Bibliographies thématiques / Targeted therapy of hematological malignancies

Littérature scientifique sur le sujet « Targeted therapy of hematological malignancies »

Auteur : Grafiati

Publié le 11 mars 2023

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Articles de revues sur le sujet "Targeted therapy of hematological malignancies"

Kachlany, Scott C., Amy Le et Benjamin A. Belinka. « Leukotoxin (Leukothera™), a Targeted Therapy for Hematological Malignancies ». Blood 116, n^o 21 (19 novembre 2010) : 3284. http://dx.doi.org/10.1182/blood.v116.21.3284.3284.

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Abstract Abstract 3284 Leukotoxin (Leukothera™) is a bacterial protein toxin that naturally targets and kills disease associated white blood cells (WBCs) expressing the activated form of leukocyte function antigen-1 (LFA-1). While leukotoxin has minimal effects on resting and healthy cells, it causes significant death of malignant WBCs associated with leukemias and lymphomas. Leukotoxin is a unique biologic in that it already provides both toxicity and specificity without requiring fusion of the protein to other molecules such as antibody fragments or cytokines. In vivo efficacy was demonstrated in an HL-60 SCID mouse leukemia model previously. In the present work, we compared leukotoxin to the standard chemotherapeutic agents, doxorubicin and cytarabine in a SCID mouse model using THP-1 leukemia cells. Mice (n=14 per group) were injected with THP-1 cells intravenously (i.v.) and then administered either leukotoxin or standard agents i.v. Mice received three doses, once daily, of leukotoxin (1.5 mg/kg) or five doses of doxorubicin (0.5 mg/kg) or cytarabine (10 mg/kg) once daily. Leukemic mice that were treated with leukotoxin maintained and increased body weight more effectively than those which received vehicle alone or the standard agents. The leukotoxin-treated mice showed significantly (p<0.001) higher mean survival than mice treated with vehicle or cytarabine over the 60-day observation period. Necropsy and histopathology of animals after the 60-day period revealed that test animals treated with vehicle or standard agents developed internal tumors on organs such as the thymus and lymph nodes. In contrast, none of the leukotoxin-treated mice developed internal tumors. To determine if leukotoxin could block migration of malignant cells, and thus formation of internal tumors, we performed a cellular migration assay using activated monocytes and human brain endothelial cells. It was found that even a low dose of leukotoxin (10 ng/ml) caused significant suppression (>80%) of monocyte migration across an endothelial barrier. Hence, leukotoxin has the potential to not only deplete malignant WBCs, but may also prevent their spread to other tissues. To test the general safety of leukotoxin, mice were injected with 1 mg/kg for three weeks. None of the mice showed signs of illness or changes in normal behavior and all continued to gain weight throughout the study period. In addition, to determine if a neutralizing antibody response to leukotoxin was generated, we challenged mice with high doses of leukotoxin and assayed monoclonal antibody from ten independent hybridomas. Results showed that antibody was able to bind to and recognize leukotoxin, but did not cause significant neutralization in a bioassay. In conclusion, leukotoxin may represent a highly effective and safe option for patients with hematologic malignancies, especially those with relapsed and refractory disease. Disclosures: Kachlany: Actinobac Biomed, Inc.: Consultancy, Equity Ownership. Belinka:Actinobac Biomed, Inc.: Employment, Equity Ownership.

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Kuriakose, Philip. « Targeted Therapy for Hematologic Malignancies ». Cancer Control 12, n^o 2 (avril 2005) : 82–90. http://dx.doi.org/10.1177/107327480501200203.

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Background: The introduction of monoclonal antibodies, either as native molecules or conjugated to radioisotopes or other toxins, has led to new therapeutic options for patients with hematologic malignancies. In addition, the use of small molecules against specific cell surface receptors, enzymes, and proteins has become an important strategy in the treatment of such disorders. Methods: The author reviewed the published clinical trials of monoclonal antibody and other targeted therapies in hematologic malignancies. Results: Results from several trials demonstrate a therapeutic benefit for the use of monoclonal antibodies (either native or conjugated) and other targeted therapies, used alone or in combination with standard cytotoxic chemotherapy. Conclusions: Targeted therapy of hematologic malignancies seems to be an effective and less toxic approach to the treatment of such disorders. Nevertheless, additional studies are needed to determine where and when such management fits into a therapeutic regimen for any given disorder, whether upfront or as salvage therapy, alone or in combination with chemotherapy (concurrent or sequential).

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Joshi, Dolly, Kanjaksha Gosh et Babu Rao Vundinti. « MicroRNAs in hematological malignancies : a novel approach to targeted therapy ». Hematology 17, n^o 3 (mai 2012) : 170–75. http://dx.doi.org/10.1179/102453312x13376952196656.

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Ma, Haiqing, Saradhi Mallampati, Gang An et Jin Wang. « Targeted Therapy in Hematological Malignancies : From Basic Research to Clinical Practice ». BioMed Research International 2015 (2015) : 1–2. http://dx.doi.org/10.1155/2015/157570.

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Podhorecka, Monika, Justyna Markowicz, Agnieszka Szymczyk et Johannes Pawlowski. « Target Therapy in Hematological Malignances : New Monoclonal Antibodies ». International Scholarly Research Notices 2014 (30 octobre 2014) : 1–16. http://dx.doi.org/10.1155/2014/701493.

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Apart from radio- and chemotherapy, monoclonal antibodies (MoAbs) represent a new, more selective tool in the treatment of hematological malignancies. MoAbs bind with the specific antigens of the tumors. This interaction is a basis for targeted therapies which exhibit few side effects and significant antitumor activity. This review provides an overview of the functional characteristics of MoAbs, with some examples of their clinical application. The promising results in the treatment of hematological malignancies have led to the more frequent usage of MoAbs in the therapy. Development of MoAbs is a subject of extensive research. They are a promising method of cancer treatment in the future.

