Gotowe bibliografie tematyczne / COMBINATORIAL THERAPY

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Gotowa bibliografia na temat „COMBINATORIAL THERAPY”

Autor: Grafiati

Data publikacji: 11 września 2023

Data aktualizacji: 16 stycznia 2024

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Artykuły w czasopismach na temat "COMBINATORIAL THERAPY"

Stritzker, J., i A. A. Szalay. "Single-agent combinatorial cancer therapy". Proceedings of the National Academy of Sciences 110, nr 21 (10.05.2013): 8325–26. http://dx.doi.org/10.1073/pnas.1305832110.

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Baust, J. G. "Cryoablation: An Emergent Combinatorial Therapy". Cryobiology 92 (luty 2020): 272. http://dx.doi.org/10.1016/j.cryobiol.2019.11.010.

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Koh, Yoon Woo. "Combinatorial Targeted Therapy in Thyroid Cancer". Korean Journal of Otorhinolaryngology-Head and Neck Surgery 53, nr 4 (2010): 203. http://dx.doi.org/10.3342/kjorl-hns.2010.53.4.203.

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Mittra, Arjun, i Debu Tripathy. "Looking ahead to rational combinatorial therapy". Community Oncology 9, nr 2 (luty 2012): 40–41. http://dx.doi.org/10.1016/j.cmonc.2012.02.002.

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Sabbatino, Francesco, Yangyang Wang, Ravin Poudel, Matteo Ligorio, Elvira Favoino, Xinhui Wang, Jennifer Wargo, Soldano Ferrone, Keith D. Lillemoe i Cristina R. Ferrone. "Novel combinatorial therapy for pancreatic adenocarcinoma". Journal of the American College of Surgeons 217, nr 3 (wrzesień 2013): S137. http://dx.doi.org/10.1016/j.jamcollsurg.2013.07.319.

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Anitha, A., S. Maya, Amal J. Sivaram, U. Mony i R. Jayakumar. "Combinatorial nanomedicines for colon cancer therapy". Wiley Interdisciplinary Reviews: Nanomedicine and Nanobiotechnology 8, nr 1 (10.06.2015): 151–59. http://dx.doi.org/10.1002/wnan.1353.

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Vojvodic, Sladjana, Gabor Katona i Miroslav Sarac. "Combinatorial pharmacogenomic test for successful antidepressant treatment of a major depressive disorder". Medical review 74, nr 3-4 (2021): 117–22. http://dx.doi.org/10.2298/mpns2104117v.

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Introduction. The combinatorial pharmacogenomic test has shown the potential to predict antidepressant response, tolerability, selection, and dosage in the treatment of a major depressive disorder. A case of successful management of antidepressant therapy adjustment is reported by using the combinatorial pharmacogenomic test. Case Report. A 53-year old man, severely disabled due to a rare genetic disease, Usher syndrome type 3, was treated with numerous antidepressants. However, episodes of major depression recurred, along with frequent suicidal thoughts. A combinatorial pharmacogenomic test was considered to design a potentially effective antidepressant therapy. Conclusion. According to the results of the combinatorial pharmacogenomic test, the patient constantly received inadequate antidepressant therapy, which did not lead to an improvement of depression due to moderate gene-drug interaction. The patient was prescribed nortriptyline, which proved to be one of the few most adequate according to the test. He showed improvement with subjectively more tolerable depression without suicidal thoughts and episodes of major depression. This case showed that the combinatorial pharmacogenomic testing may contribute to better selection of antidepressant therapy.

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Sabei, Fahad Y., Olena Taratula, Hassan A. Albarqi, Adel M. Al-Fatease, Abraham S. Moses, Ananiya A. Demessie, Youngrong Park i in. "A targeted combinatorial therapy for Ewing's sarcoma". Nanomedicine: Nanotechnology, Biology and Medicine 37 (październik 2021): 102446. http://dx.doi.org/10.1016/j.nano.2021.102446.

