3639.
Повний текст джерелаNguyen, J. P., M. Bianca, R. D. Huff, N. Tiessen, Y. Kim, V. Hou, M. Heller, M. D. Inman, and J. A. Hirota. "Development of a Novel Combinatorial Therapy for Cystic Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2580.
Повний текст джерелаLam, Kit S. "From Combinatorial Chemistry to Nanocarriers for Cancer Therapy and Imaging." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/acp.2012.as3e.4.
Повний текст джерелаLam, Kit S. "From Combinatorial Chemistry to Nanocarriers for Cancer Therapy and Imaging." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/acpc.2012.as3e.4.
Повний текст джерелаSrivastava, Jyoti, Devaraja Rajasekaran, Ayesha Siddiq, Rachel Gredler, Chadia L. Robertson, Maaged A. Akiel, Xue-Ning Shen, et al. "Abstract 5400: A novel combinatorial therapy for hepatocellular carcinoma (HCC)." 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.am2015-5400.
Повний текст джерелаBölükbas, Deniz Ali, Stefan Datz, Charlotte Meyer-Schwickerath, Malamati Vreka, Sabine van Rijt, Oliver Eickelberg, Georgios Stathopoulos, Thomas Bein, and Silke Meiners. "Combinatorial delivery of targeted mesoporous silica nanoparticles for lung cancer therapy." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2841.
Повний текст джерелаBinder, Zev A., Yibo Yin, Radhika Thokala, and Donald M. O'Rourke. "Abstract LB-340: Combinatorial platform for CART cell therapy for glioblastoma." 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-lb-340.
Повний текст джерелаChakraborty, Sanjukta, Rachana R. Maniyar, Sina Dadafarin, Ghada Ben Rahoma, Sarnath Singh, Augustine Moscatello, Jan Geliebter, and Raj K. Tiwari. "Abstract 3237: Combinatorial immune checkpoint inhibitor therapy in anaplastic thyroid cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3237.
Повний текст джерелаЗвіти організацій з теми "COMBINATORIAL THERAPY"
Baia, Gilson S. Combinatorial Therapy Approaches for NF2-Deficient Meningiomas. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada567130.
Повний текст джерелаBaia, Gilson S. Combinatorial Therapy Approaches for NF2-Deficient Meningiomas. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada584501.
Повний текст джерела