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Leni, Zaira, Geetha Parakkal et Alexandre Arcaro. « Emerging Metabolic Targets in the Therapy of Hematological Malignancies ». BioMed Research International 2013 (2013) : 1–12. http://dx.doi.org/10.1155/2013/946206.

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During the last decade, the development of anticancer therapies has focused on targeting neoplastic-related metabolism. Cancer cells display a variety of changes in their metabolism, which enable them to satisfy the high bioenergetic and biosynthetic demands for rapid cell division. One of the crucial alterations is referred to as the “Warburg effect”, which involves a metabolic shift from oxidative phosphorylation towards the less efficient glycolysis, independent of the presence of oxygen. Although there are many examples of solid tumors having altered metabolism with high rates of glucose uptake and glycolysis, it was only recently reported that this phenomenon occurs in hematological malignancies. This review presents evidence that targeting the glycolytic pathway at different levels in hematological malignancies can inhibit cancer cell proliferation by restoring normal metabolic conditions. However, to achieve cancer regression, high concentrations of glycolytic inhibitors are used due to limited solubility and biodistribution, which may result in toxicity. Besides using these inhibitors as monotherapies, combinatorial approaches using standard chemotherapeutic agents could display enhanced efficacy at eradicating malignant cells. The identification of the metabolic enzymes critical for hematological cancer cell proliferation and survival appears to be an interesting new approach for the targeted therapy of hematological malignancies.

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Liang, Xuewu, Hong Liu et Yingjie Zhang. « Novel-targeted therapy for hematological malignancies with JAK and HDAC dual inhibitors ». Future Medicinal Chemistry 11, n^o 15 (août 2019) : 1849–52. http://dx.doi.org/10.4155/fmc-2019-0168.

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Jurcic, Joseph G. « Targeted Alpha-Particle Therapy for Hematologic Malignancies ». Seminars in Nuclear Medicine 50, n^o 2 (mars 2020) : 152–61. http://dx.doi.org/10.1053/j.semnuclmed.2019.09.002.

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Jurcic, Joseph G. « Targeted Alpha-Particle Therapy for Hematologic Malignancies ». Journal of Medical Imaging and Radiation Sciences 50, n^o 4 (décembre 2019) : S53—S57. http://dx.doi.org/10.1016/j.jmir.2019.05.008.

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Gao, Rili, Yikai Zhang, Chengwu Zeng et Yangqiu Li. « The role of NFAT in the pathogenesis and targeted therapy of hematological malignancies ». European Journal of Pharmacology 921 (avril 2022) : 174889. http://dx.doi.org/10.1016/j.ejphar.2022.174889.

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Thèses sur le sujet "Targeted therapy of hematological malignancies"

Amdouni, Hela. « Synthèse et étude de nouveaux analogues de l’acadésine pour circonvenir les résistances dans les hémopathies malignes ». Thesis, Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4065/document.

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La lutte contre le cancer est certainement l’un des défis majeurs de ce 21ème siècle. Les résistances qui émergent contre les agents de thérapie ciblée présentent un aspect particulièrement épineux de cette problématique. La thèse présentée ici s’inscrit dans ce cadre. Elle vise à développer des molécules bioactives pouvant circonvenir les résistances apparues contre les traitements de certaines hémopathies malignes : la leucémie myéloïde chronique (LMC) et le syndrome myélodysplasique (SMD). Après avoir mis au point une méthodologie de synthèse monotope permettant de transformer un azoture en un 5-alcynyl-1,2,3-triazole, nous avons synthétisé deux séries de produits : nucléosidique et non nucléosidique. Pour chacune de ces séries, des relations structure-activité ont été établies. Après plusieurs cycles d’optimisation, trois composés lead très efficaces contre des lignées cellulaires résistantes de LMC et SMD, ont été sélectionnés. De surcroît, leur mode d’action s’est révélé très intéressant : il repose (partiellement ou entièrement, suivant le composé) sur un processus cellulaire qui connaît un véritable regain d’intérêt, à savoir l’autophagie. Une évaluation in vivo a été réalisée et a permis de valider l’activité prometteuse de notre composé lead nucléosidique. Par ailleurs, des études visant à déterminer la localisation intracellulaire et les cibles moléculaires de nos produits sont actuellement en cours
The fight against cancer is certainly one of the biggest challenges of the 21st century. Resistance that comes up against targeted therapy agents presents a particularly important aspect of this issue. The thesis presented here takes part within that framework. It aims at developing bioactive molecules able to circumvent resistance that have emerged against the treatment of certain hematological malignancies: chronic myeloid leukemia (CML) and myelodysplastic syndrome (MDS). Having developed a one-pot synthesis methodology that converts azides into 5-alkynyl-1,2,3-triazole, we synthesized two series of products: nucleosidic and non-nucleosidic. For each of these series, structure-activity relationships have been established. After running several cycles of optimization, three lead compounds particularly active on resistant cell lines of CML and MDS were selected. Further, their mode of action proved to be very interesting. It is based (partially or fully, depending on the compound) on a cellular process, which is experiencing a real renewed interest, the autophagy. An in vivo evaluation confirmed the promising activity of our nucleosidic lead compound. Moreover, studies aiming at determining the intracellular localization and molecular targets of our products are currently in progress

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Jokinen, E. (Elina). « Targeted therapy sensitivity and resistance in solid malignancies ». Doctoral thesis, Oulun yliopisto, 2014. http://urn.fi/urn:isbn:9789526205755.

