Relevant bibliographies by topics / Target therapies

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Target therapies'

Author: Grafiati
Published: 28 January 2023
Last updated: 22 June 2025

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Journal articles on the topic "Target therapies"

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

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

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

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

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

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

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Dissertations / Theses on the topic "Target therapies"

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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.
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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)<br>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
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DI, STEFANO ANNA LUISA. "MOLECULAR MARKERS OF GLIOMAS Implications for diagnosis and new target therapies." Doctoral thesis, Università degli studi di Pavia, 2017. http://hdl.handle.net/11571/1203374.

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The 2016 WHO classification of gliomas integrates molecular alterations (ie IDH mutations, and 1p19q codeletion) to histological features, defining distinct histo-molecular entities: IDH wild-type gliomas (mostly glioblastomas), and IDH mutated gliomas, divided according to 1p19q status into astrocytomas (1p19q intact) and oligodendrogliomas (1p19q codeleted). The first part of the manuscript is a contribution to molecular classification based on TERT promoter mutational status. We also contributed to GWAS analysis, and investigated the association between the risk loci and specific molecular entities, showing that some loci are associated with glioblastoma and IDH wild-type gliomas (rs2736100 near RTEL1, rs6010620 near TERT, rs3851634 near POLR3B) whereas others are associated to IDH mutated gliomas (rs4295627 and rs55705857 near CCDC26, rs498872 near PHLDB1, rs7572263 near IDH1, rs11196067 near VTI1A, rs648044, near ZBTB16 and rs12230172). Notably, rs4295627 and rs55705857 near CCD26 resulted strongly associated to 1p19q codeletion and to risk of oligodendrogliomas (P=2.31 x10-94). The second part of this work is devoted to the characterization of a specific oncogenic fusion between FGFR and TACC genes, which initially reported 3% of glioblastoma (GBM) and other human cancers and is proposed as a new therapeutic target. 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. These data support the systematic screening for FGFR-TACC fusion in all IDH wild-type glioma patients who can benefit from FGFR inhibition. In the third 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. Preliminary follow-up during radio-chemotherapy regimen and anti-IDH therapy showed a decrease in 2 HG production. In conclusion, MEGA-PRESS is a reliable tool for IDH mutation prediction at pre-surgical stages and for measuring the activity of anti-cancer drugs. Long-term monitoring will help to clarify the prognostic and predictive value of 2 HG decrease during anti-cancer treatment.<br>The 2016 WHO classification of gliomas integrates molecular alterations (ie IDH mutations, and 1p19q codeletion) to histological features, defining distinct histo-molecular entities: IDH wild-type gliomas (mostly glioblastomas), and IDH mutated gliomas, divided according to 1p19q status into astrocytomas (1p19q intact) and oligodendrogliomas (1p19q codeleted). The first part of the manuscript is a contribution to molecular classification based on TERT promoter mutational status. We also contributed to GWAS analysis, and investigated the association between the risk loci and specific molecular entities, showing that some loci are associated with glioblastoma and IDH wild-type gliomas (rs2736100 near RTEL1, rs6010620 near TERT, rs3851634 near POLR3B) whereas others are associated to IDH mutated gliomas (rs4295627 and rs55705857 near CCDC26, rs498872 near PHLDB1, rs7572263 near IDH1, rs11196067 near VTI1A, rs648044, near ZBTB16 and rs12230172). Notably, rs4295627 and rs55705857 near CCD26 resulted strongly associated to 1p19q codeletion and to risk of oligodendrogliomas (P=2.31 x10-94). The second part of this work is devoted to the characterization of a specific oncogenic fusion between FGFR and TACC genes, which initially reported 3% of glioblastoma (GBM) and other human cancers and is proposed as a new therapeutic target. 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. These data support the systematic screening for FGFR-TACC fusion in all IDH wild-type glioma patients who can benefit from FGFR inhibition. In the third 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. Preliminary follow-up during radio-chemotherapy regimen and anti-IDH therapy showed a decrease in 2 HG production. In conclusion, MEGA-PRESS is a reliable tool for IDH mutation prediction at pre-surgical stages and for measuring the activity of anti-cancer drugs. Long-term monitoring will help to clarify the prognostic and predictive value of 2 HG decrease during anti-cancer treatment.
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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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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.<br>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.
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Dussol, Manon. "Delta-opioïd receptor : a potential new target for migraine and headache therapies." Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2023. http://theses.bu.uca.fr/nondiff/2023UCFA0142_DUSSOL.pdf.

