Готові списки джерел за темами / Target therapies

Добірка наукової літератури з теми "Target therapies"

Автор: Grafiati
Опубліковано: 28 січня 2023

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Зміст

  1. Статті в журналах
  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій
  6. Звіти організацій

Статті в журналах з теми "Target therapies":

1

Lazzari, Ludovico, Marcella De Paolis, Daniella Bovelli, and Enrico Boschetti. "Target therapies-induced Cardiotoxicity." European Oncology & Haematology 09, no. 01 (2013): 56. http://dx.doi.org/10.17925/eoh.2013.09.1.56.

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2

&NA;. "Rheumatoid arthritis therapies target TNF." Inpharma Weekly &NA;, no. 1173 (February 1999): 2. http://dx.doi.org/10.2165/00128413-199911730-00002.

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3

Bearz, A., M. Berretta, A. Lleshi, and U. Tirelli. "Target Therapies in Lung Cancer." Journal of Biomedicine and Biotechnology 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/921231.

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Targeting intracellular signaling molecules is an attractive approach for treatment of malignancies. In particular lung cancer has reached a plateau regarding overall survival, and target therapies could offer the possibility to improve patients' outcome beyond cytotoxic activity. The goal for target therapies is to identify agents that target tumor-specific molecules, thus sparing normal tissues; those molecules are called biomarkers, and their identification is recommended because it has a predictive value, for example, provides information on outcome with regard to a specific treatment. The increased specificity should lead to decreased toxicity and better activity. Herein we provide an update of the main target therapies in development or already available for the treatment of nonsmall cell lung cancer.
4

Silvestris, Nicola, Antonio Gnoni, Anna Brunetti, Leonardo Vincenti, Daniele Santini, Giuseppe Tonini, Francesca Merchionne, et al. "Target Therapies in Pancreatic Carcinoma." Current Medicinal Chemistry 21, no. 8 (February 2014): 948–65. http://dx.doi.org/10.2174/09298673113209990238.

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5

Hampton, Tracy. "Novel Therapies Target Myasthenia Gravis." JAMA 298, no. 2 (July 11, 2007): 163. http://dx.doi.org/10.1001/jama.298.2.163.

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6

Meijer, G. A., and J. J. Oudejans. "Targeted Therapies; Who Detects the Target?" Analytical Cellular Pathology 27, no. 3 (January 1, 2005): 165–67. http://dx.doi.org/10.1155/2005/235650.

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7

Wakabayashi, Hiroshi. "Molecular target therapies in rheumatic diseases." Okayama Igakkai Zasshi (Journal of Okayama Medical Association) 126, no. 3 (2014): 227–30. http://dx.doi.org/10.4044/joma.126.227.

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8

Robson, Andrew. "Three different therapies to target PCSK9." Nature Reviews Cardiology 18, no. 8 (June 4, 2021): 541. http://dx.doi.org/10.1038/s41569-021-00581-w.

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9

Hirsch, Etienne. "Parkinson's disease: A target for therapies?" Journal of the Neurological Sciences 429 (October 2021): 118011. http://dx.doi.org/10.1016/j.jns.2021.118011.

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10

Gillis, David. "Two Novel Therapies Target Cellular Microenvironment." Oncology Times 24, no. 2 (February 2002): 38. http://dx.doi.org/10.1097/01.cot.0000294265.17109.36.

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Більше джерел
Також вас можуть зацікавити розширені добірки на тему "Target therapies" для конкретних типів джерел:
Статті в журналах Дисертації Книги

Дисертації з теми "Target therapies":

1

Holt, Sandra. "Fatty acid amide hydrolase - A target for anti-inflammatory therapies?" Doctoral thesis, Umeå universitet, Farmakologi, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-504.