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Kwong, L. N., i M. A. Davies. "Targeted therapy for melanoma: rational combinatorial approaches". Oncogene 33, nr 1 (18.02.2013): 1–9. http://dx.doi.org/10.1038/onc.2013.34.

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Mukerjee, A., A. P. Ranjan i J. K. Vishwanatha. "Combinatorial Nanoparticles for Cancer Diagnosis and Therapy". Current Medicinal Chemistry 19, nr 22 (1.06.2012): 3714–21. http://dx.doi.org/10.2174/092986712801661176.

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Rozprawy doktorskie na temat "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.

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Epilepsy is a neurological disease characterized by a persistent predisposition to generate seizures, that affects about 1% of the world population. About 30% of epileptic patients are drug-resistant, thus refractory to currently available anti-epileptic drugs (AEDs). Less than 10% of these drug-resistant patients are eligible for resective brain surgery, often due to generalized or multiple epileptic foci, or due to proximity of the epileptic focus to eloquent brain areas. Therefore, gene therapy may represent a doable approach for the unmet medical need of these patients. Neuropeptide Y (NPY) can act as an endogenous anticonvulsant. NPY expression is increased both in rodent and human hippocampal sections from temporal lobe epilepsy surgical samples, despite the strong loss of hilar GABAergic interneurons. Therefore, NPY-based gene therapy may represent a novel approach for the treatment of focal epilepsies. Ideally, however, such vectors should contain multiple elements (at least NPY and Y2Rs driven by appropriate promoters). In the past, great advancements in the field of viral vectors based on HSV-1 have been made by our laboratory. We therefore aimed at combining the potential of HSV vectors to accommodate large payloads with the complexity of the NPY system to create an “ideal” combinatorial therapeutic cassette. However, residual concerns on the safety and translatability of our new generation HSV-1 based vectors (named J∆NI8) let us first characterize their electrophysiological properties in primary neuronal culture, to assess both safety and efficacy profiles. Surprisingly and disappointingly, we show that mutations in the envelope glycoprotein B (gB), which is responsible for viral entry and cell fusion, might arise during viral vector production. In turn, mutated gB can increase firing frequency while reducing both input resistance and resting membrane potential of transduced neurons. Altogether, these data suggest that careful evaluation of envelope glycoproteins is needed to develop safe HSV-1 replication-defective vectors for the treatment of CNS disorders. We, therefore, decided to move to LV vectors, a more robustly characterized platform despite a more limited packaging capacity compared with HSV vectors. To potentiate the protective effect of NPY, we developed a combinatorial gene therapy approach based on the expression of NPY together with its receptor (Y2). Since Y2 receptors act mainly pre-synaptically to reduce glutamate release by lowering Ca2+ influx, transgenes expression was driven by the minimal CamKII promoter, thereby biasing their expression in excitatory neurons. We characterized the ability of our lentiviral vectors to express NPY and its functional Y2 receptor in hippocampal neurons and mouse brains. Telemetry video-EEG monitoring was then used to assess the effect of the therapeutic genes on the epileptic phenotype of a genetic mouse model of epilepsy. We found that the combined expression of NPY and Y2 is sufficient to reduce both the frequency and duration of seizures in the Synapsin triple-KO epilepsy model. These data further strengthen the hypothesis that strategies aimed at the delivery of NPY and Y2 may be successful for the treatment of epilepsy, particularly for pharmaco-resistant and genetic forms of the disease.
L'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.

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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.

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Thesis (Ph.D.)--Boston University
PLEASE 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

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Tavallai, Mehrad. "INTRODUCING NOVEL COMBINATORIAL TARGETED THERAPIES IN MULTIPLE TYPES OF CANCER". VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4088.