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Objectif : La migraine est un trouble hautement invalidant, pour lequel les traitements disponibles manquent d'efficacité chez de nombreux patients, soulignant ainsi la nécessité de nouveaux traitements. Le récepteur opioïde delta (DOR) est devenu une cible thérapeutique prometteuse pour la migraine. Chez la souris, les agonistes du DOR inhibent l'allodynie associée à la migraine. Cependant, des différences d'espèces (rat vs souris), régionales (trijumeau vs spinal) et de mécanisme (périphérique vs central) existent dans la contribution du DOR dans la régulation des céphalées de type migraine. Par conséquent, cette étude étudie la distribution du DOR dans le ganglion trigéminal (TG) et les mécanismes du potentiel antimigraineux d'un agoniste du DOR, SNC80, en utilisant un nouveau modèle de migraine chez le rat des deux sexes.Méthodes : En utilisant le RNAscope (hybridation in situ), l'électrophysiologie in vivo et l'analyse comportementale chez des rats des deux sexes, nous avons évalué i) la distribution du DOR dans le TG de rats en condition physiologique ii) l'effet du SNC80 sur les réponses de neurones WDR du sous noyau caudal (TNC) à des stimuli mécaniques non-nociceptifs/nociceptifs ainsi qu'à des stimuli électriques nociceptifs chez le rat en condition physiologique, et iii) la distribution du DOR dans le TG, l'effet antimigraineux du SNC80 et de ses sites d'actions dans un modèle de migraine chez le rat utilisant l'hypersensibilité mécanique (HM) cutanée comme substitut de la douleur associée à la migraine.Résultats : Nous montrons que le DOR est principalement exprimé par des neurones myélinisés de grand diamètre du TG, ainsi que par une sous-population de neurones peptidergiques exprimant CGRP, mais très rarement par des neurones non peptidergiques non myélinisés se liant à l'IB4. Conformément à la distribution du DOR dans le TG, le SNC80, régule les réponses mécaniques évoquées à la fois non-nociceptives et nociceptives des neurones WDR du TNC ainsi que la douleur mécanique céphalique aiguë chez les rats naïfs. Cependant, l'effet antinociceptif du SNC80 varie en fonction de la voie d'administration, étant efficace par voie intracisternale ou intraveineuse, mais pas par voie sous-cutanée. Il n'y a pas de différence entre les sexes ni dans la distribution du DOR ni dans la régulation de la sensibilité mécanique aiguë céphalique par le SNC80 chez les rats naïfs, ni dans l'HM céphalique aiguë induite par une administration aiguë d'ISDN. Néanmoins, l'ISDN chronique a augmenté l'expression de l'ARNm de DOR chez les rats femelles, mais pas mâles, et cette surexpression était principalement limitée aux neurones de plus grand diamètre du TG. En accord avec ces résultats, le SNC80 diminue l'HM céphalique inter-ictale chronique (basale) établie après des administrations répétées d'ISDN ainsi que l'HM céphalique ictale chronique dans les deux sexes, étant plus puissant chez les rats femelles que les rats mâles. Le traitement par SNC80 a entraîné une diminution de l'expression de c-Fos évoquée par le toucher dans le TNC, renforçant l'hypothèse selon laquelle le SNC80 peut empêcher le développement d'une sensibilisation centrale chronique au sein du TNC. Enfin, l'administration intracisternale et systémique de SNC80 peut inhiber l'HM céphalique ictale aiguë induite par l'ISDN. L'effet anti-allodynique de l'administration systémique a été partiellement inversé par la naloxone-méthiodide, ce qui suggère que les DOR périphériques et centraux régulent les céphalées de type migraine chez le rat.Conclusion : La présente étude a démontré que l'activation des DOR présente un potentiel antimigraineux chez les rats des deux sexes, étant plus puissant chez les femelles que chez les mâles. Les données renforcent la pertinence des agonistes du DOR pour traiter la migraine, une douleur à forte prévalence chez les femmes. Les agonistes du DOR produisent des effets antimigraineux via les DOR périphériques et centraux<br>Objective: Migraine is a highly incapacitating disorder, with available treatments lacking efficacy in many patients, thus highlighting the need for new treatments. The delta opioid receptor (DOR) has emerged as a very promising therapeutic target for migraine. In mice, DOR agonists inhibit the allodynia associated with migraine. However, species (rat vs mouse), regional (trigeminal vs spinal) and mechanism (peripheral vs central) differences exist in the contribution of DORs in the regulation of migraine-like headache. Therefore, this study investigates the distribution of DORs within the trigeminal ganglia (TG) and the mechanisms of the antimigraine potential of a DOR agonist, SNC80, using a new rat model of migraine of both sexes.Methods: Using RNAscope (in situ hybridization), in vivo electrophysiology and behavioral analysis in rats of both sexes, we assessed, i) the DOR distribution in rat TG under physiological conditions, ii) the effect of the DOR agonist SNC80 on the responses of WDR neurons in the trigeminal nucleus caudalis (TNC) to innocuous/noxious mechanical as well as to noxious electrical stimuli in rats under physiological conditions, and iii) DOR distribution in TG, the antimigraine effect of the SNC80 and its site(s) in a rat model of migraine using cutaneous mechanical hypersensitivity (MH) as a surrogate of pain associated with migraine headache. Results: We addressed the role of DOR in a preclinical model of migraine in both female and male rats. We show that DOR mRNA is predominantly expressed in large-diameter myelinated TG neurons, as well as by a subpopulation of CGRP peptidergic, but very rarely by IB4-binding nonpeptidergic, unmyelinated fibers. Consistent with the distribution of DORs in TG, the DOR agonist, SNC80, regulates both innocuous and noxious mechanically-evoked responses of trigeminal WDR neurons as well as acute cephalic mechanical pain in naïve rats. However, the antinociceptive effect of SNC80 varies depending on the route of administration, being effective by intracisternal or intravenous, but not subcutaneous route. There is no sex difference: neither in the distribution of DORs in TG, nor in the regulation of cephalic physiological mechanical sensitivity, nor in the acute ISDN-induced ictal cephalic MH. Nevertheless, chronic ISDN increased DOR mRNA expression in female, but not male, rats, and this overexpression was predominantly restricted to larger diameter TG neurons. Consistently, the DOR agonist could reverse both the established chronic interictal (basal) and ictal cephalic MH in both sexes, being nevertheless more potent in female than in male rats. SNC80-treatment results in decreased touch-evoked c-Fos expression in TNC, boosting the hypothesis that SNC80 can prevent the development of chronic central sensitization within TNC. Finally, intracisternal and systemic SNC80 administration can partially and completely, respectively, inhibit ISDN-induced acute ictal cephalic MH. The anti-allodynic effect of systemic SNC80 was partially reversed by naloxone-methiodide, suggesting that both peripheral and central DORs regulate migraine-like headache in rats.Conclusion: The present study demonstrated that activation of DORs exhibits an antimigraine potential in rats of both sexes, being more potent in females than in males. The data strengthens therelevance of DOR agonists to treat migraine, a pain with a high prevalence in women. DOR agonists produce anti-migraine effects through both peripheral and central DORs
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ULTIMO, Simona. "Inhibition of the PI3K/Akt/mTOR signaling pathway as a therapeutic target for Acute Lymphoblastic Leukemia." Doctoral thesis, Università degli studi di Ferrara, 2018. http://hdl.handle.net/11392/2487845.