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Anti-inflammatory drugs are a widely used class of therapeutic agents, but the use of non-steroidal anti-inflammatory drugs (NSAID) is hampered by their gastrointestinal side-effects. Recent reports that cyclooxygenase-2 inhibitors may cause cardiovascular events underline the importance of identifying new therapeutic strategies for the treatment of inflammation. One such target could be agents modifying the endogenous cannabinoid (endocannabinoid) system, since there is evidence that this system plays a role in our natural defence against inflammation. The levels of the endocannabinoid anandamide (arachidonoyl ethanolamide, AEA) are low under normal conditions, and stand under strict regulatory control of synthesising and degrading enzymes. Fatty acid amide hydrolase (FAAH) is the main enzyme degrading AEA, hydrolysing it to ethanolamine and arachidonic acid. The focus of this thesis lies in exploring the pharmacology of FAAH to evaluate its possibilities as a target for new anti-inflammatory drugs. In Papers I and II, the effects of the ambient pH on the properties of FAAH were investigated, since tissue pH is known to decrease under inflammatory conditions. In homogenates, it was found that the activity of FAAH decreased as the assay pH was decreased, consistent with the known pH profile of the enzyme. More importantly, the sensitivity of the enzyme to inhibition by FAAH inhibitors changed. In particular, the sensitivity of the enzyme to inhibition by the NSAID ibuprofen increased seventeen-fold as the assay pH decreased from 8.37 to 5.28. A similar pattern was found using intact C6 glioma cells when the extracellular, but not the intracellular pH was reduced. Thus, at an extracellular pH value of 6.2, (R)-ibuprofen, (S)-flurbiprofen and (R,S)-flurbiprofen inhibited the metabolism of AEA with IC50 values of 26, 14 and 15 µM, respectively. These values are in theory reachable upon normal dosing of the compounds. In Paper III, the effect of the selective FAAH inhibitor URB597 and the NSAID indomethacin were investigated in vivo upon the oedema response to carrageenan administration in the paw of anaesthetised mice. Both compounds reduced the oedema in a manner completely blocked by the CB2 receptor antagonist SR144528. In Paper IV, the effect of inflammation upon endocannabinoid synthesis was investigated in mice. Lipopolysaccharide-induced pulmonary inflammation was found not to affect the release of AEA to any obvious extent, and did not change the activities of the AEA synthesising enzymes N-acyl transferase or N-acyl phosphatidylethanolamine phospholipase D, or of FAAH in lung tissue. The results of this thesis would suggest that FAAH inhibitors can produce anti-inflammatory effects, and that the endocannabinoid system contributes to the actions of the NSAID indomethacin in the carrageenan model of inflammation, but that an increased endocannabinoid synthesis (a prerequisite for FAAH inhibition as a therapeutic strategy) is not an obligatory response to an inflammatory stimulus.
2

Di, Stefano Anna Luisa. "Molecular markers of gliomas : implications for diagnosis and new target therapies." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066015.

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Le travail de thèse est dédié à la caractérisation de fusions spécifiques oncogéniques entre les gènes FGFR et TACC dans les gliomes. Nous avons analysé 907 gliomes pour la présence du gène de fusion FGFR3-TACC3. Nous avons montré que les fusions FGFR3-TACC3 ne touchent que les gliomes IDH wild-type (3%), sont mutuellement exclusives avec l'amplification de EGFR et avec la forme tronquée EGFRvIII et inversement, sont associées à l'amplification de CDK4 et de MDM2 et à la délétion du 10q. Les fusions FGFR3-TACC3 sont associées à une expression intense et diffuse de FGFR3 en immunohistochimie (IHC) et l'IHC pour FGFR3 est un marqueur prédictif très sensible de la présence des fusions FGFR3-TACC3. Les patients porteurs d'une fusion FGFR3-TACC3 ont une survie globale significativement plus longue comparés aux patients avec gliome IDH wild-type. Nous avons traité deux patients porteurs d'un gène de fusion FGFR3-TACC3 avec un inhibiteur tyrosine-kinase (TK) spécifique pour FGFR et nous avons observé une stabilisation de maladie et une réponse mineur chez un patient. Dans la deuxième section nous avons optimisé une nouvelle séquence de spectroscopie différentielle-MEGA-PRESS-pour la détection de l'oncometabolite 2-hydroxyglutarate (2 HG) qui s'accumule de manière spécifique dans les gliomes IDH mutés. Nous avons analysé de façon prospective une cohorte de 25 patients avant chirurgie pour probable gliome de grade II et grade III. Nous avons trouvé que la MEGA-PRESS est hautement spécifique (100%) et sensible (80%) dans la prédiction de la présence de la mutation IDH. Son taux est corrélé aux concentrations de 2 HG mesurés sur tissu congelé par spectrométrie de masse (GC-MS/MS)
This work is devoted to the characterization of a specific oncogenic fusion between FGFR and TACC genes in gliomas. Overall, we screened 907 gliomas for FGFR3-TACC3 fusions. We found that FGFR3-TACC3 fusions exclusively affect IDH wild-type gliomas (3%), and are mutually exclusive with the EGFR amplification and the EGFR vIII variant, whereas it co-occurs with CDK4 amplification, MDM2 amplification and 10q loss. FGFR3–TACC3 fusions were associated with strong and homogeneous FGFR3 immunostaining. We show that FGFR3 immunostaining is a sensitive predictor of the presence of FGFR3-TACC3 fusions. FGFR3-TACC3 glioma patients had a longer overall survival than those patients with IDH wild-type glioma. We treated two patients with FGFR3–TACC3 rearrangements with a specific FGFR-TK inhibitor and we observed a clinical improvement in both and a minor response in one patient. In the second section, we developed a non-invasive diagnostic tool by 1H-magnetic resonance spectroscopy in IDH mutant gliomas. We optimized a uniquely different spectroscopy sequence called MEGA-PRESS for the detection of the oncometabolite 2-hydroxyglutarate (2 HG) that specifically accumulates in IDH mutant gliomas. We analysed a prospective cohort of 25 patients before surgery for suspected grade II and grade III gliomas and we assessed specificity and sensitivity, correlation with 2 HG concentrations in the tumor and associations with grade and genomic background. We found that MEGA-PRESS is highly specific (100%) and sensitive (80%) for the prediction of IDH mutation and correlated with 2 HG levels measured by gas chromatography-tandem mass spectrometry (GC-MS/MS) in frozen tissue
3

Han, Yanyan. "Functional characterization of FMNL1 as potential target for novel anti-tumor therapies." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-112968.