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The cancers of liver, colon and breast are amongst the top five most prevalent and most fatal worldwide. As the Raf/MEK/ERK pathway is frequently deregulated in hepatocellular carcinoma (HCC), sorafenib, a Raf kinase inhibitor, became the first systemic therapy approved for the treatment of patients with HCC. However, sorafenib only produced modest effects with low response rates in the clinic. Similarly, regorafenib, which was approved for the treatment of metastatic colorectal cancer (CRC), has had a poor response rate in the clinic. Since phosphodiesterase type 5 has been reported to be overexpressed in HCC and CRC, we hypothesized that sildenafil, a phosphodiesterase type 5 inhibitor, could enhance the toxicities of sorafenib and regorafenib in HCC and CRC cells, respectively. Our in vitro data indicated that the drugs interacted strongly to kill cancer cells via induction of ER stress, autophagy and apoptosis. In accordance with these findings, our in vivo data demonstrated a significant reduction in tumor growth. The second study in this manuscript was conducted based on the growing body of evidence about the significant contribution of EGFR and JAK/STAT signaling to the breast tumorigenesis. Our preliminary in vitro data demonstrated that the concurrent inhibition of these two pathways by lapatinib, a dual ERBB1/2 inhibitor, and ruxolitinib, a JAK1/2 inhibitor, synergistically killed breast cancer cells of all types, including the resistant triple negative subtype. Our mechanistic studies showed that the combination of ruxolitinib and lapatinib triggered cytotoxic mitophagy, and autophagy-dependent activation of BAX and BAK leading to the mitochondrial dysfunction.

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Valencia, 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.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, February 2013.
"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.

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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.

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Advanced and metastatic melanoma prognosis is poor. Recent approval of targeted and immune therapies markedly improved overall survival rates, but nevertheless, the majority of patients experience recurrence and resistance, as well as treatment discontinuation due to severe toxicities. To explore new promising therapeutic approach in melanoma, I made use of our cohort of metastatic melanoma patient-derived xenografts (PDXs) to perform drop-out genetic screens, by means of a shRNA library targeting actionable genes, for which drugs are already available and can be repurposed for melanoma treatment. An innovative ex vivo transwell-based migration screen allowed me to isolate numerous actionable vulnerabilities, concordantly essential also for in vivo tumor growth, thus showing that this ex vivo migration system can be exploited as a valuable preclinical platform to assess patients sensitivity profiles. Based on these results, I identified one promising combinatorial therapy approach, that notably showed remarkable efficacy when tested in vivo. Moreover, in order to specifically investigate the metastatic process, I set up a relevant model of spontaneous metastasis, in which I performed drop-out actionable screen. Many metastasis-specific actionable dependencies were isolated, notably proving high functional heterogeneity among individual lesions. Several identified candidates showed unanticipated role in driving melanoma metastasis and I further studied one of them, whose silencing reduced melanoma invasion and metastasis formation, suggesting that its therapeutic exploitation could represent an innovative treatment approach to inhibit melanoma metastasis dissemination.

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Mary, Bareford. "Sorafenib enhances pemetrexed-induced cytotoxicity through and autophagy-dependent mechanism in cancer cells". VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2870.

