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Добірка наукової літератури з теми "Leukemia Physiopathology"
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Статті в журналах з теми "Leukemia Physiopathology"
Mitani, Kinuko. "11. Molecular Physiopathology and Molecular Targeting Therapy of Leukemia." Nihon Naika Gakkai Zasshi 96, no. 9 (2007): 2013–19. http://dx.doi.org/10.2169/naika.96.2013.
Повний текст джерелаMitani, Kinuko. "11. Molecular Physiopathology and Molecular Targeting Therapy of Leukemia." Nihon Naika Gakkai Zasshi 96, Suppl (2007): 87b—88a. http://dx.doi.org/10.2169/naika.96.87b.
Повний текст джерелаSiviero-Miachon, Adriana Aparecida, Angela Maria Spinola-Castro, and Gil Guerra-Junior. "Adiposity in childhood cancer survivors: insights into obesity physiopathology." Arquivos Brasileiros de Endocrinologia & Metabologia 53, no. 2 (March 2009): 190–200. http://dx.doi.org/10.1590/s0004-27302009000200011.
Повний текст джерелаPasquer, Hélène, Maëlys Tostain, Nina Kaci, Blandine Roux, and Lina Benajiba. "Descriptive and Functional Genomics in Acute Myeloid Leukemia (AML): Paving the Road for a Cure." Cancers 13, no. 4 (February 11, 2021): 748. http://dx.doi.org/10.3390/cancers13040748.
Повний текст джерелаGueiderikh, Anna, Frédérique Maczkowiak-Chartois, Guillaume Rouvet, Sylvie Souquère-Besse, Sébastien Apcher, Jean-Jacques Diaz, and Filippo Rosselli. "Fanconi anemia A protein participates in nucleolar homeostasis maintenance and ribosome biogenesis." Science Advances 7, no. 1 (January 2021): eabb5414. http://dx.doi.org/10.1126/sciadv.abb5414.
Повний текст джерелаRossignol, Julien, Laura Polivka, Leila Maouche-Chrétien, Laurent Frenzel, Patrice Dubreuil, and Olivier Hermine. "Recent advances in the understanding and therapeutic management of mastocytosis." F1000Research 8 (November 22, 2019): 1961. http://dx.doi.org/10.12688/f1000research.19463.1.
Повний текст джерелаFernández-Torres, Javier, Denhi Flores-Jiménez, Antonio Arroyo-Pérez, Julio Granados, and Alberto López-Reyes. "HLA-B*40 Allele Plays a Role in the Development of Acute Leukemia in Mexican Population: A Case-Control Study." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/705862.
Повний текст джерелаSoulier, Jean. "Fanconi Anemia." Hematology 2011, no. 1 (December 10, 2011): 492–97. http://dx.doi.org/10.1182/asheducation-2011.1.492.
Повний текст джерелаSchinke, Carolina D., Cody Ashby, Yan Wang, Ruslana G. Tytarenko, Eileen Boyle, Christopher Wardell, Pingping Qu, et al. "The Mutational Landscape of Primary Plasma Cell Leukemia." Blood 132, Supplement 1 (November 29, 2018): 114. http://dx.doi.org/10.1182/blood-2018-99-116758.
Повний текст джерелаTelliam, Gladys, Christophe Desterke, Olivier Féraud, Frank Griscelli, Noufissa Oudrhiri, Micheline Fontaine Arnoux, Radhia Najar, Herve Acloque, Annelise Bennaceur-Griscelli, and Ali G. Turhan. "Blast Crisis in a Dish: Generation of a Blast Crisis Model in Chronic Myeloid Leukemia (CML) Using Patient-Specific Induced Pluripotent Stem Cells ( iPSC)." Blood 128, no. 22 (December 2, 2016): 933. http://dx.doi.org/10.1182/blood.v128.22.933.933.
Повний текст джерелаДисертації з теми "Leukemia Physiopathology"
Voyle, Roger Bruce. "Mechanisms of intracellular and extracellular cytokine production from the human leukaemia inhibitory factor gene." Title page, contents and summary only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phv975.pdf.