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4

Zincke, Fabian. "Biomarker based therapies in high risk cancer patients - MACC1 as molecular target." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21021.

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Das metastasierende kolorektale Karzinom stellt eine große Herausforderung in der Krebstherapie dar. Verlässliche und effiziente Biomarker zur Prognose des Krankheitsverlaufes oder der Therapieantwort (Prädiktion) sind rar. Metastasis-associated in colon cancer 1 (MACC1) ist ein prognostischer, prädiktiver und kausaler Biomarker für verschiedene Tumorentitäten. Durch die Induzierung von Zielgenen, wie z.B. MET, beeinflusst es Signalwege wie MEK/ERK und AKT/β-catenin und fördert so Zellproliferation und -motilität sowie Tumorprogression und Metastasierung in vivo. Diese Arbeit sollte neue Strategien erforschen diese Prozesse durch die Inhibition von MACC1 auf Transkriptions- und Signaltransduktionsebene zu unterbinden. Mit zwei verschiedenen Screeningmethoden konnten wir Statine als potente transkriptionelle Inhibitoren von MACC1 als auch phosphotyrosin (pY)-abhängige Interaktionen von MACC1 mit essentiellen Signalmolekülen identifizieren: SHP2, GRB2, SHC1, PLCG1 und STAT5B. Statine verringerten MACC1-spezifische Proliferation und Koloniebildung in vitro als auch Tumor Wachstum und Metastasierung in vivo bei Dosen äquivalent der humanen Standardtherapie zur Blutlipidsenkung. Mutation der pY-Bindungsstellen reduzierte die Aktivität des MACC1-induzierten ERK Signalwegs sowie Zellmigration und -proliferation. Anhand unserer Daten orchestriert MACC1, abhängig von MET und EGFR, neue SHP2/SRC/ERK und PKA/SRC/CREB Signalkaskaden zu einem malignen Phänotyp. Gezielte Intervention restringierte die MACC1-abhängige Koloniebildung, was neue therapeutische Interventionspunkte identifiziert und eine hervorragende Basis für Untersuchungen zur Kombinationstherapie darstellt. Die weitere Erforschung der spatiotemporalen Organisation des MACC1 Signalosoms und assoziierter Signalkaskaden soll das volle therapeutische Potential von MACC1 ausschöpfen. Wir empfehlen zudem Statine in der Krebstherapie bzw. -prävention, besonders bei MACC1-stratifzierten Patienten, anzuwenden.
Metastatic colorectal cancer still represents a major challenge in therapy. Reliable and efficient biomarkers for early prognosis of disease course or treatment response (prediction) remain scarce. Metastasis-associated in colon cancer 1 (MACC1) has been established as prognostic, predictive and causal biomarker for several tumor entities. Its induction of target genes such as MET affects several signaling pathways including MEK/ERK and AKT/β-catenin. Thus, it promotes cellular proliferation and motility as well as tumor progression and metastasis formation in vivo. This study intended to explore new strategies to inhibit these processes by targeting MACC1 on transcriptional and signaling level. By two distinct screening methods, we identified statins as potent MACC1 transcriptional inhibitors as well as phosphotyrosine (pY)-dependent interactions of MACC1 with crucial signaling molecules: SHP2, GRB2, SHC1, PLCG1 and STAT5B. Statins showed MACC1-specific reduction of proliferation and colony formation in vitro as well as restriction of tumor growth and metastasis formation in vivo at doses equivalent to human standard lipid reduction therapy. Mutation of the pY-interaction sites abrogated MACC1-dependent ERK signaling as well as cell migration and proliferation. Our data further suggest that MACC1 governs SHP2/SRC/ERK and PKA/SRC/CREB axes conferring a malignant phenotype in response to MET and EGFR. Targeted intervention restricted MACC1-dependent colony formation which indicates new drug intervention points for MACC1 signaling and provides an excellent baseline for further investigations of combinatorial treatments. Additional research about the spatiotemporal organization of MACC1 signalosome formation and downstream signaling will reveal the entire potential of MACC1 as therapeutic target, whereas statins should already be considered for cancer therapy or prevention, especially in patients stratified for MACC1 expression.
5

Kyle, Fiona. "LRH-1 as a target for the development of new breast cancer therapies." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/55285.