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Acute Lymphoblastic Leukemia (ALL) is a malignant disorder characterized by the abnormal clonal proliferation of B-cell progenitors (B-ALL) or immature stage thymocytes (T-ALL). Constitutive activation of the PI3K/Akt/mTOR network is a common feature of B- and T-ALL, influencing cell growth and survival. The PI3K/Akt/mTOR inhibitors are currently being developed for clinical use either as single agents or in combination with conventional chemotherapy for T-ALL patient treatment. In this study it has been investigated the effects of a panel of PI3K/Akt/mTOR inhibitors on healthy human CD4+ T-cells when compared with T-ALL cell lines. Then, it has been verified whether a multi-inhibition treatment against Akt protein could enhance the efficacy of individual drug administration and overcome drug resistance as well as to obtain a decrease in single drug concentration, by testing the effects of combined treatments with three Akt inhibitors with different mode of action, GSK690693, MK-2206 and Perifosine on T-ALL cell lines. Combined administration of the drugs displayed a significant synergistic cytotoxic effect and affected PI3K/Akt/mTOR pathway at much lower concentration than single drug use. Highest synergistic effect for full inhibition of Akt was also related to the timing of every drug administration. The results obtained suggested that targeting Akt as a key protein of PI3K/Akt/mTOR pathway with multiple drugs might represent a new and promising pharmacological strategy for treatment of T-ALL patients. It has also been investigated the role of microRNAs (miRNAs), a class of small noncoding RNAs, which play a role in various biological processes, including proliferation, apoptosis and tumorigenesis. The dysregulation of miRNAs is implicated in invasion in several human cancer types and leukemia is not an exception. By using in vitro models, it has been done an analysis of the effect of PI3K signaling inhibitors on expression of miRNA level involved in ALL disease and PI3K activation. The results obtained have shown that these drugs could modulate miRNA expression. Therefore, the regulation of miRNA expression profiling in ALL by using PI3K signaling inhibitors could be used as a new therapeutic approach in the near future. In addition, it has been analyzed the efficacy of PI3K signaling pathway inhibitors in B- and T-ALL cell lines harboring the Abl1 tyrosine kinase gene fusion that lead to an aberrant cell proliferation. It has been studied the effects of anti Bcr-Abl1 drugs such as Imatinib, Nilotinib and GZD824 associated with PI3K signaling inhibitors. Drugs against PI3K/Akt/mTOR cascade administered in combination with Imatinib, Nilotinib and GZD824 decreased cell viability, induced apoptosis and autophagy in a marked synergistic manner. These findings suggested that selected PI3K/Akt/mTOR inhibitors used in combination with anti Bcr-Abl1 drugs may be an attractive novel therapeutic intervention in Ph+ B- and T-ALL.<br>La Leucemia Linfoblastica Acuta (LLA) è un tumore maligno ematologico caratterizzato da una proliferazione clonale incontrollata di progenitori della linea cellulare di tipo B (LLA-B) o timociti allo stadio immaturo (LLA-T). L’attivazione della via di trasduzione del segnale di PI3K/Akt/mTOR è una caratteristica comune della LLA-B e T ed influisce sulla crescita e sopravvivenza cellulare. Gli inibitori della via di PI3K/Akt/mTOR sono attualmente in fase di studio per uso clinico, sia come singoli agenti che in combinazione con la convenzionale chemioterapia utilizzata nel trattamento dei pazienti affetti da LLA-T. In questo studio sono stati analizzati gli effetti di un pannello di inibitori della via di PI3K/Akt/mTOR su linfociti T-CD4+ di individui sani e confrontati con linee cellulari tumorali umane di LLA-T. Successivamente è stato verificato se il trattamento di inibizione multipla della proteina Akt potesse aumentare l’efficacia dei farmaci somministrati singolarmente e superare la resistenza al farmaco ottenendo la riduzione della concentrazione del singolo agente. Pertanto, sono stati studiati e testati gli effetti di tre inibitori su linee cellulari umane di LLA-T diretti contro Akt ma con differenti modi di azione: GSK690693, MK-2206 e Perifosina. Questa combinata somministrazione di farmaci ha mostrato un significativo effetto sinergico ed ha influito sulla via di PI3K/Akt/mTOR ad una concentrazione molto più bassa rispetto a quella del singolo farmaco. Il più elevato effetto sinergico per una totale inibizione di Akt è stato associato alla tempistica adottata per ciascuna somministrazione. I risultati ottenuti hanno suggerito che, mirare Akt come bersaglio chiave nella via del segnale di PI3K/Akt/mTOR con la somministrazione multipla di farmaci, potrebbe rappresentare una nuova e promettente strategia per il trattamento dei pazienti affetti da LLA-T. E’ stato inoltre studiata l’azione dei microRNA (miRNA), una classe di piccoli RNA non codificanti che giocano un ruolo in vari processi biologici, quali la proliferazione, la morte cellulare e la genesi del cancro. La regolazione incontrollata dei miRNA è implicata nell’invasione di diversi tumori umani e la leucemia non è esclusa. Usando modelli in vitro è stata eseguita un’analisi degli effetti degli inibitori della via del segnale di PI3K sui livelli di espressione dei miRNA coinvolti nella LLA e nell’attivazione di PI3K. I risultati emersi hanno mostrato che questi farmaci potrebbero modulare l’espressione dei miRNA, pertanto, la regolazione dei loro profili di espressione nella LLA, utilizzando gli inibitori diretti contro la via di PI3K, potrebbe costituire un nuovo terapeutico approccio per il prossimo futuro. Infine, è stata valutata l’efficacia degli inibitori della via del segnale di PI3K nelle linee cellulari di LLA-B e T caratterizzate dalla proteina di fusione Abl1 che causa una proliferazione cellulare incontrollata. Sono stati studiati gli effetti di farmaci contro il gene Bcr-Abl1 come Imatinib, Nilotinib e GZD824 utilizzati in combinazione con i farmaci diretti contro la via di PI3K. La combinazione di questi farmaci ha mostrato una ridotta vitalità cellulare, innescando il processo di morte e autofagia cellulare in maniera sinergica. Questi dati hanno suggerito che la selezione di inibitori diretti contro la via di PI3K/Akt/mTOR somministrati in combinazione con farmaci contro il gene di fusione Bcr-Abl1, potrebbe rappresentare un allettante nuovo intervento terapeutico da prendere in considerazione nel trattamento della LLA-B e T portatrice del cromosoma Philadelphia (Ph+).
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Ito, Koichi. "Galectin-1 as a Potent Target for Cancer Therapy: Role in the Tumour Microenvironment." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/367472.