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Abstract Cancer is a major global killer and a challenge for the healthcare worldwide. Earlier cancer has been treated with surgery, radiation, chemotherapy and hormonal therapy. Unfortunately the efficiency of these therapies has shown to be limited and this has raised an enthusiasm for development of new, targeted cancer therapies that are based on activated oncogenes. The challenge of the targeted therapies is therapy resistance, de novo, adaptive and acquired. This work investigated targeted therapy sensitivity and resistance in lung cancer, breast cancer, colorectal cancer, and melanoma cell lines. The results of this study indicate that in some non-small cell lung cancer cell lines, dual PI3K and MEK inhibition is a more efficacious treatment than inhibition of either solely. It was also showed that the maximal effect of the dual inhibition can be achieved with alternative dosing schedules that are potentially more tolerable in clinical use. Furthermore, by combining ABT-263, entinostat or dasatinib to the dual PI3K and MEK inhibition, the efficiency of the therapy can be increased. Bcl-xl downregulation is a major determinant of the apoptotic response to the triple inhibitor treatment. The current work showed that cancer stem cells can mediate resistance to targeted therapies. Since these cells follow the stochastic model, concurrent therapy with a targeted agent and a stem cell targeting drug might be needed for maximal therapeutic efficiency. This study also showed that Gö6976 acts as a potent inhibitor of mutant EGFR despite the presence of T790M, the most important mechanism of acquired resistance for EGFR tyrosine kinase inhibitors in lung cancer, both in vitro and in vivo
Tiivistelmä Syöpä on yksi johtavia kuolemanaiheuttajia ja tauti on maailmanlaajuinen haaste terveydenhuollolle. Perinteiset syöpähoidot käsittävät kirurgian, sädehoidon, kemoterapian ja hormonaalisen hoidon, mutta näiden rinnalle on noussut uusia, aktivoituneiden onkogeenien signaalien estoon perustuvia hoitoja. Tämä työ tutki kohdennettuja syöpähoitoja ja näihin hoitoihin liittyvää resistenssiä keuhko-, rinta- ja paksusuolen syövän sekä melanooman solulinjoissa. Tulokset osoittavat, että joissakin ei-pienisoluisen keuhkosyövän solulinjoissa yhdistetty PI3K- ja MEK-esto aiheuttaa tehokkaamman vasteen kuin kummankaan signaalireitin esto yksistään. Tässä työssä näytettiin myös, että maksimaalinen vaste yhdistetylle PI3K- ja MEK-estolle voidaan saavuttaa vaihtoehtoisilla annostelutavoilla, jotka ovat voisivat olla paremmin siedettyjä kliinisessä käytössä kuin kahden lääkkeen jatkuva annostelu. Tämä tutkimus osoitti lisäksi, että kaksoiseston tehokkuutta voidaan lisätä yhdistämällä hoitoon kolmas lääkeaine, ABT-263, entinostaatti tai dasatinibi. Bcl-xl proteiinilla on keskeinen rooli apoptoottisen vasteen määrittäjänä näille kolmen lääkkeen käsittelyille. Tämä työ osoitti, että syövän kantasolut voivat välittää resistenssiä kohdennetuille syöpähoidoille. Nämä solut noudattavat niin kutsuttua stokastista mallia, joten parhaan vasteen saaminen saattaa edellyttää että hoito kohdentuu sekä erilaistuneisiin että kantasolutyyppisiin syöpäsoluihin. Tässä tutkimuksessa osoitettin lisäksi, että Gö6976 toimii mutatoituneen EGFR:n estäjänä, huolimatta kehittyvää keuhkosyövissä resistenssiä välittävästä T90M mutaatiosta, sekä in vitro -että in vivo -malleissa

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Lundin, Jeanette. « Targeted CD52 therapy in lymphoid malignancies : a clinical and immunological study / ». Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-441-0/.

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Günther, Thomas [Verfasser], Hans-Jürgen [Akademischer Betreuer] Wester, Matthias [Gutachter] Eiber et Hans-Jürgen [Gutachter] Wester. « Novel GRPR-targeted antagonists with improved pharmacokinetics for imaging and therapy of GRPR-expressing malignancies / Thomas Günther ; Gutachter : Matthias Eiber, Hans-Jürgen Wester ; Betreuer : Hans-Jürgen Wester ». München : Universitätsbibliothek der TU München, 2021. http://d-nb.info/1233428055/34.

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DELLA, CRISTINA Pietro Argeo. « Construction of a macromolecular recombinant drug for the targeted therapy of hematological malignancies ». Doctoral thesis, 2009. http://hdl.handle.net/11562/337455.