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Estrogen drives the growth and development of estrogen receptor alpha (ERα) positive breast cancer and ERα is the target for hormonal therapies that inhibit its activity. A substantial proportion of patients become resistant to these therapies, demonstrating a need for new therapies. Gene expression microarray studies have been performed with a view to identifying potential novel therapeutic targets, biomarkers or forming the basis of identifying a molecular signature for endocrine resistance. These studies have identified candidate genes whose expression is altered in models of endocrine resistance. Investigation of the molecular pathways particularly highlights cell survival and regulation of apoptosis and indicates that these pathways play a key role in the development of resistance. Microarray analysis also identified the liver receptor homolog 1 (LRH-1, NR5A2), a member of the nuclear receptor superfamily of transcription factors, as an estrogen regulated gene in MCF7 cells. Functional analysis showed that LRH-1 regulates breast cancer cell growth, acting in part by regulating ERα expression. Gene expression profiling of MCF-7 cells following RNAi for LRH-1 identified LRH-1 regulated genes. LRH-1 is known to regulate expression of CYP19A1 (aromatase), responsible for estrogen biosynthesis through the aromatisation of aromatase. Together, our findings identify LRH-1 as a potential therapeutic target for breast cancer treatment. Results of screening for small molecule inhibitors of LRH-1 will be presented, together with analysis of gene expression profiling for LRH-1 regulated genes.
6

Cunniff, Brian. "Mitochondrial structure and function as a therapeutic target in malignant mesothelioma." ScholarWorks @ UVM, 2014. http://scholarworks.uvm.edu/graddis/249.

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Malignant mesothelioma (MM) is a rare tumor associated with occupational exposure to asbestos with no effective treatment regime. Evaluation of mitochondrial function in human MM cell lines revealed a common tumor phenotype: in comparison to immortalized or primary human mesothelial cells, MM tumor cells displayed a more oxidized mitochondrial environment, increased expression of mitochondrial antioxidant enzymes, and altered mitochondrial metabolism. Earlier work by our laboratory indicated that increases in mitochondrial reactive oxygen species (mROS) in MM cell lines supports expression of FOXM1, an oncogenic transcription factor that contributes to increased cell proliferation and chemoresistance. These studies sought to investigate targeting of mitochondrial structure and function as a therapeutic avenue in MM. MM cells have reduced mitochondrial reserve capacity, a redox vulnerability exploitable by pro-oxidant therapeutics. Targeting of the mitochondrial peroxidase peroxiredoxin 3 (PRX3) with the anti-cancer compound thiostrepton (TS) induces irreversible modifications to PRX3 protein, increased mROS, and selective MM cell death. Mass spectrometry showed TS targets conserved cysteine residues in PRX3. In vitro and in MM cells, TS failed to modify human PRX3 harboring mutations to Cys108, Cys127 or Cys229. Pre-incubation of MM cells with dimedone blocked cysteine adduction of PRX3 by TS, suggesting adduction requires an active PRX3 catalytic cycle. Studies with immortalized and primary human mesothelial cells showed adduction of PRX3 by TS occurred at a much lower rate in normal cells than MM cells, and this difference correlated with markedly decreased cytotoxicity. Moreover, MM cells transduced with shRNA to PRX3 grew more slowly and were less sensitive to TS than their wild type counterparts, indicating PRX3 is a major target of TS in MM cells. Studies with a xenoplant mouse model of MM showed TS alone or in combination with the TRX2 inhibitor gentian violet significantly reduced tumor volume. Tumor cell mitochondria have an increased mitochondrial membrane potential, therefore numerous drugs have been developed that selectively accumulatte into energized mitochondria to enhance drug efficacy and specificity. Here two mitochondrial-targeted nitroxides, Mito-carboxy-proxyl (MCP) and Mito-TEMPOL (MT), were investigated for their anti-cancer effects. Treatment of MM cells with MCP or MT led to rapid disruption of the mitochondrial reticulum, increased oxidant levels, and reduced FOXM1 and PRX3 protein expression. Immunostaining revealed a pool of cytoplasmic FOXM1 associated with PRX3 in mitochondria, suggesting PRX3 participates in regulating FOXM1 expression. Combination of MCP or MT with TS led to synergistic effects on MM cell viability. Upregulation of mitochondrial antioxidant enzymes is an adaptive response that ameliorates mitochondrial oxidative stress and supports tumor cell survival. Studies here indicate that enhanced dependency on the PRX3 catalytic cycle in tumor cells promotes inactivation of PRX3 by TS, providing a therapeutic window dependent on a mitochondrial phenotype common to many human tumor types. Therefore TS, alone or in combination with other agents, may prove useful in the management of intractable tumors such as MM.
7

Ruscito, Ilary [Verfasser]. "Harnessing tumor angiogenesis to explore ovarian cancer immune suppression and address target-therapies outcomes / Ilary Ruscito." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1235400476/34.