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Despite many new and significant discoveries made in cancer research in the last few decades, only limited improvements in overall responses to treatment have occurred. The frustrating gaps between the scientific evidence and minor advances in clinical outcomes as well as unacceptable treatment failure must be overcome by improving current cancer therapies and developing more effective anti-cancer strategies. The term “tumour heterogeneity” refers to the formation of a tumour containing areas with distinguishable phenotypic features within its microenvironment. The realisation that a tumour tissue is not a cluster of single clonally derived cells but rather comprises a well-organised and tumour-protective environment necessitates a drastic change in the direction of cancer research to breakdown these protective barriers. Over the last century, the field of glycobiology has grown in significance and attracted a number of scientists from a variety of fields including immunology and oncology. Involvement of carbohydrates is critical for pathological aspects of cancer progression and metastasis as well as for normal biological systems such as immune reaction and recognition. Therefore, the studies of lectin-glycan interactions currently are providing much opportunity for unveiling many novel pathological features of cancer. Galectin-1 is a β-galactoside binding protein abundantly secreted by almost all types of malignant tumour cells and its expression plays vital pro-tumourigenic roles within the tumour microenvironment. In particular, galectin-1 suppresses the T cell-mediated anticancer immune responses, inducing apoptosis of the activated effector T cells by binding to their glycosylated surface receptors.<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy (PhD)<br>School of Medical Science<br>Griffith Health<br>Full Text
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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.
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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.
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Books on the topic "Target therapies"

