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dc.contributor.authorSouza, Iandara Maíra Lopes de-
dc.date.available2023-11-24-
dc.date.available2023-11-27T14:40:52Z-
dc.date.issued2023-07-27-
dc.identifier.urihttp://repositorioinstitucional.uea.edu.br//handle/riuea/5374-
dc.description.abstractChronic Myeloid Leukemia is a hematologic malignancy that affects cells of the myeloid lineage. The vast majority of patients have the Philadelphia chromosome, which produces a hybrid protein with increased tyrosine kinase activity. Treatment is performed with tyrosine kinase inhibitors, which block oncoprotein expression. The inhibitors act in the control of immature cells, being of extreme importance the molecular monitoring of the patients. In recent years, the importance of microvesicles has been studied, as they can be used as a marker of relapse during the disease, and provide information on drug resistance. Since they play an important role in intercellular communication and studies indicate that their release increases in pathological processes. The aim of this study was to characterize the profile of microvesicles in patients with Chronic Myeloid Leukemia at diagnosis and during the first year of treatment. This research is a descriptive and exploratory study, of the bidirectional type. Thirty patients of both sexes were recruited, divided into two groups: 15 patients with CML, and 15 blood donors, as a control group. Peripheral blood samples were collected from patients in four moments (at diagnosis, in cytoreduction, 3 months and 6 months of treatment with tyrosine kinase inhibitors), while in the control group peripheral blood was collected in only one moment. The samples were processed and phenotypic quantifications and analyzes were performed through the flow cytometry technique using surface markers to identify progenitor cells, myeloid cells, leukocytes, dendritic cells, monocytes, neutrophils, T cells, B cells, platelets, erythrocytes and endothelial cells. The research results showed that microvesicles released from progenitor cells (CD34), neutrophils (CD16 and CD66), erythrocytes (CD235a), dendritic cells (CD11c) and endothelial cells (CD51/61) are significantly more expressed in patients with CML than diagnosis compared to the control group. However, at the beginning of treatment with tyrosine kinase inhibitors, a decrease in the amount of microvesicles released from progenitor cells, myeloid cells, leukocytes, dendritic cells, monocytes, neutrophils, T cells, B cells, erythrocytes and endothelial cells can be observed. In addition, changes in the interactions between populations of microvesicles can be observed over the course of patient follow-up. Future investigations are needed with a larger number of participants and with longer follow-up, in order to validate these findingspt_BR
dc.languageporpt_BR
dc.publisherUniversidade do Estado do Amazonaspt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectLeucemia mieloide crônicapt_BR
dc.subjectVesículas extracelularespt_BR
dc.subjectMicrovesículaspt_BR
dc.subjectCélulas hematopoéticaspt_BR
dc.subjectchronic myeloid leukemiapt_BR
dc.titleCaracterização das microvesículas circulantes e seu potencial uso como biomarcador no diagnóstico e tratamento de pacientes com LMCpt_BR
dc.title.alternativeCharacterization of circulating microvesicles and their potential use as a biomarker in the diagnosis and treatment of patients with CMLpt_BR
dc.typeDissertaçãopt_BR
dc.date.accessioned2023-11-27T14:40:52Z-
dc.contributor.advisor-co1Costa, Allyson Guimarães da-