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Acquired cellular resistance to traditional chemotherapeutics is a common obstacle in the treatment of most cancer cell types. This resistance occurs as a result of changes in the underlying molecular mechanisms of disease progression. The development of novel chemotherapeutic approaches designed to enhance the efficacy of protypical anti-cancer drugs is important in order to overcome this issue. Such approaches will aid in understanding the biomolecular phenomena responsible for drug resistance and disease progression. Combining signaling pathway inhibitors has become an effective strategy for enhancing tumor cell death by targeting multiple pathways known to regulate cell survival. Pemetrexed, an FDA-approved anti-folate drug, targets thymidylate synthase (TS) and a secondary folate-dependent enzyme, 5’ aminoimidazole-carboximide ribonucleotide formyltransferase (AICART); both important for DNA synthesis. Studies performed by our collaborator demonstrated that TS inhibition causes intracellular accumulation of ZMP+ and activation of AMPK which is known to induce autophagy in mammalian cells. Previous studies from our lab and others showed that sorafenib, a multi-kinase inhibitor of Raf-1 and class III receptor tyrosine kinases, was able to induce a cytotoxic form of autophagy in a variety of tumor cell types. Combination treatment using pemetrexed and sorafenib in these cancer cells resulted in an enhancement of autophagy and cell lethality beyond that of individual drugs alone. Inhibition of autophagy suppressed the toxic interactions of these drugs in all cell types examined. Pemetrexed/sorafenib cotherapy also proved to be an effective treatment for triple negative breast cancer cells having advanced to a stage of estrogen independence. Fulvestrant-resistant MCF7 cells were more sensitive to the drug combination than parental, estrogen-dependent MCF7 cells. Breast cancer cells cotreated with pemetrexed and sorafenib exhibited enhanced MEK/ERK signaling, Src activation that was dependent on platelet-derived growth factor β (PDGFRβ) downregulation, elevated protein phosphatase 2A (PP2A) activity, and increased de novo ceramide synthesis. Studies using a mouse model of experimentally-induced breast cancer validated drug combination effectiveness through inhibition of tumor growth, while no deleterious effects on normal tissues were observed. The data presented demonstrates that pemetrexed/sorafenib cotreatment augments chemosensitivity in both in vitro and in vivo systems. Based upon these findings, a Phase I clinical trial involving pemetrexed and sorafenib in breast cancer patients with solid, recurrent tumors was begun in 2011. In conclusion, this work strongly supports a promising therapeutic utility for the pemetrexed/sorafenib combination in treatment of various cancer cell types.

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KUMAR, SUNIL. "COMBINATORIAL THERAPY FOR TUMOR TREATMENT". Thesis, 2023. http://dspace.dtu.ac.in:8080/jspui/handle/repository/20430.

