Bibliografie tematiche / Leukemia Physiopathology

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Letteratura scientifica selezionata sul tema "Leukemia Physiopathology"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 14 febbraio 2022

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Articoli di riviste sul tema "Leukemia Physiopathology"

1

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.

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Mitani, 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.

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3

Siviero-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.

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Abstract (sommario):
As childhood cancer treatment has become more effective, survival rates have improved, and a number of complications have been described while many of these patients reach adulthood. Obesity is a well-recognized late effect, and its metabolic effects may lead to cardiovascular disease. Currently, studies concerning overweight have focused on acute lymphocytic leukemia and brain tumors, since they are at risk for hypothalamic-pituitary axis damage secondary to cancer therapies (cranial irradiation, chemotherapy, and brain surgery) or to primary tumor location. Obesity and cancer have metabolic
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4

Pasquer, 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.

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Over the past decades, genetic advances have allowed a more precise molecular characterization of AML with the identification of novel oncogenes and tumor suppressors as part of a comprehensive AML molecular landscape. Recent advances in genetic sequencing tools also enabled a better understanding of AML leukemogenesis from the preleukemic state to posttherapy relapse. These advances resulted in direct clinical implications with the definition of molecular prognosis classifications, the development of treatment recommendations based on minimal residual disease (MRD) measurement and the discove
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5

Gueiderikh, 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.

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Abstract (sommario):
Fanconi anemia (FA), the most common inherited bone marrow failure and leukemia predisposition syndrome, is generally attributed to alterations in DNA damage responses due to the loss of function of the DNA repair and replication rescue activities of the FANC pathway. Here, we report that FANCA deficiency, whose inactivation has been identified in two-thirds of FA patients, is associated with nucleolar homeostasis loss, mislocalization of key nucleolar proteins, including nucleolin (NCL) and nucleophosmin 1 (NPM1), as well as alterations in ribosome biogenesis and protein synthesis. FANCA coim
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6

Rossignol, 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.

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Abstract (sommario):
Mastocytosis is a rare disease due to the abnormal accumulation of mast cells in various tissues. Its clinical presentation is heterogeneous depending on mast cell infiltration and mediators release. In some cases, it is associated with hematological malignancies. Prognosis varies from very good with a life expectancy similar to the general population in indolent forms of the disease to a survival time of just a few months in mast cell leukemia. Although in most cases a somatic KIT D816V mutation is found in tumor mast cells, the physiopathology of the disease is not yet fully understood. Addi
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7

Fernández-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.

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Among oncohematological diseases, acute lymphoid leukemia (ALL) and acute myeloid leukemia (AML) are characterized by the uncontrolled production and accumulation of blasts that can lead to death. Although the physiopathology of these diseases is multifactorial, a genetic factor seems to be at play. Several studies worldwide have shown association of ALL and AML with several alleles of the major histocompatibility complex (MHC).Objective. To determine gene frequencies of HLA-B alleles in Mexicans (individuals with Native American genetic background admixed with European descent) with ALL and A
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8

Soulier, Jean. "Fanconi Anemia." Hematology 2011, no. 1 (December 10, 2011): 492–97. http://dx.doi.org/10.1182/asheducation-2011.1.492.

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Abstract Fanconi anemia (FA) is the most frequent inherited cause of BM failure (BMF). Fifteen FANC genes have been identified to date, the most prevalent being FANCA, FANCC, FANCG, and FANCD2. In addition to classical presentations with progressive BMF during childhood and a positive chromosome breakage test in the blood, atypical clinical and/or biological situations can be seen in which a FA diagnosis has to be confirmed or eliminated. For this, a range of biological tools have been developed, including analysis of skin fibroblasts. FA patients experience a strong selective pressure in the
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9

Schinke, 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.

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Abstract Introduction: Primary Plasma Cell Leukemia (pPCL) is a rare form of multiple myeloma (MM) that is characterized by an aggressive disease course with >20% peripherally circulating plasma cells (PCs) and poor clinical outcome. Despite the advances of modern anti-MM therapy, pPCL patients continue to experience low median overall survival (OS) suggesting a distinct biological background. Due to its low incidence of 1-2% of all MM patients, studies on physiopathology remain challenging and are limited. The aim of this study was to elucidate the differences in biology and outcome betwee
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10

Telliam, 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.