dc.contributor.advisor-co1Latteshttp://lattes.cnpq.br/7531662673281014pt_BR
dc.contributor.advisor1Tarragô, Andréa Monteiro-
dc.contributor.advisor1Latteshttp://lattes.cnpq.br/4644326589690231pt_BR
dc.contributor.referee1Tarragô, Andréa Monteiro-
dc.contributor.referee1Latteshttp://lattes.cnpq.br/4644326589690231pt_BR
dc.contributor.referee2Almeida, Maria Edilene Martins de-
dc.contributor.referee2Latteshttp://lattes.cnpq.br/9637683978812335pt_BR
dc.contributor.referee3Mourão, Lucivana Prata de Souza-
dc.contributor.referee3Latteshttp://lattes.cnpq.br/1135734404648095pt_BR
dc.creator.Latteshttp://lattes.cnpq.br/7592758890357555pt_BR
dc.description.resumoA Leucemia Mieloide Crônica é uma neoplasia hematológica que afeta as células da linhagem mieloide. A grande maioria dos pacientes apresentam o cromossomo Philadelphia, que produz uma proteína híbrida com a atividade tirosina quinase aumentada. O tratamento é realizado com inibidores tirosina quinase, que bloqueiam a expressão da oncoproteína. Os inibidores atuam no controle de células imaturas sendo de extrema importância o monitoramento molecular dos pacientes. Nos últimos anos tem sido estudado a importância das Microvesículas, pois elas podem ser usadas como marcador de recidiva durante a doença, e fornecer informações sobre resistência à farmacos. Visto que elas têm um papel importante na comunicação intercelular e estudos indicam que sua liberação aumenta em processos patológicos. O objetivo deste estudo foi caracterizar o perfil de Microvesículas em pacientes com Leucemia Mieloide Crônica ao diagnóstico e durante o primeiro ano de tratamento. Esta pesquisa se trata de um estudo descritivo e exploratório, do tipo bidirecional. Foram recrutados trinta pacientes de ambos os sexos, divididos em dois grupos: 15 pacientes com LMC, e 15 doadores de sangue, como grupo controle. As coletas das amostras de sangue periférico dos pacientes foram realizadas em quatro momentos (ao diagnóstico, em citorredução, 3 meses e 6 meses de tratamento com inibidores tirosina quinase), enquanto que no grupo controle coletou-se sangue periférico em apenas um momento. As amostras foram processadas e foram realizadas as quantificações e análises fenotípicas através da técnica de Citometria de fluxo usando marcadores de superfície para identificar células progenitoras, células mieloides, leucócitos, células dendríticas, monócitos, neutrófilos, células T, células B, plaquetas, eritrócitos e células endoteliais. Os resultados da pesquisa demonstraram que as microvesículas liberas de células progenitoras (CD34), neutrófilos (CD16 e CD66), eritrócitos (CD235a), células dendríticas (CD11c) e células endoteliais (CD51/61) são significativamente mais expressas nos pacientes com LMC ao diagnóstico em comparação ao grupo controle. Contudo, ao inicio do tratamento com inibidores tirosina quinase, pode-se observar a diminuição da quantidade de microvesículas liberadas de células progenitoras, células mieloides, leucócitos, células dendríticas, monócitos, neutrófilos, células T, células B, eritrócitos e células endoteliais. Além disso, foram observadas mudanças nas interações entre as populações de microvesículas ao longo do acompanhamento dos pacientes. Investigações futuras são necessárias com o número maior de participantes e os acompanhando por mais tempo, para assim validar esses achados.pt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.programPPGH -PROGRAMA DE PÓS-GRADUAÇÃO EM CIÊNCIAS APLICADAS À HEMATOLOGIApt_BR