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Cancer is a complex and multifaceted disease that continues to pose a significant challenge to global health. As the second leading cause of death worldwide. Early detection and noninvasive techniques of detecting cancer are necessary to improve treatment outcomes, save lives and improve the quality of life. Biopsies of tumors are often expensive and invasive and raise the risk of serious complications like infection, excessive bleeding, and puncture damage to nearby tissues and organs. Early detection biomarkers are often variably expressed in different patients and may even be below the detection level at an early stage. Hence PBMC that shows alteration in gene profile as a result of interaction with tumor antigens may serve as a better early detection biomarker. Also, such alterations in immune gene profile in PBMCs are more detectable in a wide variety of cancer patients despite their variability in different cancer mutants. Tumor cell biomarkers lack specificity, and tumor heterogeneity complicates accurate diagnosis and treatment. Changing biomarker expression affects treatment responses, and technical challenges impact utility. Synthetic drugs targeting tumor cells often trigger tumour cells to acquire resistance against them. Tumor progression is an outcome of tumor growth regulation in conjunction with tumor evasion by immune modulation. Therefore, understanding of immunological biomarkers is equally important. Hence, designing a prudent chemotherapeutic combination requires a detailed understanding of gene regulation altering cancer prognosis and its impact on immune regulation . Immunotherapy also has its side effects and does not provide an adequate response in all patients, and its inherent variability in patient response often makes them prohibitive. Hence, a concomitant targeting of tumour cells and modulation of immune cell function may be a particularly beneficial mechanism for cancer treatment. Machine learning tools are crucial for early cancer detection and immune modulation due to their ability to analyze complex data and identify patterns that may not be apparent through viii | P a g e traditional methods. Potential diagnostic biomarkers were predicted for breast cancer using eXplainable Artificial Intelligence (XAI) on XGBoost machine learning (ML) models trained on a binary classification dataset containing the expression data of PBMCs from 252 breast cancer patients and 194 healthy women. After effectively adding SHAP values further into the XGBoost model, ten important genes related to breast cancer development were discovered to be effective potential biomarkers. It was discovered that SVIP, BEND3, MDGA2, LEF1-AS1, PRM1, TEX14, MZB1, TMIGD2, KIT, and FKBP7 are key genes that impact model prediction. These genes may serve as early, non-invasive diagnostic and prognostic biomarkers for breast cancer patients. The impact of concomitant intervention cancer progression and immune regulation therefore necessitated identification of such biomarkers that have dual impact. Gene expression data of HNSC tumor samples and PBMCs of tumor patient datasets were analysed for the identification of differentially expressed genes. 110 DEGs were found to be common in both datasets. Further, it was identified that these 110 DEGs were involved in biological processes related to tumor regulation. Potential Immunological biomarkers were identified for HNSC cancer. The Genes that play a role in both tumour growth and immune suppression were identified by enrichment analysis followed by gene expression analysis. 10 such genes were shortlisted, Foxp3, CD274, IDO1, IL-10, SOCS1, PRKDC, AXL, CDK6, TGFB1, FADD. CD274 and IDO1 were found to have the highest degree of interaction based on their network of interactions. Synthetic drugs including many of FDA approved drugs might cause significant side effects, leading to adverse impacts on patients' quality of life. Additionally, some cancer cells may develop resistance to synthetic drugs over time, reducing treatment efficacy. Moreover, targeted therapies may only be effective in cancers with specific molecular characteristics, limiting their broad applicability. To address these limitations, ongoing research focuses on developing more targeted and personalized therapies, combining synthetic drugs with other ix | P a g e treatment modalities, and exploring alternative natural compounds with multi-target effects. Multi-target natural compounds offer the advantage of targeting multiple pathways involved in cancer progression without significant side effects. These compounds, derived from plants and other natural sources, hold promise in cancer treatment due to their diverse mechanisms of action and potential for reduced toxicity. Natural compounds that help in tumour suppression as well as functional immune modulation were identified for their dual roles. Np care and GEO databases were used for retravel of natural compounds. 102 potential anti-cancer natural compounds treatment gene expression data was analysed and key differentially regulated genes by them were identified. These 102 natural compounds were analysed for their ability to alter the expression of 110 commonly differentially expressed (identified in first objective). Salidroside was altering maximum number of 66 gene from them. Gallic acid and Shikonin were found to be the natural compounds that target CD274 and IDO1 respectively. Galic acid is extracted from leaves of bearberry, in pomegranate root bark, gallnuts, witch hazel, both in free-state and as part of the tannin molecule, whereas Shikonin is found in the extracts of dried root of the plant Lithospermum erythrorhizon. Studies have demonstrated that both Shikonin and Gallica acid exhibits anti-cancer properties. Single drug treatment can lead to the development of drug resistance, where cancer cells become less responsive to the treatment over time. Some cancers may be inherently resistant to certain drugs, restricting their effectiveness. Moreover, high doses of a single drug can cause severe side effects, impacting patients' quality of life. Additionally, single-drug therapy may not be effective due to the heterogeneity of cancer cells, allowing potential tumor recurrence. Combination therapy targets cancer cells through multiple pathways, reduces drug resistance, and enhances efficacy of treatment outcomes. Synergistic interactions can improve efficacy while minimizing side effects, advancing personalized cancer care for better patient outcomes. A combination of Salidroside, Ginsenoside Rd, Oridonin, Britanin, and Scutellarein was x | P a g e chosen such that they could alter the expression of 108 genes out of the selected 110 genes. The combination was further analyzed for regulating pathways and biological processes that were affected. Expression data analysis of HNSC cancer exhibited 1745 differentially expressed genes. Gallic acid treatment results in the downregulation of 120 genes and upregulation of 35 genes while Shikonin results in the downregulation of 660 genes and upregulation of 38 genes. Pathway analysis of these genes that were modulated by Gallic acid and Shikonin showed them to be crucially involved in pathways that were essential for cancer prognosis. Further Gallic acid and shikonin treatment impact on cancer cell line was analysed individually as well as in combination with the help of in vitro experiments. Gallic acid showed IC50 value of 46.87, 59.37, and 93.75 at 12h, 24h, and 48h treatment, respectively. Shikonin showed IC50 value of 13.86, 11.95, and 10.89 at 12h, 24h, and 48h treatment, respectively. Lowest percentage of cell viability was observed for combination of 80 µl Gallic acid and 16 µl of Shikonin. So, this combination of gallic acid and shikonin could be effective for the HNSC cancer treatment. Our studies showed a multifaceted, multi-dimensional tumor regression by altering autophagy, apoptosis, inhibiting cell proliferation, angiogenesis, metastasis and inflammatory cytokines production. Thus, the study has helped develop a unique combination of natural compounds that will markedly reduce the propensity of development of drug resistance in tumors and immune evasion by the tumors. This study is crucial to developing a combinatorial natural therapeutic cocktail with accentuated immunotherapeutic potential.