Повний текст джерелаMello, Mônika Conchon Ribeiro de. ""Avaliação da resposta clínica e citogenética em portadores de leucemia mielóide crônica, tratados com inibidor da tirosina quinase (imatinib)"." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/5/5136/tde-11082005-150129/.
Повний текст джерелаSTI571 (Imatinib, Glevec) is an inhibitor of the Bcr-Abl tyrosine kinase that is central to the pathogenesis of chronic myelogenous leukemia (CML). A total of 110 patients with CML chronic phase (CP) who failed or were intolerant to interferon, accelerated phase (AP) and blastic crisis (BC) were treated with imatinib from December 2000 until September 2003. Complete hematologic response and major cytogenetic response were observed in 95,9% and 69,4% respectively of patients in CP and 93,2% and 36,4% in AP. Only 2 patients are alive in BC. Imatinib is well tolerated with high rates of response
Corazza, Francis. "Contribution à l'étude de la physiopathologie de l'anémie et de la thrombocytopénie associées à une affection néoplasique chez l'enfant." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210291.
Повний текст джерелаthrombopoïétine, respectivement, dans l’anémie et la thrombocytopénie observées
chez des enfants souffrant d’une hémopathie maligne.
Par le dosage simultané de la forme soluble du récepteur de la transferrine et de
l’érythropoïétine dans le sérum nous avons montré que l’anémie observée chez ces
patients est bien la conséquence d’une réduction du nombre de progéniteurs
érythropoïétiques (atteinte médullaire centrale) mais que celle-ci n’est pas la
conséquence d’une production insuffisante d’érythropoïétine. Nous avons fait la
même observation chez des enfants souffrant d’une tumeur solide non
hématologique et chez des patients en cours de traitement par chimiothérapie.
Chez ces derniers patients, en appliquant un modèle de culture de moelle à long
terme, nous avons pu démontrer l’existence d’une altération du microenvironnement
médullaire, probablement induite par la chimiothérapie, se
traduisant par une réduction de son aptitude à supporter le développement de la
lignée érythroïde. Ceci expliquant au moins partiellement l’inadéquation de la
réponse érythropoïétique observée chez ces patients en réponse à l’anémie.
Dans la dernière partie du travail, nous avons montré que la thrombocytopénie très
fréquemment observée chez les patients leucémiques s’accompagne dans la
majorité des cas d’une élévation exponentielle de la concentration de
thrombopoïétine, excepté dans les cas de leucémies de la lignée myéloïde. Chez ces
derniers la concentration de thrombopoïétine est proche des valeurs observées chez
des sujets normaux alors qu’elle devrait être 10 à 100 fois plus élevée compte tenu
du nombre de plaquettes extrêmement bas. Nous avons pu montrer que ces taux
très bas sont la conséquence de la liaison de la thrombopoïétine à un récepteur
spécifique et fonctionnel présent à la surface des cellules leucémiques myéloïdes
qui, en l’utilisant comme facteur de croissance, (stimulant leur prolifération et
retardant leur mort cellulaire) « consomment » la thrombopoïétine présente dans le
sérum.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
Arnaud, Marie-Pierre. "Physiopathologie des leucémies aigues lymphoblastiques de la lignée B à remaniement ETV6/RUNX1 : rôle de la protéine CD9." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1S064/document.