dc.relation.references1. Swerdlow SH et al. WHO Classification of tumours of haematopoietic and lymphoid tissues. World Health Organization. 2017. 2. Santos VM dos, Leite RG de M, Ferreira KF, Miranda T do A, Aguiar CN. Diagnóstico de leucemia mieloide crônica em fase acelerada: relato de caso. Brasília Médica. 2018;55:22–6. 3. Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2022 update on diagnosis, therapy, and monitoring. Am J Hematol. 2022;97:1236–56. 4. Vieira F da C, Bonito D, Borducchi DM, del Giglio A, Bollmann PW. Desfecho e preditores de resposta aos inibidores de Tirosinoquinase de 2a geração em pacientes com Leucemia Mielóide Crônica em fase crônica resistentes ao Imatinibe. Clin Oncol Lett. 2018;3(01–02):45–52. 5. Apperley JF. Chronic myeloid leukaemia. Lancet [Internet]. 2015;385(9976):1447–59. Available at: http://dx.doi.org/10.1016/S0140-6736(13)62120-0 6. Azevedo LD, Bastos MM, Oliveira AP de;,Boechat N. Sínteses e propriedades de fármacos inibidores da tirosina quinase BCR-ABL, utilizados no tratamento da leucemia mieloide crônica. Quim Nov [Internet]. 2017;40(7):791–809. Available at: http://dx.doi.org/10.21577/0100- 4042.20170027 7. Bonavigo AG, Sarturi PR. Comparação entre o diagnóstico citogenético e por biologia molecular das leucemias mieloides crônicas (LMC): uma revisão bibliográfica Comparison between cytogenetic and molecular biology diagnosis of chronic myeloid leukemias (CML): a bibliographic r. RBAC. 2018;50:47–50. 8. Deininger MW, Shah NP, Altman JK, Berman E, Bhatia R, Bhatnagar B, et al. Chronic myeloid leukemia, version 2.2021. JNCCN J Natl Compr Cancer Netw. 2020;18(10):1385–415. 9. Bruford EA, Antonescu CR, Carroll AJ, Chinnaiyan A, Cree IA, Cross NCP, et al. HUGO Gene Nomenclature Committee (HGNC) recommendations for the designation of gene fusions. Leukemia. 2021;35:3040–3. 10. Leukemia WHO Classification of Haematolymphoid Tumours, 5th edition, 2022 [Internet]. Springer Nature. 2022. Available at: https://doi.org/10.1038/s41375-022-01625- x%0AINTRODUCTION 11. Martins P, Andrade RJ. Tratamento da leucemia mieloide crônica com inibidores da tirosino quinase. Rev Thêma Sci. 2018;8(no 1E):161–71. 12. Sampaio MM et al. Chronic myeloid leukemia-from the Philadelphia chromosome to specific target drugs: A literature review. In: World Journal of Clinical Oncology. 2021. p. 69–94. 13. Hu Y, Li Q, Hou M, Peng J, Yang X, Xu S. Magnitude and temporal trend of the chronic myeloid leukemia: on the basis of the global burden of disease study 2019. JCO Glob Oncol. 2021;(7):1429–41. 14. Bavaro L, Martelli M, Cavo M, Soverini S. Mechanisms of disease progression and resistence to tyrosine kinase inhibitor therapy in chronic myeloid leukemia: An update. Int J Mol Sci. 80 2019;20:1–23. 15. Hochhaus A, Baccarani M, Silver RT, Schiffer C, Apperley JF, Cervantes F, et al. European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia. Leukemia [Internet]. 2020;34(4):966–84. Available at: http://dx.doi.org/10.1038/s41375-020-0776-2 16.Ribeiro AC de A, Pratti JES, Nogueira TA, Cordeiro BC. Acompanhamento farmacoterpêutico e a detecção de reações adversas a inibidores de tirosinoquinase utilizados no tratamento da leucemia mielóide crônica / Pharmacotherapeutic follow-up and detection of adverse reactions to tyrosinokinase inhibitors used in. Brazilian J Heal Rev. 2020;3(6):19438–54. 17. Dingli D, Traulsen A, Pacheco JM. Chronic Myeloid Leukemia: Origin, Development, Response to Therapy, and Relapse. Clin Leuk. 2008;2(2):133–9. 