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Articoli di riviste sul tema "Leukemia Physiopathology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 14 febbraio 2022

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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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2

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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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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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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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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11

Mascarenhas, Cintia, Lara Woldmar, Maria Helena Almeida, Rosangela Vieira Andrade, Anderson Ferreira Cunha, and Carmino A. De Souza. "Evaluation of Peroxiredoxins (PRDX1, PRDX2 and PRDX6) Expression in Patients with Chronic Myeloid Leukemia (CML) Treated with Imatinib in First Line." Blood 124, no. 21 (December 6, 2014): 5545. http://dx.doi.org/10.1182/blood.v124.21.5545.5545.

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Abstract Introduction: Satisfactory response is present for the majority of chronic myeloid leukemia (CML) patients (pts) in chronic phase (CP) treated with tyrosine kinase inhibitors (ITK) . However, some pts exhibit suboptimal response or treatment failure. The probability of achieving optimal response may be related with several factors. The oxidative stress modulation is tightly related with the physiopathology of various hematologic diseases and can cause cell death, apoptosis and necrosis. Peroxiredoxins (Prdx) are a family of multifunctional antioxidant thioredoxin-dependent peroxidases

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12

de Melo Campos, Paula, Joao Machado-Neto, Adriana Silva Santos Duarte, Rafaela Mendonça, Irene Lorand-Metze, Fernando F. Costa, Sara T. O. Saad, and Fabiola Traina. "IRS2 Associates With JAK2 and May Be Involved In Cell Proliferation Pathways In Chronic Myeloproliferative Neoplasms." Blood 122, no. 21 (November 15, 2013): 1598. http://dx.doi.org/10.1182/blood.v122.21.1598.1598.

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Abstract Background Polycythemia Vera (PV), Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF) are BCR-ABL1 negative Chronic Myeloproliferative Neoplasms (MPN) characterized by increased myeloid proliferation, with predominant erythroid, megakaryocytic and megakaryocytic/granulocytic expansion, respectively. The finding of a recurrent mutation in the gene of the tyrosine-kinase Janus kinase 2 (JAK2 V617F) in these diseases has raised the hypothesis that this could be the main cause of their development. However, the evidence that MPN patients have a very similar response to JAK2 in

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13

Wang, Lining, Emmanuel Raffoux, Xavier Thomas, Ibrahim Yakoub-Agha, Jean Henri Bouhris, Stephane de Botton, Mauricette Michallet, et al. "Skin Immune Stimulation By Infections and Drug Toxicities during Induction and/or Consolidations Increases Incidence of Skin Acute Graft Versus Host Disease in Acute Myeloid Leukemia: A Study on Behalf of SFGM-TC and ALFA." Blood 126, no. 23 (December 3, 2015): 1946. http://dx.doi.org/10.1182/blood.v126.23.1946.1946.

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Abstract Introduction: 60-70% of AML patients have an indication of allogeneic hematopoietic stem cell transplantation (allo-HSCT) during their treatment. Among those who undergo allo-HSCT, prognosis and quality of life depended on presence or absence of graft versus host disease (GvHD). Immune stimulation supports the principle of GvHD and graft versus leukemia (GvL) after allo-HSCT. The impact of immune activation prior to allo-HSCT on the pathogenesis of GvHD has never been evaluated. The aim of this study was to determine whether immune stimulation induced by infection or drug toxicity bef

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14

Bousta, Abderrahmane, Sabrina Bondu, Alexandre Houy, Nicolas Cagnard, Carine Lefevre, Delphine Bernard, Marc-Henri Stern, Michaela Fontenay, and Olivier Kosmider. "Gene Expression and Alternative Splicing Datasets Analyses of MDS with Ring Sideroblasts Highlight Alternative Branchpoint Usage in Genes Involved in Iron Metabolism and Erythropoiesis." Blood 128, no. 22 (December 2, 2016): 1972. http://dx.doi.org/10.1182/blood.v128.22.1972.1972.