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L’impiego di agenti citotossici capaci di riconoscere in modo specifico molecole presenti sulla superficie di una cellula tumorale rappresenta una tecnica molto promettente per il trattamento di diverse neoplasie ed è particolarmente efficace per la cura di leucemie e linfomi. Appartengono a questa classe di sostanze le immunotossine, proteine composte da un dominio di derivazione anticorpale e da un dominio tossico solitamente di origine batterica o vegetale: l’anticorpo lega selettivamente l’antigene bersaglio e, a seguito di endocitosi, consente il rilascio all’interno della cellula della componente tossica che interferisce con i processi metabolici necessari alla sopravvivenza cellulare. Tra i diversi marcatori di superficie associati a leucemie e linfomi, uno dei target molecolari di maggior interesse per questo tipo di approccio terapeutico, è il CD22, una glicoproteina di membrana con funzioni co-recettoriali la cui espressione è limitata ai linfociti B. Il presente lavoro di tesi descrive la generazione e la successiva caratterizzazione funzionale di una immunotossina in cui il motivo di legame alla superficie cellulare è costituito da un frammento anticorpale a singola catena (scFv) specifico per l’antigene CD22, mentre l’azione citotossica è svolta da una forma tronca dell’esotossina A di Pseudomonas aeruginosa, proteina in grado di inibire il meccanismo di sintesi proteica eucariotica. Attraverso il clonaggio delle sequenze codificanti per le regioni variabili della catena pesante (VH) e della catena leggera (VL) di un anticorpo monoclonale murino anti-CD22, è stato possibile assemblare il costrutto che codifica per l’scFv ed esprimere la proteina ricombinante in un sistema di espressione eterologo quale Escherichia coli. Mediante analisi di immunofluorescenza e saggi immunoenzimatici è stato verificato che il frammento anticorpale possiede una buona affinità di legame all’antigene e mantiene le stesse caratteristiche di specificità mostrate dall’anticorpo monoclonale parentale. Successivamente l’scFv è stato unito attraverso fusione genetica al dominio enzimatico della tossina batterica. L’immunotossina risultante, espressa in Escherichia coli, è stata estratta a partire da aggregati insolubili accumulati nel compartimento citosolico del batterio e purificata tramite cromatografia di affinità con rese di circa 1-2 mg per litro di coltura batterica. La proteina ricombinante possiede proprietà di legame specifiche per l’antigene non dissimili da quelle osservate per l’scFv, inoltre, secondo quanto accertato mediante saggi di citotossicità, induce in modo selettivo l’inibizione della proliferazione di linee cellulari esprimenti la proteina CD22 con una IC50 di 1- 10 nM (per IC50 si intende la concentrazione in grado di inbire il 50% della proliferazione IV cellulare). Essa sembra quindi conservare inalterate sia le caratteristiche di riconoscimento specifico del frammento anticorpale che l’attività enzimatica della tossina. Ulteriori studi serviranno a valutare l’opportunità di sottoporre l’immunotossina ad un processo di ottimizzazione finalizzato all’ottenimento di un nuovo farmaco biotecnologico per il trattamento di neoplasie ematologiche nell’uomo.
The use of cytotoxic agents capable to selectively target surface molecules on a malignant cell is a promising approach for the treatment of cancer, especially hematologic malignacies. Immunotoxins, in particular, are polypeptides comprising an antibody-derived domain and a toxic portion, usually represented by a bacterial or plant toxin: the antibody specifically binds a target antigen and, following endocytosis, delivers the toxic payload to the interior of the cell, interfering with fundamental metabolic pathways. Among several leukemia/lymphoma-associated surface antigens, one of the most attractive molecular targets for this kind of therapeutic strategy is CD22, a membrane glycoprotein with coreceptor functions, whose expression is restricted to B lymphocytes. The present thesis describes the construction and characterization of a recombinant immunotoxin in which the binding domain is represented by a CD22-specific single-chain antibody fragment (scFv), while the cytotoxic activity is carried out by a truncated version of Pseudomonas aeruginosa Exotoxin A, a bacterial toxin that inhibits the mechanism of protein synthesis in eukaryotes. Through the molecular cloning of sequences coding for the variable domains of heavy and light chains (VH and VL, respectively) of an anti-CD22 murine monoclonal antibody, it was possible to assemble a plasmid construct coding for a scFv that was eventually produced in a bacterial expression system. Immunofluorecence analysis on CD22-positive cells and immunoenzymatic assays on the purified antigen proved that the antibody fragment maintains the binding specificity of the parental monoclonal antibody, exhibiting a fairly good affinity for CD22. The scFv was later genetically fused to the enzymatic domain of a bacterial toxin. The resulting immunotoxin was expressed in Escherichia coli and recovered from insoluble cytoplasmic aggregates after purification by affinity chromatography, with yields of 1-2 mg from a 1 litre culture. The binding properties of the recombinant immunotoxin are comparable to those of the scFv; V moreover, as ascertained through cell-proliferation assays, it can selectively poison CD22- expressing cells with an IC50 (i.e. concentration inhibiting 50% of the maximal cell proliferation) around 1-10 nM. It can be concluded that our anti-CD22 immunotoxin combines the binding qualities of the scFv antibody and the potent enzymatic activity of the bacterial toxin. After further characterization we will explore the opportunity to start a process of molecular optimization, aiming at the construction of a novel biotechnological drug for the treatment of hematological malignancies in humans.

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CASTAGNA, Monica. « Targeting CD38 antigen as a therapeutic strategy for hematological malignancies ». Doctoral thesis, 2013. http://hdl.handle.net/11562/537549.