18. Moisoiu V, Teodorescu P, Parajdi L, Pasca S, Zdrenghea M, Dima D, et al. Assessing measurable residual disease in chronic myeloid leukemia. BCR-ABL1 IS in the avant-garde of molecular hematology. Front Oncol. 2019;9(September):1–8. 19. Cross NCP, White HE, Colomer D, Ehrencrona H, Foroni L, Gottardi E, et al. Laboratory recommendations for scoring deep molecular responses following treatment for chronic myeloid leukemia. Leukemia. 2015;29(5):999–1003. 20. Cavalcanti, Heloísa Nelson; Silva Fiho, Tiago João; Queiroz LMG. Vesículas extracelulares: o que sabemos até agora. Clin Lab Res Dent. 2021;1–8. 21. Sedgwick AE, D’Souza-Schorey C. The biology of extracellular microvesicles. Traffic. 2018;19(5):319–27. 22. Aharon A, Rebibo-Sabbah A, Tzoran I, Levin C. Extracellular vesicles in hematological disorders. Rambam Maimonides Med J. 2014;5(4):e0032. 23. Meldolesi J. Exosomes and Ectosomes in Intercellular Communication. Curr Biol [Internet]. 2018;28(8):R435–44. Available at: https://doi.org/10.1016/j.cub.2018.01.059 24. Bode AP, Hickerson DHM. Characterization and quantitation by flow cytometry of membranous microparticles formed during activation of platelet suspensions with ionophore or thrombin. Platelets. 2000;11(5):259–71. 25. Taylor R. Interpreation of the correlation coefficients: A Basic Review. J Diagnostic Med Sonogr. 1990;6(1):35–9. 26. Hughes A, Clarson J, Tang C, Vidovic L, White DL, Hughes TP, et al. CML patients with deep molecular responses to TKI have restored immune effectors and decreased PD-1 and immune suppressors. Blood. 2017;129(9):1166–76. 27. Li Q, Zhong Z, Zeng C, Meng L, Li C, Luo Y, et al. A clinical observation of chinese chronic myelogenous leukemia patients after discontinuation of tyrosine kinase inhibitors. Oncotarget. 2016;7(36):58234–43. 28. García-Suárez J, Gil-Fernández JJ. Epidemiología de la leucemia mieloide crónica en España y sus posibles implicaciones terapéuticas. Rev Clin Esp [Internet]. 2016;216(6):311–2. Available 81 at: http://dx.doi.org/10.1016/j.rce.2016.05.003 29. Harrington P, Dillon R, Radia D, McLornan D, Woodley C, Asirvatham S, et al. Chronic myeloid leukaemia patients at diagnosis and resistant to tyrosine kinase inhibitor therapy display exhausted T-cell phenotype. Br J Haematol. 2022;198:1011–5. 30. Alves R de CS. Análise de pacientes com leucemia mieloide crônica com resistência primária ou secundária ao mesilato de imatinibe. Rev Bras Hematol e Hemoteraia. 2009;31(3):166–77. 31. Albuquerque PMS de, Ximenes DIJ, Diniz M de FFM. Avaliação da qualidade de vida de portadores de leucemia mieloide crônica em João Pessoa-PB no período de 2015 a 2016. Rev Eletrônica Acervo Saúde / Electron J Collect Heal REAS/EJCH. 2019;11(14):1–8. 32. Dal Ponte ES, Wagner SC, Linden R, Schirmer H. Study of correlation between imatinib mesylate plasma levels and hematological profile of patients undergoing treatment for chronic myeloid leukemia. J Bras Patol e Med Lab. 2017;53(3):159–64. 33. Oliveira RF, Maia MM, Sousa RD. Leucemia Mieloide Crônica (LMC): aspectos fisiopatológicos, diagnóstico e tratamentos. Rev FIMCA. 2021;8(1):12–8. 34. Himmelstein MS, Sanchez DT. Masculinity impediments: internalized masculinity contributes to healthcare avoidance in men and women. J Health Psychol. 2016;21(7):1283–92. 35. Gomes R, Nascimento EF do, Araújo FC. Por que os homens buscam menos os serviços de saúde do que as mulheres? As explicações de homens com baixa escolaridade e homens com ensino superior Why do men use health services less than women? Explanations by men with low versus higher education. Cad Saúde Publica - Rio Janeiro. 2007;23(3):565–74. 