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8

Semenchenko, Kostyantyn. "Development of tumour therapies : from target validation of TTLL12 to tests of a small molecule XRP44X in pre-clinical models of cancer." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ107.

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Les modifications post-traductionnelles de la tubuline sont des cibles attrayantes pour la thérapie du cancer. TTLL12 est impliqué dans la détyrosination de la tubuline, la triméthylation de l’histone H4K20 et le cancer de la prostate. La thèse porte sur les effets de la surexpression de TTLL12 sur ces modifications à différents stades du cycle cellulaire et sur la sensibilité à des agents ciblant les microtubules. Les résultats montrent que TTLL12 affecte ces modifications indépendant du cycle cellulaire et réduit la sensibilité des cellules à paclitaxel. XRP44X est un nouvel inhibiteur de la signalisation Ras-ERK-Elk3. Ses propriétés antitumorigène ont été montré in vitro et dans certaines études in vivo. Le projet de thèse était une continuation des études pré-cliniques sur XRP44X dans des modèles de cancer de la prostate de souris. Les résultats montrent que XRP44X est un inhibiteur efficace de la tumorigenèse et des métastases, ce qui peut être dû à son effet sur Elk3
Tubulin posttranslational modifications are an attractive target for cancer therapy. TTLL12 isinvolved in tubulin detyrosination, histone H4K20 trimethylation and prostate cancer. The thesis addresses the effects of TTLL12 overexpression on these tubulin and histone modifications at different stages of the cell cycle and on sensitivity to microtubule-targeting agents. The results show that TTLL12 over expression affects tubulin detyrosination and H4K20 trimethylation independently of cell cycle phase and reduces cell sensitivity totaxanes.XRP44X is a novel inhibitor of Ras-ERK1/2-Elk3 signalling and tubulin-binding agent. Itsantitumorigenic properties had been shown in vitro and in initial in vivo studies. The thesis project was a continuation of pre-clinical studies on XRP44X in mouse prostate cancer models. The results show that XRP44X is an effective inhibitor of tumorigenesis and metastasis in prostate cancer, which may be due to its effect on Elk3
9

Zincke, Fabian [Verfasser], Ulrike [Gutachter] Stein, Edda [Gutachter] Klipp, and Stephan Michael [Gutachter] Feller. "Biomarker based therapies in high risk cancer patients - MACC1 as molecular target / Fabian Zincke ; Gutachter: Ulrike Stein, Edda Klipp, Stephan Michael Feller." Berlin : Humboldt-Universität zu Berlin, 2020. http://d-nb.info/1202775608/34.

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10

Trouvilliez, Sarah. "Caractérisation des interactions entre TrkA, CD44 et les molécules de leur signalisation dans les cancers du sein triple négatifs." Thesis, Université de Lille (2022-....), 2022. http://www.theses.fr/2022ULILS104.