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Rhee, Younghwa. "Efficacy of losartan and growth hormone combinatorial therapy in DyW mice". Thesis, 2015. https://hdl.handle.net/2144/16344.

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Merosin-deficient CMD type 1A (MDC1A) is the second most common form of congenital muscular dystrophy (CMD) that presents at or near birth. MDC1A is caused by a mutation in the LAMA2 gene which encodes a protein called laminin-2. The clinical manifestations of MDC1A include profound muscle weakness, muscle hypotonia, loss of independent ambulation, and respiratory failure. There is still no cure or effective treatment available for MDC1A patients. In this study we use the Lama2dyW (DyW) mouse model which shares analogous phenotypes with the MDC1A disease in humans. To this point, therapy development has mainly utilized single-mode therapy. While effective in attenuating some aspects of pathology, no single treatment has been able to completely ameliorate the multi-faceted pathology of laminin-2 deficiency. Therefore this study utilizes a combinatorial treatment strategy with Losartan and Growth Hormone to target multiple pathologies simultaneously. Losartan, an angiotensin II type 1 (AT1) receptor antagonist, is commonly used in hypertensive patients for its abilities to induce vasodilation. In the context of dystrophy, blocking AT1 receptor with losartan inhibits AT1-mediated TGF- signaling leading to decreased fibrosis, normalized muscle architecture, and improved muscle function and regeneration. Losartan does not, however, induce weight gain in models of muscular dystrophy. Growth hormone (GH) is well known to stimulate postnatal skeletal muscle growth as well as overall body weight mainly through Insulin-like Growth Factor 1 (IGF-1). IGF-1 induces muscle growth via Akt-mediated mTOR activation leading to increases in protein synthesis and consequent muscle fiber hypertrophy. Thus we hypothesize that the combination of Losartan and GH would alleviates chronic inflammation and fibrosis as well as induce weight/muscle gain in DyW mice. Dual treatment led to significant gains in total body weight as well as muscle function. In addition to the improvements of weights and activities, dual-treated mice showed a more normalized distribution of fiber size without increased total fiber number suggesting that dual treatment led to muscle hypertrophy not seen in untreated or Losartan-treated DyW mice. Myogenesis associated genes, and specifically late markers of myogenic differentiation were also significantly upregulated in dual-treated mice indicating a more complete and robust myogenic repair compared to untreated and Losartan-treated DyW mice, respectively. Dual treatment also led to increased expression of IGF-1 and IGF-1R as well as the glucose transporter glut4 suggesting that this strategy also affects insulin signaling. This study suggests that a combinatorial anti-fibrotic and pro-myogenic therapy achieves a more comprehensive amelioration of downstream pathologies greater than single-mode therapies and may be a more suitable treatment regimen for complex pathologies such as MDC1A.

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JAIN, SHALEEN. "PREPARATION OF TUMOR TARGETING COMBINATORIAL THERAPY USING NANOPARTICLE CONJUGATED NATURAL COMPOUNDS". Thesis, 2020. http://dspace.dtu.ac.in:8080/jspui/handle/repository/18150.