36. Lucena R. Os homens (ainda) não vão ao médico [Internet]. Diário de Pernabunco. 2019. Available at: https://www.diariodepernambuco.com.br/noticia/opiniao/2019/10/os-homensainda- nao-vao-ao-medico.html 37. Sossela FR, Zoppas BC de A, Weber LP. Leucemia Mieloide Crônica: aspectos clínicos, diagnóstico e principais alterações observadas no hemograma. Rev Bras Análises Clínicas. 2017;49(2):127–30. 38. Bonfim ACS, Anjos BS, França KFC, Couto LA, Santos RWF, Santana VHS, et al. O papel da citogenética e da biologia molecular no diagnóstico da leucemia mieloide crônica. Brazilian J Heal Rev. 2022;5(2):5153–64. 39. Viganò I, Di Giacomo N, Bozzani S, Antolini L, Piazza R, Gambacorti Passerini C. First-line treatment of 102 chronic myeloid leukemia patients with imatinib: A long-term single institution analysis. Am J Hematol. 2014;89(10):E184–7. 40. Yang H, Zhou H, Huang Z, Tao K, Huang N, Peng Z, et al. Induction of CML-specific immune response through cross-presentation triggered by CTP-mediated BCR-ABL-derived peptides. Cancer Lett. 2020;482:44–55. 41. Jabbour E, Saglio G, Hughes TP, Kantarjian H. Suboptimal responses in chronic myeloid leukemia: Implications and management strategies. Cancer. 2012;118(5):1181–91. 82 42. Bernardi S, Farina M. Exosomes and extracellular vesicles in myeloid Neoplasia: The multiple and complex roles played by these “magic bullets”. Biology (Basel). 2021;10(2):1–24. 43. Hsieh YC, Kirschner K, Copland M. Improving outcomes in chronic myeloid leukemia through harnessing the immunological landscape. Leukemia [Internet]. 2021;35(5):1229–42. Available at: http://dx.doi.org/10.1038/s41375-021-01238-w 44. Hughes A, Yong ASM. Immune effector recovery in chronic myeloid leukemia and treatmentfree remission. Front Immunol. 2017;8(469):1–12. 45. Al-amleh EK, Al-sanabra OM, Alqaisi KM, Alqaraleh M, Al-nahal J, Hamadneh L, et al. Investigation of the effect of imatinib and hydroxyurea combination therapy on hematological parameters and gene expression in chronic myeloid leukemia (CML) patients. J Clin Med. 2022;11(4954):1–15. 46. Cortes J, Kantarjian H. How I treat newly diagnosed chronic phase CML. Blood [Internet]. 2012;120(7):1390–7. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916560/ 47. Kapor S, Čokić V, Santibanez JF. Mechanisms of hydroxyurea-induced cellular senescence: an oxidative stress connection? Oxid Med Cell Longev [Internet]. 2021;2021. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8545575/ 48. Huang M, Facca C, Fatmi Z, Baïlle D, Bénakli S, Vernis L. DNA replication inhibitor hydroxyurea alters Fe-S centers by producing reactive oxygen species in vivo. Sci Rep. 2016;6(29361):1–12. 49. Santos SS, dos Santos IG, Silva CV da, Cazedey ECL. Qualitative Analýsis of Hydroxyurea. Drug Anal Res [Internet]. 2020;4(1):18–21. Available at: https://seer.ufrgs.br/index.php/dar/article/view/100682/58267 50. Singh A, Xu Y. The Cell killing mechanisms of hydroxyurea. Genes (Basel). 2016;7(99):1– 15. 51. Aswad MH, Kissova J, Ovesna P, Rihova L, Penka M. The clinical significance of circulating microparticles concerning thrombosis in BCR/ABL1-negative myeloproliferative neoplasms. In Vivo (Brooklyn). 2021;35:3345–53. 52. Zhu X, You Y, Li Q, Zeng C, Fu F, Guo A, et al. BCR-ABL1-positive microvesicles transform normal hematopoietic transplants through genomic instability: Implications for donor cell leukemia. Leukemia. 2014;28(8):1666–75. 53. Muralidharan-Chari V, Clancy JW, Sedgwick A, D’Souza-Schorey C. Microvesicles: Mediators of extracellular communication during cancer progression. J Cell Sci. 2010;123(10):1603–11. 