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Il successo di terapie convenzionali come la chemioterapia e la radioterapia per il trattamento delle neoplasie è stato limitato a causa di diversi fattori come la chemioresistenza ai farmaci e la tossicità periferica causata dalla mancanza di specificità di questi approcci. Per questo motivo l’interesse per le terapie selettive che prevedono l’uso di immunotossine, specialmente per il trattamento di tumori ematologici, è in aumento. Le immunotossine sono proteine chimeriche costituite da un ligando selettivo per la cellula bersaglio (dominio di origine anticorpale, citochina o fattore di crescita) che media il legame e l’internalizzazione della porzione tossica legata chimicamente o fusa geneticamente, generalmente rappresentata da una tossina di origine vegetale o batterica che agisce interferendo con la sintesi proteica. In questo lavoro viene descritta la costruzione di nuove proteine di fusione ad uso terapeutico progettate per indurre apoptosi selettivamente in neoplasie umane dei linfociti B e la valutazione dell’effetto potenziante ottenuto attraverso l’associazione delle immunotossine con farmaci coinvolti in meccanismi metabolici intracellulari. Il dominio di legame delle nostre immunotossine è rappresentato da frammenti anticorpali a singola catena (scFv) diretti verso l’antigene CD38, una molecole di superficie espressa ad alti livelli dai linfociti B di un sottogruppo particolarmente aggressivo di Leucemia Linfatica Cronica (CLL) che evolve in una patologia dall’esito prognostico sfavorevole, nota come Sindome di Richter, e dalle plasmacellule tumorali immature nel Mieloma Multiplo (MM). L’scFv è fuso ad una porzione tossica che agisce inibendo il meccanismo della sintesi proteica negli organismi eucarioti e nel caso delle nostre immunotossine è rappresentato da una forma tronca della Esotossina A prodotta dal batterio Pseudomonas aeruginosa (PE40) o in alternativa dalla tossina di origine vegetale saporina. Abbiamo inizialmente progettato una immunotossina con PE40 ed una con saporina contenenti un scFv derivato da un anticorpo monoclonale (mAb) sviluppato e caratterizzato nel nostro laboratorio. Tutti i costrutti ricombinanti sono stati prodotti nel sistema di espressione di origine batterica Escherichia coli e purificati da corpi di inclusione tramite IMAC. Tuttavia, l’scFv 1E8 non ha consentito di preservare l’efficienza di legame dell’anticorpo parentale. Inoltre, le immunotossine ricombinanti ottenute dalla fusione dell’scFv 1E8 con PE40 o saporina hanno mostrato una bassa affinità di legame nei confronti delle cellule bersaglio esprimenti la molecola CD38 e, di conseguenza, è stata rilavata solo una trascurabile attività citotossica. Con la progettazione della forma divalente dell’scFv 1E8, il nostro scopo è stato quello di aumentare l’affinità di legame dei costrutti. Nonostante i risultati sconfortanti del saggio di legame in citometria a flusso, la molecola DIV1E8-SAP ha dimostrato di inibire la sintesi proteica di cellule CD38-positive con una IC50 nell’ordine del sub-nanomolare. Successivamente abbiamo progettato due immunotossine ricombinanti dirette verso l’antigene CD38, il cui dominio di legame era costituito da un scFv derivato da un mAb con una specificità epitopica diversa da quella del precedentemente descritto 1E8. Le immunotossine AT13/5-PE e AT13/5-SAP hanno dimostrato buone proprietà di legame con una elevata affinità e specificità per l’antigene CD38 espresso sulla superficie di cellule derivate da Linfoma di Burkitt e cellule di mieloma. Abbiamo dimostrato l’abilità si queste immunotossine di inibire la sintesi proteica nelle linee cellulari studiate e ne abbiamo chiaramente dimostrato un effetto dose-risposta. Il blocco della sintesi proteica causato dalle immunotossine derivate da AT13/5 ha determinato infine l’innesco del processo di apoptosi e la morte cellulare. Attraverso saggi di apoptosi abbiamo dimostrato la capacità di AT13/5-PE e AT13/5-SAP di indurre apoptosi in cellule Daudi e RPMI8226. Abbiamo perciò provato che l’associazione delle nostre immunotossine con molecole terapeutiche che agiscono su diversi bersagli dalla cascata di traduzione del segnale coinvolta nella crescita cellulare, nella sopravvivenza e nella proliferazione, potrebbe essere sinergica in alcune linee cellulari. In particolare abbiamo osservato che farmaci coinvolti nell’inibizione di Bcl-2, Bcl-xL e Bcl-w (noti come BH3-mimetics) possono aumentare la potenza delle nostre immunotossine. Abbiamo infine dimostrato una prima prova di concetto riguardo l’efficacia delle immunotossine derivate da AT13/5 su linfociti B derivati da pazienti affetti da CLL, tuttavia questo studio necessita di essere implementato con una casistica più ampia.
The success of conventional chemotherapy and radiotherapy for the treatment of cancer has been limited due to several factors like chemoresistance to drugs and peripheral toxicity caused by the lack of specificity of these approaches. For this reason the interest in targeted therapies using immunotoxins (ITs) especially for the treatment of hematological malignancies is increasing. Immunotoxins are chimeric proteins with a cell-selective ligand (antibody-derived domain, cytokine or growth factor) which drives the binding and internalization of a chemically linked or genetically fused toxic portion, generally represented by a plant or bacterial toxin which acts by interfering with protein synthesis. Here we report on the construction of novel therapeutic fusion proteins designed to induce target antigen-restricted apoptosis in human B-cell neoplasias and the evaluation of the potentiating effect obtained by the association of the ITs with drugs involved in intracellular metabolic pathways. The binding portion of our ITs is represented by a single-chain antibody fragment (scFv) directed against CD38 antigen, a surface molecule highly expressed by B lymphocytes of a particularly aggressive sub-group of Chronic Lymphocytic Leukemia (CLL) leading to the prognostically unfavorable Richter’s Syndrome and by the neoplastic immature plasma cells in Multiple Myeloma (MM). The scFv is fused to a toxic portion which acts by inhibiting the mechanism of protein synthesis in eukaryotes and in our ITs is represented by a truncated version of the bacterial toxin Pseudomonas aeruginosa Exotoxin A (PE40) or alternatively by the plant toxin saporin. We firstly designed a PE40- and a saporin-based IT comprising a scFv derived from a monoclonal antibody (mAb) developed and characterized in our laboratory. All the recombinant constructs were produced in the bacterial expression system E. coli and purified from inclusion bodies by IMAC. However, the scFv format (1E8) did not allow to preserve the binding efficiency of the parental monoclonal. Moreover, the recombinant ITs created by the fusion of 1E8 scFv with PE40 or saporin showed a low binding affinity to the CD38 target cells and, as a consequence, only negligible citotoxic activity was detected. With the creation of the divalent form of the 1E8 scFv, our purpose was to increase the binding affinity of the constructs. Despite the discouraging results of the flow-cytometric binding assay, DIV1E8-SAP demonstrated to inhibit protein synthesis of CD38-positive cells with an IC50 in the sub-nanomolar range. Then we designed two anti-CD38 recombinant ITs whose binding portion was a scFv derived from a mAb with an epitope specificity different from that of the previously described 1E8. AT13/5-PE and AT13/5-SAP showed good binding properties with a high affinity and specificity for CD38 antigen expressed on the surface of Burkitt’s lymphoma cells and myeloma cells. We proved the ability of these ITs to inhibit protein synthesis in the cell lines studied and we clearly demonstrated a dose-response effect of the ITs. The arrest of protein synthesis caused by the AT13/5-derived ITs finally leads to the triggering of the apoptotic cascade and to cell death. By using apoptosis assays we demonstrated the capability of AT13/5-PE and AT13/5-SAP to induce apoptosis of Daudi and RPMI8226 cells. Then we proved that the association of our ITs with therapeutic molecules acting on different targets of the signal transduction cascade involved in cell growth, survival and proliferation, could be synergistic in some cell lines. In particular we observed that drugs involved in the Bcl-2, Bcl-xL and Bcl-w inhibition (BH3-mimetics) can increase the potency of our ITs. Finally we demonstrated a first proof of concept about the efficacy of AT13/5-derived ITs on B-lymphocytes derived from CLL patient, but this study needs to be implemented with a wider number of cases.