Повний текст джерелаDespite improvements in survival rates, approximately 20% of children suffering from acute lymphoblastic leukemia (B-ALL) present relapses from bone marrow or from B-extramedullary sites, such as the testes or ovaries, particularly in cases of late relapse of ETV6/RUNX1-ALL. Virgine Gandemer showed in 2007, that the expression of CD9, a protein from the tetraspanin superfamily, can be used to distinguish ETV6/RUNX1 lymphoblastic leukemia from other types of ALL. CD9 expression has been correlated with the risk of metastasis and is associated with a poor clinical outcome in various types of cancer. Moreover CD9 has been implicated in hematopoietic and leukemic stem cell homing. We hypothesized, that CD9 protein, through its functional properties on migration and homing, could be a key actor of B-ALL relapses. The purpose of our study was then to investigate, first the transcriptional regulation of CD9 in ETV6/RUNX1 B-ALL and secondly, the effect of CD9 expression on motility and engrafment of B lymphoblasts. The analysis of CD9 transcriptional regulation previously made in the team, suggested that it could be regulated by miRNAs. We identified a cluster of 3 miRNAs potentially implicated in the regulation of CD9 expression in ETV6/RUNX1 B-ALL. This result has to be confirmd by more functional analysis. We investigated the role of CD9 in the dissemination of B-ALL. We identified CD9 as a potential regulator of B-ALL cell adhesion and a new factor involved in CXCR4-mediated migration and homing, through the promotion of actin rearrangement in response to CXCL12. We also characterized the effect of CD9 protein expression on RAC1 activation, which had an impact on blast migration and engraftment. Finally, we described, for the first time, the influence of CD9, mediated by RAC1 signaling, on B-cell chemotactic migration and homing in the testis. Our work provides evidence for an impact of CD9 on the ability of pre-B leukemic cells to disseminate to testes, through its effects on migration and homing, and suggests that CD9 may be a key player in late relapses of B-ALL, which are currently poorly understood
Labiad, Yasmine. "Contribution de l’approche transcriptomique dans la physiopathologie et le traitement des hémopathies malignes." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4068.
Повний текст джерелаThe aim of this research is to demonstrate transcriptomic approach contribution in the physiopathology and treatment of hematological malignancies. In particular, how microarrays technology is used to study several oncohematology difficulties; which remain deaths-related infection, as well as the failure to obtain remission and death related relapse. In the first part, our focus was to study natural killer cells (Nks) in patients affected with acute myeloid leukemia (AML). We compared transcriptomic AML-NKs signature with healthy donors-NKs signature and suggested that ETS-1 transcription factor is a good candidate able to regulate the natural cytotoxicity receptors (NCRs), whose coding genes, are located on two different chromosomes even if their expression remain strongly coordinated.Our second part, aimed to predict sepsis using a transcriptomic approach in the case of autologous stem cell transplantation (auto-HSCT). Using the same model, in the third part, we highlighted the melphalan high-dose chemotherapy effect on peripheral blood mononuclear cells and identified a potential good biomarker of early relapse in patients affected by myeloma in the case of auto-HSCT.Our final focus was to analyze gene expression profile of HIV-related large diffuse B-cell lymphoma type in order to verify the existence of subgroups described in immune-competent patients
"The non-apoptotic role of caspase-3 activation and its modulation in erythroid differentiation of TF-1 cells." Thesis, 2006. http://library.cuhk.edu.hk/record=b6074279.
Повний текст джерелаAs a whole, we have illustrated that the activated caspase-3, mediated most likely by the mitochondrial pathway, is an essential component in the differentiation of TF-1 cells. Its activation was nevertheless not coupled with DNA fragmentation due to some protective mechanisms such as CAD downregulation, Hsp70 upregulation and overexpression of Bcl-XL. Our study therefore provides some insights in the understanding of the relationship between human erythropoiesis and apoptosis and a better understanding in this regard will undoubtedly facilitate the development of new drugs in the treatment of different hematopoietic diseases.
Caspases play a central role in apoptosis. Their activations during the process are accounted for different biochemical and morphological changes in apoptotic cells. Yet in recent years, increasing studies had shown that caspases were also involved in some non-apoptotic cellular events, including T and B-lymphocytes activation, as well as the terminal differentiation of lens cells, megakaryocytes and erythrocytes.