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Cancer, a multifactorial disease, caused by several genetic and environmental factors and their interactions in which normal cells become progressively transformed to malignant cells, is currently the most studied topic. Numerous receptors and pathways have been identified for cancer that play a crucial role in its progression. Natural compounds obtained from various medicinal plants have shown a promising potential in targeting cancer in multiple ways. In the present project we are exploring the design of a combinatorial cancer therapy. At first, different bioactive compounds were screened using literature reviews and researches conducted previously and molecular docking simulations were performed against different receptors involved in cancer associated pathways, particularly breast cancer as India’s most prevalent cancer. In this project, AutoDock was used for molecular docking and later, PyMol 2.3.2 was used for identifying the binding amino acid residues of ligands against targeting receptors. From the results conducted, the binding energies were assessed and it is hereby proposed that, combination of Withferin A, Curcumin, Rutin and Selicib shows highest binding energies against selected key receptors in breast cancer, which can be further explored for combinatorial efficacy. Furthermore, for effective drug delivery, BSA nanoparticles were designed using desolvation process in which the effective size was found to be 160nm with a charge of -100mV. Thus this project holds significant implications for the development of combinatorial therapy using natural compounds and designing new protocols for their in-vivo delivery using nanoparticles, which eventually may have exciting potential for applicability in various cancers.

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Bao, Xuhui. "Immunotoxin Monotherapy and Combinatorial Therapy With Immune Checkpoint Inhibitors for Malignant Brain Tumors". Diss., 2016. http://hdl.handle.net/10161/13365.

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Glioblastoma 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

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Książki na temat "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.

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1966-, Seeberger Peter H., red. Solid support oligosaccharide synthesis and combinatorial carbohydrate libraries. New York: Wiley, 2001.

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Ganai, Shabir Ahmad. Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy. Springer Singapore Pte. Limited, 2021.

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Ganai, Shabir Ahmad. Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy. Springer Singapore Pte. Limited, 2020.

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Andersson, Patrik, i Christian Ostheimer, red. 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.

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Atta-ur-Rahman i M. Iqbal Choudhary, red. Frontiers in Cardiovascular Drug Discovery: Volume 4. BENTHAM SCIENCE PUBLISHERS, 2019. http://dx.doi.org/10.2174/97816810839951180401.

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Frontiers in Cardiovascular Drug Discovery is an eBook series devoted to publishing the latest advances in cardiovascular drug design and discovery. Each volume brings reviews on the biochemistry, in-silico drug design, combinatorial chemistry, high-throughput screening, drug targets, recent important patents, and structure-activity relationships of molecules used in cardiovascular therapy. The eBook series should prove to be of great interest to all medicinal chemists and pharmaceutical scientists involved in preclinical and clinical research in cardiology. The fourth volume of the series covers the following topics: -Aspirin administration -Adenosine receptor targeting for cardiovascular therapy -Drug treatment of patients with coronary stenting -Immunosuppressive drugs in heart transplantation -PCSK9 inhibition for lowering LDL-C levels.

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Kahn, Michael. High Throughput Screening for Novel Anti-Inflammatories (Progress in Inflammation Research). Birkhauser, 2000.

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Części książek na temat "COMBINATORIAL THERAPY"

Dalasanur Nagaprashantha, Lokesh. "Combinatorial Cancer Therapy". W Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7158-7.

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Nagaprashantha, Lokesh Dalasanur. "Combinatorial Cancer Therapy". W Encyclopedia of Cancer, 1180–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_7158.

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Winbanks, Catherine E., i Paul Gregorevic. "Combinatorial Gene Therapy Strategies for Treating Muscular Dystrophies". W Muscle Gene Therapy, 117–39. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1207-7_8.

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Rothenberg, S. Michael, Joan Fisher, David Zapol, David Anderson, Yasumichi Hitoshi, Philip Achacoso i Gany P. Nolan. "Intracellular Combinatorial Chemistry with Peptides in Selection of Caspase-like Inhibitors". W Gene Therapy, 171–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72160-1_18.

