Academic literature on the topic 'Targeted therapy of hematological malignancie'

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Journal articles on the topic "Targeted therapy of hematological malignancie"

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Armitage, James O. "Targeted therapy and hematological malignancy." Targeted Oncology 4, no. 1 (February 14, 2009): 1–2. http://dx.doi.org/10.1007/s11523-008-0098-1.

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Kachlany, Scott C., Amy Le, and Benjamin A. Belinka. "Leukotoxin (Leukothera™), a Targeted Therapy for Hematological Malignancies." Blood 116, no. 21 (November 19, 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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Joshi, Dolly, Kanjaksha Gosh, and Babu Rao Vundinti. "MicroRNAs in hematological malignancies: a novel approach to targeted therapy." Hematology 17, no. 3 (May 2012): 170–75. http://dx.doi.org/10.1179/102453312x13376952196656.

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Ma, Haiqing, Saradhi Mallampati, Gang An, and 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, and Johannes Pawlowski. "Target Therapy in Hematological Malignances: New Monoclonal Antibodies." International Scholarly Research Notices 2014 (October 30, 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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Liang, Xuewu, Hong Liu, and Yingjie Zhang. "Novel-targeted therapy for hematological malignancies with JAK and HDAC dual inhibitors." Future Medicinal Chemistry 11, no. 15 (August 2019): 1849–52. http://dx.doi.org/10.4155/fmc-2019-0168.

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

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Kim, Miyoung, Jane Snowdon, S. Dilhan Weeraratne, Winnie Felix, Lionel Lim, Irene Dankwa-Mullan, Young Kyung Lee, et al. "Clinical insights for hematological malignancies from an artificial intelligence decision-support tool." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e13023-e13023. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13023.

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e13023 Background: Next generation sequencing (NGS) in hematological tumors is increasingly shaping clinical treatment decisions at the point of care. While the impact of NGS panels in solid tumors is largely therapeutic, targeted sequencing in hematological tumors can additionally provide diagnostic and prognostic insights. Additional data generated in hematological tumor sequencing makes manual interpretation and annotation of variants tedious and non-scalable. In this study we compared hematological tumor variant interpretation using an artificial intelligence decision-support system, Watsonä for Genomics (WfG), with expert guided manual curation. Methods: Patients with hematological tumors at Hallym University, College of Medicine between December 2017 and December 2018, were sequenced using the 54 gene Illumina TruSight Myeloid Panel. WfG interpreted and annotated all patients’ sequencing results, a subset of which were assessed manually to ascertain concordance. Results: 54 South Korean patients with hematological malignancies were analyzed (23 Acute Myeloid Leukemia, 12 myeloproliferative neoplasm, 5 myelodysplastic syndrome, 5 multiple myeloma and 9 others). Comparison of manual and WfG interpretation of 10 randomly selected cases yielded 90% (9/10) concordance and identification of 9 clinically actionable variants (33%) not found in manual interpretation. In total, WfG identified that 71% (38/54) of all cases had at least one clinically actionable therapeutic alteration (a variant targeted by a US FDA approved drug, off-label drug, or clinical trial). 33% (18/54) of cases had genes that were targeted by a US FDA approved therapy including JAK2, IDH1, IDH2, and FLT3. In cases without therapeutic alterations, WfG identified diagnostic or prognostic insights in an additional 20% (11/54) of patients. 9% (5/54) had no clinically actionable information. Conclusions: WfG variant interpretation correlated well with manually curated expert opinion and identified clinically actionable insights missed by manual interpretation. WfG has obviated the need for labor-intensive manual curation of clinical trials and therapy, enabling our center to exponentially scale our NGS operations.
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Miloudi, Hadjer, Vincent Camus, Antoine Taly, Brigitte Sola, and Fabrice Jardin. "Exportin 1 (or XPO1) abnormalities in hematological malignancies: from the gene to targeted therapy." Hématologie 23, no. 1 (January 2017): 43–56. http://dx.doi.org/10.1684/hma.2017.1208.

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Dissertations / Theses on the topic "Targeted therapy of hematological malignancie"

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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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Books on the topic "Targeted therapy of hematological malignancie"

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

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Book chapters on the topic "Targeted therapy of hematological malignancie"

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Booth, Christopher H., Lysette Mutkus, Karen Bussard, Erika Spaeth, Michael Andreeff, and Frank C. Marini. "Mesenchymal Stem/Stromal Cell-Targeted Therapies for Solid Tumors and Hematological Malignancies." In 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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Zehnbauer, Barbara, and Mona Nasser. "Targeted Therapy in Hematologic Malignancies." In Hematopathology, 293–323. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-262-9_9.

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Zhang, Yizhuo, Shanqi Guo, and Haifeng Zhao. "Epigenetic Regulation and Therapy in Lymphoid Malignancies." In 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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Prebet, Thomas, and Steven D. Gore. "Development of Epigenetic Targeted Therapies in Hematological Malignancies." In Epigenetic Cancer Therapy, 169–87. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-800206-3.00008-2.

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Satwani, Prakash, and Alan S. Wayne. "Antibody-Targeted Therapy for Children, Adolescents and Young Adults with Hematological Malignancies." In Hematological Malignancies in Children, Adolescents and Young Adults, 403–19. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814299619_0021.

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Samal, Priyanka, and Shahani Begum. "Drug loaded nanomaterials for hematological malignancies diagnosis and enhanced targeted therapy." In Advanced Nanomaterials for Point of Care Diagnosis and Therapy, 383–98. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-85725-3.00016-7.

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Shukry, Safa, Fadhel Hariri, and Abdul Wahab Al-Nehmi. "Target Therapy in Hematological Malignancies." In Advances in Hematologic Malignancies. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.84696.

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Coltoff, Alexander R., and Joseph G. Jurcic. "Targeted radionuclide therapy of hematologic malignancies." In Reference Module in Biomedical Sciences. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-12-822960-6.00117-4.

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Gewirtz, Alan M. "Nucleic Acid-Based, mRNA-Targeted Therapeutics for Hematologic Malignancies." In Innovative Leukemia and Lymphoma Therapy, 311–27. CRC Press, 2019. http://dx.doi.org/10.1201/9780429114670-13.

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Conference papers on the topic "Targeted therapy of hematological malignancie"

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Shah, Neil P. "Abstract IA16: Acquired resistance to targeted therapeutics in hematologic malignancies." In 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, and Thomas P. Loughran. "Abstract 48: Acid ceramidase inhibition: A targeted therapy for acute myeloid leukemia." 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.hemmal17-48.

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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." 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-b01.

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Medichelme, Chaitanya, Shagun Juneja, Anirudh Punnakal, Charu Garg, Indu Bansal, Amal Roy Chaudhoory, Anil Kumar Bansal, and Anil Kumar Anand. "Retrospective analysis of acute and late gastrointestinal and hematological toxicities with extended field radiation in gynaecological malignancies: A single institution data." In 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, and Jan S. Moreb. "Abstract 987: Unanticipated cardiotoxicity due to targeted anti-cancer therapy in hematologic malignancies patients: Natural history and risk factors." 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.am2017-987.

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Reports on the topic "Targeted therapy of hematological malignancie"

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Marenco-Hillembrand, Lina, Michael A. Bamimore, Julio Rosado-Philippi, Blake Perdikis, David N. Abarbanel, Alfredo Quinones-Hinojosa, Kaisorn L. Chaichana, and 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, December 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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