54. Taylor DD, Gercel-taylor C. The origin, function, and diagnostic potential of RNA within extracellular vesicles present in human biological fluids. Front Genet. 2013;4(142):1–12. 55. Georgatzakou HT, Fortis SP, Papageorgiou EG, Antonelou MH, Kriebardis AG. Blood cellderived microvesicles in hematological diseases and beyond. Biomolecules. 2022;12(803):1–30. 83 56. Pelissier Vatter FA, Cioffi M, Hanna SJ, Castarede I, Caielli S, Pascual V, et al. Extracellular vesicle- and particle-mediated communication shapes innate and adaptive immune responses. J Exp Med. 2021;218(8):1–14. 57. Ehsanpour A, Saki N, Bagheri M, Behzad MM, Abroun S. The expression of microvesicles in leukemia: Prognostic approaches. Cell J. 2018;21(2):115–23. 58. Miljkovic-Licina M, Arraud N, Zahra AD, Ropraz P, Matthes T. Quantification and phenotypic characterization of extracellular vesicles from patients with acute myeloid and B-cell lymphoblastic leukemia. Cancers (Basel). 2022;14(1). 59. Lin G, Finger E, Gutierrez-ramos JC. Expression of CD34 in endothelial cells, hematopoietic progenitors and nervous cells in fetal and adult mouse tissues. Eur J Immunol. 1995;25:1508–16. 60. Kaplan D, Husel W, Lewandowska K. CD34 expression on platelets. Platelets. 2003;14(2):83–7. 61. Sidney LE, Branch MJ, Dunphy S, Dua HS, Hopkinson A. Concise Review: Evidence for CD34 as a Common Marker for Diverse Progenitors. Stem Cells. 2014;32:1380–9. 62. Harada I, Sasaki H, Murakami K, Nishiyama A, Nakabayashi J. Compromised anti ‑ tumor – immune features of myeloid cell components in chronic myeloid leukemia patients. Nat Portf. 2021;11:1–10. 63. Durai V, Murphy KM. Functions of murine dendritic cells. Immunity. 2016;45(4):719–36. 64. Berckmans RJ, Nieuwland R, Böing AN, Romijn FP, Hack CE, Sturk A. Cell-derived microparticles circulate in healthy humans and support low grade thrombin generation. Thromb Haemost. 2001;85(4):639–46. 65. Reeves BN, Beckman JD. Novel pathophysiological mechanisms of thrombosis in myeloproliferative neoplasms. Curr Hematol Malig Rep. 2021;16(3):304–13. 66. Hasselbalch HC, Elvers M, Schafer AI. The pathobiology of thrombosis, microvascular disease, and hemorrhage in the myeloproliferative neoplasms. Blood. 2021;137(16):2152–60. 67. Van Der Meijden PEJ, Van Schilfgaarde M, Van Oerle R, Renné T, Ten Cate H. Platelet- and erythrocyte-derived microparticles trigger thrombin generation via factor XIIa. J Thromb Haemost. 2012;10:1355–62. 68. Tissot J, Rubin O, Canellini G. Analysis and clinical relevance of microparticles from red blood cells. Curr Opin Hematol. 2010;17(6):571–7. 69. Tuzovic M, Herrmann J, Iliescu C, Marmagkiolis K, Ziaeian B, Yang EH. Health Research Alliance. Curr Treat Options Cardiovasc Med. 2018;20(5). 70. Moliterno AR, Ginzburg YZ, Hoffman R. Clinical insights into the origins of thrombosis in myeloproliferative neoplasms. Blood. 2021;137(9):1145–53. 71. Hultcrantz M, Björkholm M, Dickman PW, Landgren O, Derolf AR, Kristinsson SY, et al. Risk of Arterial and Venous Thrombosis in Patients with Myeloproliferative Neoplasms: A population-based cohort study. Ann Intern Med. 2018;168(5):317–25. 84 72. Chauffaille M de LLF. Neoplasias mieloproliferativas: revisão dos critérios diagnósticos e dos aspectos clínicos. Rev Bras Hematol Hemoter. 2010;32(4):308–16. 73. Kolonics F, Kajdacsi E, Farkas VJ, Veres DS, Khamari D, Kittel A, et al. Neutrophils produce proinflammatory or anti-inflammatory extracellular vesicles depending on the environmental conditions. J Leukoc Biol. 2021;109(4):793–806. 