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Abstract Despite the major progress obtained in prognosis with the use of tyrosine kinase inhibitors (TKI), the great majority of patients with CML remain on long-term therapy and progression occurs in patients with either primary or secondary resistance. The mechanisms of progression towards accelerated phase (AP) and blast crisis (BC) have been studied so far only in primary patient samples in BC. Currently, there is no in vitro model to study sequentially the molecular events leading from CP to BC as only some primary sequential samples are amenable to analysis. Using induced Pluripotent St
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Più fonti

Tesi sul tema "Leukemia Physiopathology"

1

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.

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Abstract (sommario):
Addendum attached to back facing leaves. Includes bibliographical references (leaves 172-199). The findings establish leukemia inhibitory factor, and possibly oncostatin M, as new members of a small but growing class of cytokines produced in an intracellularly active form and also suggest that the production of alternate transcripts and intercellularly-retained proteins may be a common and important feature of cytokines of the IL-6 and other families.
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2

Mello, 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/.

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Abstract (sommario):
O STI (imatinib, Glivec) é um inibidor da tirosina quinase BCR-ABL, responsável pela patogênese da leucemia mielóide crônica (LMC). Um total de 110 pacientes com LMC na fase crônica (FC) que falharam ou foram intolerantes ao tratamento com interferon, fase acelerada (FA) e crise blástica (CB) foram tratados com imatinibe entre dezembro de 2000 e setembro de 2003. Resposta hematológica completa e resposta citogenética maior foram observadas em 95,9% e 69,4% respectivamente em pacientes em FC e 93,2% e 36,4% em FA. Apenas 2 pacientes na CB estão vivos. O imatinib foi bem tolerado com altas taxas
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3

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.

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Abstract (sommario):
L’objectif de notre travail était de déterminer le rôle joué par l’érythropoïétine et la<p>thrombopoïétine, respectivement, dans l’anémie et la thrombocytopénie observées<p>chez des enfants souffrant d’une hémopathie maligne.<p>Par le dosage simultané de la forme soluble du récepteur de la transferrine et de<p>l’érythropoïétine dans le sérum nous avons montré que l’anémie observée chez ces<p>patients est bien la conséquence d’une réduction du nombre de progéniteurs<p>érythropoïétiques (atteinte médullaire centrale) mais que celle-ci n’est pas la<p>conséquence d’une production insuffisante d’ér
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4

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.

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Abstract (sommario):
Malgré l'amélioration des traitements, environ 20% des patients atteints de leucémie aigue lymphoblastiques (LAL) rechutent dans la moelle osseuse ou dans des sites extra-médullaires tels que les ovaires et les testicules, ce qui est particulièrement fréquent dans les rechutes tardives de LAL-B présentant un remaniement ETV6/RUNX1. Les travaux réalisés par Virginie Gandemer en 2007, ont montré que l'expression de CD9 permettait de distinguer les leucémies ETV6/RUNX1 des autres types de leucémie. Le gène CD9 code pour une protéine de la famille des tétraspanines dont l'expression a été corrélée
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5

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.

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Abstract (sommario):
L’objectif général de cette thèse a été de mettre en évidence la contribution de l’approche transcriptomique dans la physiopathologie et le traitement des hémopathies malignes. En particulier, comment la technologie des microarrays nous a aidée à étudier diverses problématiques en onco-hématologie.Dans la première partie, notre objectif était d’étudier les cellules Natural killer (Nk) chez les patients atteints de leucémie aiguë myéloïde (LAM). Nous avons comparé la signature transcriptomique des cellules Nk de patients LAM à celle des cellules Nk de sujet sains et suggéré que le facteur de tr
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6

"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.

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Abstract (sommario):
Apart from CAD, the transient liberation of AIF during day 6 of TF-1 differentiation could pose another threat to the genomic DNA in cells. We have demonstrated the absence of AIF in the nucleus of TF-1 cells despite its release from the mitochondria by using confocal studies. Moreover, the expression of heat shock protein 70 kDa (Hsp70), a well-known antagonist of AIF, was found to be temporarily increased at day 6. Taken together, our results implied a plausible retention of AIF in the cytoplasm by Hsp70. Although Hsp70 is commonly utilized by many cancer cells to counteract AIF and avoid DN
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Libri sul tema "Leukemia Physiopathology"

1

The chemokine system in experimental and clinical hematology. Berlin: Springer Verlag, 2010.

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2

Romero, Rafael M. Focus On Leukemia Research (Horizons in Cancer Research). Nova Science Publishers, 2004.

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3

The Jak-Stat pathway in hematopoiesis and disease. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2002.

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4

1947-, Vedeckis Wayne V., ed. Hormones and cancer. Boston: Birkhäuser, 1996.

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5

1926-, 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.

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6

Gregory, Bock, Marsh Joan, and Widdows Kate, eds. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.

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