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Le cancer du sein est la tumeur maligne la plus fréquente chez les femmes dans le monde (OMS). Le cancer du sein est une maladie hétérogène et le pronostic varie en fonction des caractéristiques moléculaires. En particulier, la prise en charge des cancers du sein triple négatifs (TNBC) reste un défi clinique en raison de l'absence de thérapie spécifique et efficace. Dans ce contexte, notre équipe a mis en évidence le rôle de TrkA dans les TNBC. Plus précisément, les travaux du Pr. Toillon montrent qu'il agit non seulement via sa phosphorylation mais aussi par le biais de plateforme de récepteurs membranaires. En particulier, le NGF induit une interaction de TrkA avec la glycoprotéine CD44. Le complexe TrkA/CD44 active une signalisation indépendante du phosphorylation de TrkA impliquée dans la résistance des inhibiteurs de la phosphorylation de TrkA. Afin de cibler ce mécanisme de résistance, les interactions entre TrkA, CD44 et leurs partenaires de signalisation ont été étudiées. Tout d'abord, j'ai déterminé que le complexe TrkA/CD44 implique uniquement le variant 3 de CD44. En déterminant les motifs moléculaires impliqués, un peptide bloquant l'association TrkA/CD44v3 a été synthétisé et un mutant H112A de TrkA. J’ai ainsi confirmé l'importance des acides aminés de CD44v3 (IDDDEDFISST) et de l'acide aminé H112 de TrkA dans cette interaction. De façon intéressante, ce peptide bloquant réduit la croissance tumorale et la métastase. De plus nous avons montré que l'inhibition de CD44 n'affecte pas la liaison d’une des molécules de la signalisation de TrkA/CD44. Nous avons décrypté ensuite décrypté l’interaction TrkA/molécule de la signalisation et montré qu’un inhibiteur de cette interaction bloque la migration de cellules cancèreuses triples négatives. En conclusion, nos études ont révélé le rôle des interactions TrkA/CD44/molécules de leur signalisation dans l'agressivité des cancers du sein et la résistance des inhibiteurs de TrkA. Ceci suggère que si les inhibiteurs de la phosphorylation de TrkA actuels ne sont pas efficaces dans le TNBC, de nouveaux inhibiteurs perturbant la signalisation TrkA/CD44 pourraient être de nouvelles stratégies thérapeutiques efficaces
Breast cancer is the most common malignancy in women worldwide (WHO). Breast cancer is a heterogeneous disease and prognosis varies according to molecular characteristics. In particular, the management of triple-negative breast cancer (TNBC) remains a clinical challenge due to the lack of specific and effective therapy. In this context, our team has highlighted the role of TrkA in TNBC. More precisely, the work of Prof. Toillon shows that TrkA acts not only via its phosphorylation but also via the membrane receptor platform. In particular, NGF induces an interaction of TrkA with the glycoprotein CD44. The TrkA/CD44 complex activates a TrkA phospho-ndependent signaling involved in the resistance of TrkA inhibitors. To target this resistance mechanism, the interactions between TrkA, CD44 and their signaling partners were investigated. First, I determined that the TrkA/CD44 complex involves only CD44 variant 3. By determining the molecular motifs involved, a peptide blocking the TrkA/CD44v3 association was synthesized and an H112A mutant of TrkA. I thus confirmed the importance of the amino acids of CD44v3 (IDDDEDFISST) and of the amino acid H112 on TrkA in this interaction. Interestingly, this blocking peptide reduces tumor growth and metastasis. Furthermore, we showed that CD44 inhibition does not affect the binding of one of TrkA/CD44 signaling partners. We then deciphered the TrkA/signaling molecule interaction and showed that an inhibitor of this interaction blocks the migration of triple negative cancer cells. In conclusion, our studies revealed the role of TrkA/CD44/signaling molecule interactions in breast cancer aggressiveness and resistance to TrkA inhibitors. It suggests that if current TrkA inhibitors are not effective in TNBC, novel inhibitors disrupting TrkA/CD44 signaling could be a new therapeutic option
Більше джерел

Книги з теми "Target therapies":

1

Dzau, Victor J., and Gabor M. Rubanyi. The endothelium in clinical practice: Source and target of novel therapies. New York: M. Dekker, 1997.

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2

Albert, Jeffrey S., and Michael W. Wood. Targets and emerging therapies for schizophrenia. Hoboken (New Jersey), USA: John Wiley & Sons, 2012.

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3

Albert, Jeffrey S., and Michael W. Wood, eds. Targets and Emerging Therapies for Schizophrenia. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118309421.

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4

Los, Marek, and Spencer B. Gibson, eds. Apoptotic Pathways as Targets for Novel Therapies in Cancer and Other Diseases. New York: Springer-Verlag, 2005. http://dx.doi.org/10.1007/b102187.

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Falk Symposium (131st 2002 Freiburg im Breisgau, Germany). Targets of treatment in chronic inflammatory bowel diseases: Proceedings of Falk Symposium 131 (part II of the Gastroenterology Week, Freiburg, Germany, October 6-8, 2002). Dordrecht: Kluwer Academic, 2003.

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6

Hillis, Argye E., and Jean-Claude Baron, eds. The Ischemic Penumbra: Still the Target for Stroke Therapies? Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-635-7.

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7

Corporation, Market Intelligence Research, and Frost & Sullivan., eds. Autoimmune disease: Therapeutic markets : new therapies target causes, not symptoms. Mountain View, CA: Market Intelligence, 1992.

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8

Drouin-Ouellet, Janelle, and Roger A. Barker. Disease-Modifying Therapies in Neurodegenerative Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0016.

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The recent identification of the genetic basis of many neurodegenerative disorders (NDDs), coupled with a greater understanding of their pathophysiology, has enabled better therapeutic strategies to be identified and tried. This includes approaches that target critical specific nodes in the disease pathways, for example, agents that modulate levels of mutant huntingtin in Huntington’s disease. In addition to these highly specific targeted therapies, there is also a growing realization that more generic lifestyle therapies influencing whole brain health may also have merit in treating these conditions-such as diet and exercise. This chapter explores the different approaches and agents used to try to modify the course of a range of NDDs, and highlights their progress relative to the clinic and the patients suffering with these currently incurable conditions.
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Freeman, Charlene. Oral Medication and Insulin Therapies: A Practical Guide for Reaching Diabetes Target Goals. PESI HealthCare, 2003.

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10

Freeman, Charlene. Diabetes : A Practical Guide for Reaching Diabetes Target Goals: Oral Medication and Insulin Therapies. PESI, 2013.