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

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

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

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Albert, Jeffrey S., and Michael W. Wood. Targets and emerging therapies for schizophrenia. John Wiley & Sons, 2012.

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

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Paleari, Laura, ed. Cancer Prevention with Molecular Target Therapies. MDPI, 2023. http://dx.doi.org/10.3390/books978-3-0365-7926-9.

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Paleari, Laura, ed. Cancer Prevention with Molecular Target Therapies 3.0. MDPI, 2023. http://dx.doi.org/10.3390/books978-3-0365-7908-5.

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Paleari, Laura, ed. Cancer Prevention with Molecular Target Therapies 4.0. MDPI, 2024. http://dx.doi.org/10.3390/books978-3-7258-1951-5.

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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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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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Book chapters on the topic "Target therapies"

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Kefas, Benjamin, and Benjamin W. Purow. "microRNA: A Potential Therapy Able to Target Multiple Cancer Pathways." In Targeted Therapies. 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. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-478-4_1.

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Yamada, Yuma, Fumika Kubota, Rina Naganawa, Satrialdi, and Hideyoshi Harashima. "Cancer Photo Therapies that Target Mitochondria." In Nanomedicine and Nanotoxicology. Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-97-5288-1_4.

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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. 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. 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. John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470035439.ch1.

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

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Shay, Jerry W. "Telomerase as a Target for Cancer Therapeutics." In Gene-Based Therapies for Cancer. 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, et al. "Complement C3 as a Target of Host Modulation in Periodontitis." In Emerging Therapies in Periodontics. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42990-4_2.

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

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Conference papers on the topic "Target therapies"

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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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Yang, Yu-an, Howard Yang, Ying Hu, 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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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.
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Fernandes, Caio J., Carlos Jardim, Bruno A. Dias, et al. "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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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.
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Claret, Francois X., Thuy Vu, Terry J. Shackleford, et al. "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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Sarkar, Saugata, Amy Lutkus, James Mahaney, et al. "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.
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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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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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Alysandratos, K. D., L. R. Rodriguez, R. Acín-Pérez, et al. "Preclinical Pulmonary Fibrosis Models Identify AMP-kinase as a Candidate Druggable Target for Pulmonary Fibrosis Therapies." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6264.

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Reports on the topic "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, 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.
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Vail, Neal. Targeted Therapies for Myeloma and Metastatic Bone Cancers. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada485553.

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

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

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

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

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

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

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Agrafiotis, Apostolos, Mariana Brandão, Thierry Berghmans, Valérie Durieux, and Christiane Jungels. Immunotherapy and targeted therapies efficacy in thymic epithelial tumors: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.8.0080.

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Htet, Htet, Jwala Rebecca James Anaghan, Heethal Jaiprakash, Igor Nikolayevich Lezhitsa, and Renu Agarwal. Efficacy and safety of molecular-targeted therapies in nasopharyngeal carcinoma: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.8.0024.

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