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Banerjee, Ena Ray. "Novel Combinatorial Probiotics in Therapy and Prophylaxis". W 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.

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Mangla, Bharti, Pankaj Kumar, Kamya Goyal, Kanchan Kohli i Shammy Jindal. "Breast Cancer Therapy by Combinatorial Herbo-Synthetic Nanocarrier". W 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.

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Ganai, Shabir Ahmad. "Overview of Epigenetic Signatures and Their Regulation by Epigenetic Modification Enzymes". W 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.

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Ganai, Shabir Ahmad. "Combining Histone Deacetylase Inhibitors with Other Anticancer Agents as a Novel Strategy for Circumventing Limited Therapeutic Efficacy and Mitigating Toxicity". W 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.

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Ganai, Shabir Ahmad. "Futuristic Approaches Towards Designing of Isozyme-Selective Histone Deacetylase Inhibitors Against Zinc-Dependent Histone Deacetylases". W 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.

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Ganai, Shabir Ahmad. "Epigenetic Regulator Enzymes and Their Implications in Distinct Malignancies". W 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.

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Streszczenia konferencji na temat "COMBINATORIAL THERAPY"

Amiji, Mansoor M. "Multifunctional combinatorial-designed nanoparticles for nucleic acid therapy". W SPIE Defense + Security, redaktorzy Thomas George, Achyut K. Dutta i M. Saif Islam. SPIE, 2016. http://dx.doi.org/10.1117/12.2224764.

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Lam, Kit S., i Ruiwu Liu. "From Combinatorial Chemistry to Nanotechnology to Cancer Therapy". W The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.014.

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Wang, Yangyang, Shalin S. Patel, Juan Cong, Nan Zhang, Yuan Qi, Francesco Sabbatino, Steven Isakoff, Albert B. DeLeo, Soldano Ferrone i Xinhui Wang. "Abstract 3639: Combinatorial therapy for triple negative breast cancer". W 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.

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Nguyen, J. P., M. Bianca, R. D. Huff, N. Tiessen, Y. Kim, V. Hou, M. Heller, M. D. Inman i J. A. Hirota. "Development of a Novel Combinatorial Therapy for Cystic Fibrosis". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2580.

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Lam, Kit S. "From Combinatorial Chemistry to Nanocarriers for Cancer Therapy and Imaging". W Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/acp.2012.as3e.4.

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Srivastava, Jyoti, Devaraja Rajasekaran, Ayesha Siddiq, Rachel Gredler, Chadia L. Robertson, Maaged A. Akiel, Xue-Ning Shen i in. "Abstract 5400: A novel combinatorial therapy for hepatocellular carcinoma (HCC)". W 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.

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Bölükbas, Deniz Ali, Stefan Datz, Charlotte Meyer-Schwickerath, Malamati Vreka, Sabine van Rijt, Oliver Eickelberg, Georgios Stathopoulos, Thomas Bein i Silke Meiners. "Combinatorial delivery of targeted mesoporous silica nanoparticles for lung cancer therapy". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2841.

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Binder, Zev A., Yibo Yin, Radhika Thokala i Donald M. O'Rourke. "Abstract LB-340: Combinatorial platform for CART cell therapy for glioblastoma". W 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.

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Chakraborty, Sanjukta, Rachana R. Maniyar, Sina Dadafarin, Ghada Ben Rahoma, Sarnath Singh, Augustine Moscatello, Jan Geliebter i Raj K. Tiwari. "Abstract 3237: Combinatorial immune checkpoint inhibitor therapy in anaplastic thyroid cancer". W 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.

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Raporty organizacyjne na temat "COMBINATORIAL THERAPY"

Baia, Gilson S. Combinatorial Therapy Approaches for NF2-Deficient Meningiomas. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2012. http://dx.doi.org/10.21236/ada567130.

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Baia, Gilson S. Combinatorial Therapy Approaches for NF2-Deficient Meningiomas. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2013. http://dx.doi.org/10.21236/ada584501.

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