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Частини книг з теми "Target therapies":

1

Kefas, Benjamin, and Benjamin W. Purow. "microRNA: A Potential Therapy Able to Target Multiple Cancer Pathways." In Targeted Therapies, 155–70. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-478-4_9.

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Cortot, Alexis B., and Pasi A. Jänne. "Resistance to Targeted Therapies As a Result of Mutation(s) in the Target." In Targeted Therapies, 1–31. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-478-4_1.

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Wang, Haichao, Wei Li, Richard Goldstein, Kevin J. Tracey, and Andrew E. Sama. "HMGB1 as a Potential Therapeutic Target." In Sepsis: New Insights, New Therapies, 73–91. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470059593.ch6.

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Myall, Nathaniel J., and Sukhmani K. Padda. "BRAF: Novel Therapies for an Emerging Target." In Targeted Therapies for Lung Cancer, 79–100. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-17832-1_4.

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Siemann, Dietmar W. "Tumor Vasculature: a Target for Anticancer Therapies." In Vascular-Targeted Therapies in Oncology, 1–8. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470035439.ch1.

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6

Michaelis, Uwe, and Michael Teifel. "Cationic Lipid Complexes to Target Tumor Endothelium." In Vascular-Targeted Therapies in Oncology, 221–45. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470035439.ch13.

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7

Shay, Jerry W. "Telomerase as a Target for Cancer Therapeutics." In Gene-Based Therapies for Cancer, 231–49. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6102-0_13.

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Hajishengallis, George, Tetsuhiro Kajikawa, Evlambia Hajishengallis, Tomoki Maekawa, Xiaofei Li, George N. Belibasakis, Nagihan Bostanci, et al. "Complement C3 as a Target of Host Modulation in Periodontitis." In Emerging Therapies in Periodontics, 13–29. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42990-4_2.

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9

Dutzan, Nicolas, Loreto Abusleme, and Niki Moutsopoulos. "The IL-17/Th17 Axis as a Therapeutic Target in Periodontitis." In Emerging Therapies in Periodontics, 73–85. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42990-4_6.

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Kreipe, Hans H., and Reinhard von Wasielewski. "Beyond Typing and Grading: Target Analysis in Individualized Therapy as a New Challenge for Tumour Pathology." In Targeted Therapies in Cancer, 3–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46091-6_1.

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Тези доповідей конференцій з теми "Target therapies":

1

Pierotti, Marco A. "Abstract CN1-1: Target mutation: The dark side of targeted therapies." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-cn1-1.

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2

Yang, Yu-an, Howard Yang, Ying Hu, Peter Watson, Huaitian Liu, Thomas R. Geiger, Miriam R. Anver, et al. "Abstract 1846: Immunocompetent mouse allograft models for development of therapies to target breast cancer metastasis therapies to target breast cancer metastasis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1846.

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3

Mojarrad, Mehran. "Nanotechnology Based Cancer Therapies." In ASME 2007 2nd Frontiers in Biomedical Devices Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/biomed2007-38034.

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By all accounts cancer remains the leading cause of death for humans of age less than 85 years old. This is partly because of the fact that there has been success in addressing other competing diseases such as cardiovascular leading to an overall drop in the rate of such disease where as after four decades of research success in cancer therapy remains limited. This places a greater demand on developing new therapies to treat cancer. With recent advances in nanotechnology field as applied in medicine there are new opportunities to detect, more effectively target and treat cancer and monitor the therapy while minimizing the damage to normal tissues and cells.
4

Fernandes, Caio J., Carlos Jardim, Bruno A. Dias, Andre Hovnanian, Suzana Hoette, Luciana K. Morinaga, Milena Suesada, Ana P. Breda, Silvia Souza, and Rogerio Souza. "The Role Of Target-Therapies In Schistosomiasis-Associated Pulmonary Arterial Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5918.

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5

Sarkar, Saugata, and Marissa Nichole Rylander. "Treatment Planning Model for Nanotube-Mediated Laser Cancer Therapy." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192997.

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The goal of the project is to develop an effective treatment planning computational tool for nanotube-mediated laser therapy that maximizes tumor destruction and minimizes tumor recurrence. Laser therapies can provide a minimally invasive treatment alternative to surgical resection of tumors. However, the effectiveness of these therapies is limited due to nonspecific heating of target tissue and diffusion limited thermal deposition which often leads to healthy tissue injury and extended treatment durations. These therapies can be further compromised due to induction of molecular chaperones called heat shock protein (HSP) in tumor regions where non-lethal temperature elevation occurs causing enhanced tumor cell viability and imparting resistance to chemotherapy and radiation treatments which are generally employed in conjunction with hyperthermia.
6

Claret, Francois X., Thuy Vu, Terry J. Shackleford, Jennifer Allensworth, Qingxiu Zhang, Ling Tian, and Ronghua Zhang. "Abstract 1825: Jab1/Csn5 a new target in the resistant mechanism to HER2-targeted therapies for 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.am2014-1825.