In order to find out other unknown cellular mechanisms in erythropoiesis, mRNA differential display was employed to compare the gene expression pattern of TF-1 cells at different stages of differentiation. Several differentially expressed genes were identified and subsequently confirmed by RT PCR. These genes include formin binding protein 3, destrin and T-complex protein-1 (TCP-1). Their involvement in erythroid differentiation was still not clear at the moment but would be investigated in the near future. Furthermore, aiming at identifying the interacting proteins or inhibitors of caspase-3 in the system, a pull down assay was developed by means of the bacterial expression of a recombinant human caspase-3 mutant protein. With the mutation in the active site, the binding of our recombinant caspase-3 mutant with two known partners ICAD and BIRII (Baculovirus Inhibitor of apoptosis protein Repeat II) domain has been demonstrated. We hope in the near future that it can be employed to fish out some novel caspase-3 substrates from the differentiating TF-1 cell lysate.
In the present study, the participation of caspase in in vitro erythropoiesis was investigated using a human erythroleukemia cell line TF-1. Erythropoietin (EPO) induced erythroid maturation of TF-1 as indicated by the expression of erythroid-lineage markers like glycophorin A (GPA), transferrin receptors (CD71) and synthesis of hemoglobin (Hb). Activation of caspase-3 was observed from day 6 to day 12 during TF-1 differentiation after EPO treatment. With the administration of caspase-3 specific inhibitor, expressions of GPA and CD71 were partially blocked, suggesting that caspase-3 activation is essential in erythropoiesis in our TF-1 model.
Possible involvement of the intrinsic and extrinsic apoptotic pathways was studied by investigating respectively the activation of pro-caspase-9 and -8. It was found that caspase-9, but not -8, was activated at the corresponding time point when caspase-3 was activated. Besides, a transient mitochondrial depolarization coupled with the release of cytochrome c and apoptosis inducing factor (AIF) were detected on day 6, strongly implying a role of mitochondria in triggering the activation of executioner caspase-3. On the other hand, GPA and CD71 expressions were blocked by the application of mitochondrial depolarization inhibitor cyclosporin A (CyA). Also, the recovery of mitochondrial membrane potential was found to be correlated with an overexpression of Bcl-XL at a late stage of TF-1 differentiation, and the role of Bcl-XL was subsequently manifested further by a significant retardation of erythroid differentiation in the siRNA Bcl-XL knocked down TF-1 cells.
The exact role of caspase-3 in erythroid differentiation is far from clear at this moment. Yet, its regulation in the process is equally intriguing. On the course of TF-1 maturation, activated caspase-3 was able to cleave and de-localize the Inhibitor of Caspase-activated DNase (ICAD) from the nucleus, but at the same time DNA fragmentation was not detected by TUNEL assay nor agarose electrophoresis. Furthermore, protection against DNA fragmentation was observed in the EPO-treated TF-1 cells when challenged with a potent apoptotic inducer staurosporine (STS). These observations are in contrast to our understanding that DNA is fragmented by CAD (Caspase-activated DNase) when ICAD in the ICAD-CAD complex is cleaved by caspase-3. For these apparently contradictory observations, we demonstrated that downregulation of CAD occurred at the mRNA and protein levels during the erythroid differentiation in TF-1. This provides a cell rescuing mechanism in non-apoptotic cells with activated caspases.
Lui Chun Kin Julian.
"September 2006."
Adviser: Siu Kai Kong.
Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1620.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2006.
Includes bibliographical references (p. 239-253).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
Книги з теми "Leukemia Physiopathology"
The chemokine system in experimental and clinical hematology. Berlin: Springer Verlag, 2010.
Знайти повний текст джерелаRomero, Rafael M. Focus On Leukemia Research (Horizons in Cancer Research). Nova Science Publishers, 2004.
Знайти повний текст джерелаThe Jak-Stat pathway in hematopoiesis and disease. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2002.
Знайти повний текст джерела1947-, Vedeckis Wayne V., ed. Hormones and cancer. Boston: Birkhäuser, 1996.
Знайти повний текст джерела1926-, Cacciola E., Deisseroth Albert B. 1941-, and Giustolisi R, eds. Hemopoietic growth factors, oncogenes, and cytokines in clinical hematology: Current aspects and future directions. Basel: Karger, 1994.
Знайти повний текст джерелаGregory, Bock, Marsh Joan, and Widdows Kate, eds. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.
Знайти повний текст джерела