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Huang, Chia Ju, et 黃佳如. « Cognitive behavioral therapy for depression and anxiety in patients with hematological malignancies ». Thesis, 2011. http://ndltd.ncl.edu.tw/handle/65385533412867466652.

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碩士
長庚大學
護理學系
99
Purpose: Examine the effect of cognitive behavioral therapy on depression and anxiety in hospitalized patients with hematological malignancies. Method: A prospective study with randomization was used. Patients were assigned to one of the three groups: (1) cognitive behavioral therapy (CBT) group (n =17) ( 2) attention control group (n =19), and (3) usual-care control group (n =20). Patients in the cognitive behavioral therapy group received 6 individual CBT interventions for a total of 6 hours. Patients in the attention control group received listening support for a total of 6 hours. The main outcomes were anxiety and depression measured by the Hospital Anxiety and Depression Scale (HADS). Data were collected at baseline (before intervention), during intervention, at completion of intervention, and at 2 and 4 months after intervention. Results: The anxiety level in cognitive behavioral treatment group was significantly lower than that of usual-care group (p =0.04). No significant group effect was found for depression. There was a significant time effect (p =0.00); Patients’ anxiety and depression level decreased along the time. Patients with older age, married, lower education level, lower family income, and pain had higher level of depression. Conclusion: The cognitive behavioral therapy can reduce the anxiety level in patients with hematological malignancies. Depression and anxiety level can also decrease as time going. Key word: Cognitive behavioral therapy, hematological malignancies, depression, anxiety, prospective randomized clinical trial.

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Abdelfatah, Possnert Heba. « Detection of Thymidine Kinase 1 Activity in Whole Blood Using an Oligonucleotide System ». Thesis, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-349265.

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In today’s medical science studies, many tumor markers are being used to monitor cancer cell proliferation, but the number of assays for analysis of these markers are few. The aim of this study was to find an easier and more time-efficient way to measure the activity of a specific tumor marker called tymidine kinase 1 (TK1). This tumor marker is an important enzyme involved in cell proliferation and is a key enzyme in the salvage pathway. TK1 activity is related to the occurrence of hematological malignancies and cell activity and therefore have been used as a marker when monitoring this group of patients in treatment. Measurement of the enzyme activity in this study was performed by using an oligonucleotide assay. Detection of the enzyme activity in whole blood and in plasma has not previously been shown. The TK1 activity measured in whole blood and plasma correlated with TK1 activity measured in serum (R2=0,8651 and R2 =0,9845, respectively). It was found that it is possible to determine the TK1 activity in whole blood but only if the activity was measured on the same day as the blood samples were taken. The results shows that the activity measurement of TK1 in plasma and whole blood can be used as a marker to verify patients' therapy in cancer care. This study is only the beginning and further investigations should be made in the future to determine if the method that is subject to this study has the requested effects.

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Livres sur le sujet "Targeted therapy of hematological malignancies"

Quintás-Cardama, Alfonso. Targeted therapy for solid tumors and hematologic malignancies. Hauppauge, N.Y : Nova Science Publishers, 2010.

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service), SpringerLink (Online, dir. Rare Hematological Malignancies. Boston, MA : Springer Science+Business Media, LLC, 2008.

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Kleinberg, Michael. Managing infections in patients with hematological malignancies. New York : Humana Press, 2010.

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Ansell, Stephen M., et Various. Rare Hematological Malignancies. Springer, 2010.

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Ansell, Stephen M. Rare Hematological Malignancies. Springer, 2008.

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1946-, Cheson Bruce D., dir. Monoclonal antibody therapy of hematologic malignancies. Abingdon : Darwin Scientific, 2001.

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Cimpean, Anca Maria, Andreea Adriana Jitariu et Marius Raica. Growth Factors and Their Corresponding Receptors as Targets for Ovarian Cancer Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0011.

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Ovarian cancer remains one of the most aggressive and difficult to manage malignancies regarding evaluation and therapeutic options. The high mortality persists despite extensive research in the field. Current conventional chemotherapy does not improve disease-free survival and does not decrease recurrences amongst patients. This calls for a stringent reconsideration of the drugs selection, focused on the most targeted strategies and personalization of the therapy. Targeted agents against growth factors and their corresponding receptors are already approved as first- or second-line neoadjuvant therapy with controversial results. This chapter critically discusses the role of growth factors as vascular endothelial growth factor, fibroblast growth factors, or platelet-derived growth factors and their corresponding receptors in the pathogenesis, progression, and selection of therapeutic strategies. Other growth factors, such as nerve growth factor or endocrine gland derived growth factor, seem to have a strong involvement in ovarian carcinogenesis but their actual impact is not fully understood.

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Pereira, Luis F., Mark Bradley, Harold W. Goforth, César A. Alfonso, Joseph Z. Lux, Esteban Martínez et Michael P. Mullen. Overview of HIV-Associated Multimorbidities. Sous la direction de Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding et Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0047.

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With the advent of effective antiretroviral therapy, persons with access to and engagement in HIV medical care and antiretroviral therapy can live longer and remain healthy with what has become a chronic manageable illness. Despite advances in medical care, without access to HIV medical care and antiretroviral therapy or with access but without viral suppression, persons with HIV still experience opportunistic infections and cancers. This chapter reviews the HIV-associated multimorbidities, including pulmonary manifestations, ophthalmological complications, dermatological manifestations, gastrointestinal and hematological illnesses, as well as HIV-associated malignancies. The proposed mechanisms through which HIV may contribute to premature aging are also discussed.

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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Roy A. J. Spence OBE, Miranda Payne et Gareth Morris-Stiff. Biomarkers and cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0040.