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7

Sarkar, Saugata, Amy Lutkus, James Mahaney, Harry Dorn, Tom Campbell, Dave Geohegan, and Marissa Nichole Rylander. "Carbon Nanohorns as Photochemical and Photothermal Agents." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206796.

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Laser therapies based on photochemical or photothermal mechanisms can provide a minimally invasive and potentially more effective treatment alternative to conventional surgical resection procedures by delivering prescribed optical/thermal doses to a targeted tissue volume with minimal damage to intervening and surrounding tissues. However laser therapy effectiveness is limited due to nonspecific excitation/heating of target tissue which often results in healthy tissue injury. Nanostructures targeted to tumor cells and utilized in combination with laser excitation can enhance treatment effectiveness by increasing thermal deposition and generating toxic photo-chemical mediators in the form of reactive oxygen species for targeted cell destruction.
8

Campbell, Timothy B., and Emmanuelle Passegué. "Abstract A38: Remodeling of the malignant bone marrow niche represents a therapeutic target." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-a38.

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9

Goverdhan, Aarthi, Heng-Huan Lee, Ondrej Havranek, Richard Eric Davis, and Mien-Chie Hung. "Abstract 13: PRMT1 as a therapeutic target in diffuse large B-cell lymphoma." In Abstracts: Second AACR Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; May 6-9, 2017; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.hemmal17-13.

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10

Stylianopoulos, Triantafyllos, Alptekin Aksan, and Victor H. Barocas. "A Structural, Kinetic Model of Soft Tissue Thermomechanics." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176008.

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Sub-ablative heating of collagenous soft tissues is central to thermal therapies such as thermal capsulorrhaphy, thermokeratoplasty and skin resurfacing [1]. These therapies target the heat-induced denaturation of the collagen molecule, which starts in a temperature range of 55–75 °C. There are relatively few theoretical studies describing the heat-induced alterations in soft tissues, which are mainly phenomenological [2]. In this work, a methodology for studying the kinetics of soft tissue thermomechanics is presented and used to predict the thermal response of New Zealand white patellar tendons [3]. The modeling approach accounts for the microstructure of the tissue and utilizes information at the single-molecule level to obtain the macroscopic response.

Звіти організацій з теми "Target therapies":

1

Shujaa, Asaad Suliman, and Qasem Almulihi. The efficacy and safety of ketamine in treating refractory and super-refractory status epilepticus in pediatric and adult populations, A systemic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0011.

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Review question / Objective: This study is to assess the efficacy and safety of ketamine in treating refractory and super-refractory status epilepticus in pediatric and adult populations. Rationale: Refractory status epilepticus (RSE) is either generalized or complex partial status epilepticus (SE) that fails to respond to first and second-line therapies. Super refractory status epilepticus (SRSE) is SE that remains unresponsive despite 24 hours of therapy with general anesthesia [1, 2]. Both RSE and SRSE pose significant challenges for the managing intensivist. There exists a race against time for control of epileptic activity in the RSE/SRSE patient to preserve cortical function and reduce morbidity/mortality. However, despite the best intentions, and not uncommonly, standard frontline antiepileptic drugs (AEDs) fail to control or reduce seizure activity once seizures approach the 30-minute mark. The following review provides an analysis of ketamine in treating RSE/SRSE, focusing on the potential target population, dosing, concerns, and the role of early administration.
2

Vail, Neal. Targeted Therapies for Myeloma and Metastatic Bone Cancers. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada485553.

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3

Vail, Neal. Targeted Therapies for Myeloma and Metastatic Bone Cancers. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada454700.

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4

Rossini, J. G., and Neal Vail. Targeted Therapies For Myeloma and Metastatic Bone Cancers. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada535238.

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5

Malkin, David, and Diana Merino. Molecular Targeted Therapies of Childhood Choroid Plexus Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada592041.

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6

Vail, Neal. Targeted Therapies for Myeloma and Metastatic Bone Cancers. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada467829.

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7

Malkin, David. Molecular Targeted Therapies of Childhood Choroid Plexus Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada555024.

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8

Vail, Neal. Targeted Therapies for Myeloma and Metastatic Bone Cancers. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada555410.

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9

Cacciapaglia, Fabio, Vincenzo Venerito, Stefano Stano, Marco Fornaro, Giuseppe Lopalco, and Florenzo Iannone. Comparison of Adalimumab to other Targeted Therapies in Rheumatoid Arthritis: results from Systematic Literature review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0048.

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10

Huang, Wenbo, Masashi Nagao, Naohiro Yonemoto, and Yuji Nishizaki. Comparative Efficacy Assessment of Different Targeted Therapies and Combinations of Chemotherapeutic Agents for Osteosarcoma: A Bayesian Network Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0028.

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