74. Johnson III BJ, Kuethe JW, Caldwell CC. Neutrophil Derived Microvesicles: Emerging Role of a Key Mediator to the Immune Response. Endocr Metab Immune Disord Drug Targets. 2014;14(3):210–7. 75. Craver BM, Alaoui K El, Scherber RM, Fleischman AG. The Critical role of inflammation in the pathogenesis and progression of myeloid malignancies. Cancers (Basel). 2018;10(104):1–18. 76. Yates AG, Pink RC, Erdbrügger U, Siljander PR, Dellar ER, Pantazi P, et al. In sickness and in health: The functional role of extracellular vesicles in physiology and pathology in vivo. J Extracell vesicles. 2022;11(1). 77. Lim K, Hyun Y, Lambert-emo K, Capece T, Bae S, Miller R, et al. Neutrophil trails guide influenza-specific CD8 + T cells in the airways. Science (80- ). 2015;349(6252). 78. Kornek M, Popov Y, Libermann TA, Afdhal NH, Schuppan D. Human T cell microparticles circulate in blood of hepatitis patients and induce fibrolytic activation of hepatic stellate cells. Hepatology. 2011;53(1):230–42. 79. Caivano A, Laurenzana I, De Luca L, La Rocca F, Simeon V, Trino S, et al. High serum levels of extracellular vesicles expressing malignancy-related markers are released in patients with various types of hematological neoplastic disorders. Tumor Biol. 2015;36(12):9739–52. 80. Brück O, Blom S, Dufva O, Turkki R, Chheda H, Ribeiro A, et al. Immune cell contexture in the bone marrow tumor microenvironment impacts therapy response in CML. Leukemia. 2018;32:1643–56. 81. Raimondo S, Corrado C, Raimondi L, De Leo G, Alessandro R. Role of extracellular vesicles in hematological malignancies. Biomed Res Int. 2015;2015. 82. Cai J, Wu G, Tan X, Han Y, Chen C, Li C, et al. Transferred BCR/ABL DNA from K562 extracellular vesicles causes chronic myeloid leukemia in immunodeficient mice. PLoS One. 2014;9(8):1–11. 83. Fu FF, Zhu XJ, Wang HX, Zhang LM, Yuan GL, Chen ZC, et al. BCR-ABL1-positive microvesicles malignantly transform human bone marrow mesenchymal stem cells in vitro. Acta Pharmacol Sin [Internet]. 2017;38(11):1475–85. Available at: http://dx.doi.org/10.1038/aps.2017.116 84. Trino S, Lamorte D, Caivano A, De Luca L, Sgambato A, Laurenzana I. Clinical relevance of extracellular vesicles in hematological neoplasms: from liquid biopsy to cell biopsy. Leukemia [Internet]. 2021;35(3):661–78. Available at: http://dx.doi.org/10.1038/s41375-020-01104-1 85. Kang K, Jung J, Hur W, Park J, Shin H, Choi B, et al. The potential of exosomes derived from 85 chronic myelogenous leukaemia cells as a biomarker. Anticancer Res. 2018;38:3935–42. 86. Bernardi S, Malagola M, Polverelli N, Russo D. Exosomes in chronic myeloid leukemia: are we reading a new reliable message? Acta Haematol. 2020;143:509–10. 87. Ghafouri-fard S, Niazi V, Taheri M. Contribution of extracellular vesicles in normal hematopoiesis and hematological malignancies. Heliyon. 2021;7(e06030). 88. Zhang J, Zhao A, Sun L, Chen W, Zhang H, Chen Z, et al. Selective surface marker and miRNA profiles of CD34+ blast-derived microvesicles in chronic myelogenous leukemia. Oncol Lett. 2017;14(2):1866–74. 89. Houshmand M, Simonetti G, Circosta P, Gaidano V, Cignetti A, Martinelli G, et al. Chronic myeloid leukemia stem cells. Leukemia. 2019;33:1543–56. 90. de Almeida FC, Berzoti-Coelho MG, Toro DM, Cacemiro M da C, Bassan VL, Barretto GD, et al. Bioactive lipids as chronic myeloid leukemia’s potential biomarkers for disease progression and response to tyrosine kinase inhibitors. Front Immunol. 2022;13(840173):1–8pt_BR
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