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Biomarkers and cancer defines these markers and outlines their role in diagnosis, prognosis, prediction of response, and response assessment of a variety of cancers. Established biomarkers are reviewed, and the potential for development of new biomarkers offered by the dramatic progress in both the understanding of molecular biology and the development of laboratory techniques is emphasised. The field of signal transduction has already proved fruitful, with identification of markers allowing successful targeted therapy in a range of cancers. Progress is anticipated also in tumour imaging, with developments in both MRI and PET. Areas of clinical interest are summarised for breast, lung, colorectal, renal, and CNS malignancies.

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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne et Gareth Morris-Stiff. Principles of chemotherapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0005.

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Principles of radiation oncology outlines the physical and biological effects of ionising radiation, and its use in clinical oncology. Radiobiology, examining the response of tissue to ionising radiation, is described with regards to normal and malignant tissues. The effect of fractionation, the delivery of radiotherapy in a series of repeated exposures, is examined. The damaging effects on normal tissues are considered, particularly nonreversible late effects including carcinogenesis. Therapeutic exposure to ionising radiation is contrasted between radical and palliative radiotherapy. The physical properties of ionising radiation beams are described for superficial x-rays, megavoltage x-rays, and electrons. The process of treatment planning is summarised through beam dosimetry, target and critical organ outlining, dose planning, treatment verification, prescription and delivery. Computerised tomography is used for outlining and for verification, using cone beam CT. 0ther methods for image guided radiotherapy include fiducial markers. Increasingly intensity modulated radiotherapy is proving beneficial in reducing normal tissue damage during radical treatment. Stereotactic radiotherapy is used in the radical treatment of small unresectable malignancies. The clinical use of electron therapy, brachytherapy and intraoperative radiotherapy is described. Nuclear medicine uses unsealed radionuclides in imaging primary malignancies and their metastases, and in targeted radiotherapy. Examples include PET scanning, bone scanning, and radio iodine therapy. Whole body irradiation is used to improve outcomes after high-dose chemotherapy with stem cell or bone marrow transplantation.

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Chapitres de livres sur le sujet "Targeted therapy of hematological malignancies"

Zehnbauer, Barbara, et Mona Nasser. « Targeted Therapy in Hematologic Malignancies ». Dans Hematopathology, 293–323. Totowa, NJ : Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-262-9_9.

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Booth, Christopher H., Lysette Mutkus, Karen Bussard, Erika Spaeth, Michael Andreeff et Frank C. Marini. « Mesenchymal Stem/Stromal Cell-Targeted Therapies for Solid Tumors and Hematological Malignancies ». Dans Targeted Therapy of Acute Myeloid Leukemia, 799–819. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_43.

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Zhang, Yizhuo, Shanqi Guo et Haifeng Zhao. « Epigenetic Regulation and Therapy in Lymphoid Malignancies ». Dans Hematologic Cancers : From Molecular Pathobiology to Targeted Therapeutics, 395–418. Dordrecht : Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5028-9_17.

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Mounier, Nicolas, et Michelle A. Rudek. « Chemotherapy and Interactions with Combination Antiretroviral Therapy ». Dans HIV-associated Hematological Malignancies, 207–14. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26857-6_17.

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Barta, Stefan K. « Coinfection with Hepatitis B or C in People Living with HIV Undergoing Immunosuppressive Therapy ». Dans HIV-associated Hematological Malignancies, 227–34. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26857-6_20.

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Ramesh, Sathyadeepak. « Targeted Therapy for Cutaneous Malignancies ». Dans Foundational Papers in Oculoplastics, 389–400. Cham : Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92794-3_39.

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Furukawa, Nobufusa, et Ali Guermazi. « Abdominal Effects of Therapy in Patients Treated for Hematological Malignancies ». Dans Radiological Imaging in Hematological Malignancies, 473–84. Berlin, Heidelberg : Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18832-9_24.

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Hanna, Soheil L., et Barry D. Fletcher. « Musculoskeletal Effects of Therapy in Patients Treated for Hematological Malignancies ». Dans Radiological Imaging in Hematological Malignancies, 485–509. Berlin, Heidelberg : Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18832-9_25.

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Herbrecht, Raoul, et Yasmine Nivoix. « Antifungal Therapy in Patients with Hematological Malignancies ». Dans Pulmonary Involvement in Patients with Hematological Malignancies, 569–88. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-15742-4_44.

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Guermazi, Ali, Elida VáZquez, Eliane Gluckman et Yves Miaux. « Central Nervous System Effects of Therapy in Patients Treated for Hematological Malignancies ». Dans Radiological Imaging in Hematological Malignancies, 409–41. Berlin, Heidelberg : Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18832-9_22.

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Actes de conférences sur le sujet "Targeted therapy of hematological malignancies"

Shah, Neil P. « Abstract IA16 : Acquired resistance to targeted therapeutics in hematologic malignancies ». Dans Abstracts : AACR Precision Medicine Series : Drug Sensitivity and Resistance : Improving Cancer Therapy ; June 18-21, 2014 ; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-ia16.

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Pearson, Jennifer M., Su-Fern Tan, Arati Sharma, Todd E. Fox, Jose Luis Abad, Gemma Fabrias, David F. Claxton, David J. Feith, Mark Kester et Thomas P. Loughran. « Abstract 48 : Acid ceramidase inhibition : A targeted therapy for acute myeloid leukemia ». Dans 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.hemmal17-48.

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Eckfeldt, Craig E., Robin DW Lee, Emily J. Pomeroy, Alpay N. Temiz, Susan K. Rathe, Jing Ma, Tanja A. Gruber et al. « Abstract B01 : Mechanisms of treatment resistance following Ras targeted therapy in acute myeloid leukemia. » Dans 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-b01.

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Medichelme, Chaitanya, Shagun Juneja, Anirudh Punnakal, Charu Garg, Indu Bansal, Amal Roy Chaudhoory, Anil Kumar Bansal et Anil Kumar Anand. « Retrospective analysis of acute and late gastrointestinal and hematological toxicities with extended field radiation in gynaecological malignancies : A single institution data ». Dans 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685352.

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Purpose: The aim of this study is to report a preliminary analysis of our clinical experience with extended field pelvic (conformal) radiation, with or without concurrent chemotherapy, in gynaecological malignancies. Materials and Methods: 27 women with gynaecological malignancies (17 with Carcinoma Cervix and 10 with Carcinoma Endometrium) were treated between November 2009 and October 2015 with Extended Field abdomino-pelvic radiation. All patients were treated with conformal radiation (Intensity Modulated Radiotherpy or Volumetric Modulated Arc Therapy). All patients underwent CT Simulation followed by target and OAR delineation as per RTOG guidelines. Dose prescriped was 45-50 Gy in 1.8 Gy per fraction and boost to gross node upto 54-56 Gy. Planning was done on Eclipse Planning system, and treatment was delivered on 6 MV linac. Concurrent chemotherapy was given when indicated. All toxicities were scored according to Common Terminology Criteria for Adverse Events (CTCAE v 4.03). Dosimetric parameters were correlated with toxicities. Results: Median follow up was 9.5 months (Range 0-52 months). 14 (51.8%) patients developed Grade 1 and 2 acute hematological toxicity and 1 (0.04%) developed Grade 3 toxicity. 10 (37%) patients developed Grade 1 and 2 acute gastrointestinal toxicity and 1 (0.04%) developed grade 4 toxicity. 3 (11.12%) patients had late toxicity in the form of prolonged leucopenia, SAIO, and Irritable Bowel Syndrome. 1 patient did not complete her treatment due to persistent leucopenia (Grade 3). Conclusion: Extended field Radiation in Gynaecological malignancies is a reasonably well tolerated procedure when treated with IMRT or VMAT, with acceptable toxicity profile.

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Shah, Chintan, Yan Gong, Anita Szady, Qian Sun, carl J. Pepine, Taimour Langaee, Alexandra R. Lucas et Jan S. Moreb. « Abstract 987 : Unanticipated cardiotoxicity due to targeted anti-cancer therapy in hematologic malignancies patients : Natural history and risk factors ». Dans 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.am2017-987.

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Choudhury, Yukti, Chae Yin Cher, Min-Han Tan et Zi Yi Lim. « Abstract A41 : Ultrasensitive detection of diverse genomic alterations in hematological malignancies using a targeted amplicon-based sequencing approach ». Dans Abstracts : AACR Special Conference on Advances in Liquid Biopsies ; January 13-16, 2020 ; Miami, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.liqbiop20-a41.

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Lau, Christopher C., Keith Killian, Yuelin J. Zhu, Yonghong Wang, Marbin Pineda, Anish Thomas, Yisong Wang et al. « Abstract 1999 : A targeted exome sequencing platform for routine clinical molecular profiling of advanced thoracic malignancies relevant to targeted therapy. » Dans Proceedings : AACR 104th Annual Meeting 2013 ; Apr 6-10, 2013 ; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1999.

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Poortinga, Gretchen, Jeannine Diesch, Elaine Sanij, Nadine Hein, Jirawas Sornkum, Donald Cameron, Megan J. Bywater et al. « Abstract A31 : Elucidating mechanisms that cooperate with the therapeutic inhibition of RNA polymerase I to treat MYC-driven hematological malignancies ». Dans Abstracts : AACR Special Conference on Myc : From Biology to Therapy ; January 7-10, 2015 ; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-a31.

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Xu, Jihong, Alessandra Welker, Brandon Miller, Mark Calhoun, Jose Otero, Catherine Czeisler, J. Brad Elder et al. « Abstract 3682 : Characterization of PolyDots, a novel nanomicelle drug delivery system, for targeted therapy of neurological malignancies ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3682.

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Libert, Diane, Constance M. Yuan, Haneen Shalabi, Dalia Salem, Bonnie Yates, Cindy Delbrook, Terry Fry, John Shern, Maryalice Stetler-Stevenson et Nirali Shah. « Abstract 1440 : Evolution of CD19 expression in pediatric B-cell malignancies in the era of targeted therapy ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1440.

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Rapports d'organisations sur le sujet "Targeted therapy of hematological malignancies"

Zhao, Kangjia, Jiwen Sun, Nanping Shen, Mengxue He, Haishan Ruan, Geng Lin, Jiali Ma et Yanhua Xu. Treatment-Related Adverse Events of Chimeric Antigen receptor T-Cell (CAR-T) Cell Therapy in B-cell hematological malignancies in the Pediatric and Young Adult Population : A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, juillet 2022. http://dx.doi.org/10.37766/inplasy2022.7.0034.

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Marenco-Hillembrand, Lina, Michael A. Bamimore, Julio Rosado-Philippi, Blake Perdikis, David N. Abarbanel, Alfredo Quinones-Hinojosa, Kaisorn L. Chaichana et Wendy J. Sherman. The Evolving Landscape of Leptomeningeal Cancer from Solid Tumors : A Systematic Review of Clinical Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, décembre 2022. http://dx.doi.org/10.37766/inplasy2022.12.0112.

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Review question / Objective: Among adult patients with leptomeningeal carcinomatosis from solid tumors (population) treated with chemotherapy, targeted therapy, or immunotherapy (intervention and comparator) what are the differences in overall survival (OS) and progression-free survival (PFS) and treatment response based on clinical trial outcomes? Eligibility criteria: Included articles reported 1) human subjects ≥ 18 years 2) diagnosis of leptomeningeal carcinomatosis from solid tumors confirmed by imaging or cerebrospinal fluid (CSF) cytology and clinical or neurological symptoms 3) clinical trials 4) with either PFS or MOS outcomes listed. Book chapters, case reports, review articles, observational studies, ed-itorials, and publications of leptomeningeal cancer from hematological tumors and studies consisting solely of pediatric patients were excluded from the analysis.

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