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Abstract Introduction SF3B1 hotspot mutations are associated with various cancers like uveal melanoma, chronic lymphocytic leukemia and myelodysplastic syndrome with ring sideroblasts (MDS-RS). These mutations affect RNA splicing by the use of alternative branchpoints resulting in an aberrant 3' splice site (ss) selection. RNA-sequencing (RNA-seq) analyzed to quantify exon-exon junctions identified aberrantly spliced transcripts in target genes, and half of them are predicted to be degraded by non-sense mediated decay. For this reason, target genes in SF3B1-mutated MDS remain partially charact

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15

Duployez, Nicolas, Elise Labis, Alice Marceau-Renaut, Christine Ragu, Arnaud Petit, Anne Auvrignon, Christophe Roumier, et al. "Genomic Landscape of Pediatric CBF-AML By SNP-Array Karyotyping and Extensive Mutational Analysis." Blood 124, no. 21 (December 6, 2014): 1007. http://dx.doi.org/10.1182/blood.v124.21.1007.1007.

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Abstract Background. Core binding factor (CBF) acute myeloid leukemia (AML) includes AML with t(8;21) and inv(16) leading to RUNX1-RUNX1T1 or CBFB-MYH11 fusion genes. These recurrent genetic abnormalities are both associated with disruption of genes encoding subunits of the CBF, a heterodimeric transcription factor involved in hematopoiesis. Although the fusion proteins appear to be crucial for the leukemogenic process, considerable experimental evidence indicates that they are not sufficient to induce AML on their own. Due to their high sensitivity to chemotherapy with high complete remission

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16

Martin, Mickaël, Anne Marie Knapp, Dana Ghergus, Fabien Delmotte, Laurent Vallat, Cédric Schleiss, Raoul Herbrecht, et al. "ZAP-70 Expression in Non Tumoral B Cells: Role in B Tolerance Breakdown?" Blood 132, Supplement 1 (November 29, 2018): 1114. http://dx.doi.org/10.1182/blood-2018-99-118237.

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Abstract Abnormal expression of the tyrosine kinase ZAP-70 by tumoral B cells in chronic lymphocytic leukemia (CLL) is associated with bad prognosis, related to B cell receptor (BCR) hypersignalling, clonal expansion and autoimmune cytopenia (AIC) occurrence, these latter being mostly induced by polyclonal IgG from the residual non tumoral B cells. We previously shown that ZAP-70 is expressed by these non tumoral B cells in CLL, positively associated with its expression in CLL B cells and with AIC occurrence (Ghergus et al. Poster ASH 2017). Here, we show for the first time a potential role of

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17

Fattizzo, Bruno, Jessica Rosa, Juri Alessandro Giannotta, Luca Baldini, and Nicola Stefano Fracchiolla. "The Physiopathology of T- Cell Acute Lymphoblastic Leukemia: Focus on Molecular Aspects." Frontiers in Oncology 10 (February 28, 2020). http://dx.doi.org/10.3389/fonc.2020.00273.

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18

Arenas, Víctor, Jose Luis Castaño, Juan José Domínguez-García, Lucrecia Yáñez, and Carlos Pipaón. "A Different View for an Old Disease: NEDDylation and Other Ubiquitin-Like Post-Translational Modifications in Chronic Lymphocytic Leukemia." Frontiers in Oncology 11 (September 23, 2021). http://dx.doi.org/10.3389/fonc.2021.729550.

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Despite the enormous amount of molecular data obtained over the years, the molecular etiology of chronic lymphocytic leukemia (CLL) is still largely unknown. All that information has enabled the development of new therapeutic approaches that have improved life expectancy of the patients but are still not curative. We must increase our knowledge of the molecular alterations responsible for the characteristics common to all CLL patients. One of such characteristics is the poor correlation between mRNA and protein expression, that suggests a role of post-translational mechanisms in CLL physiopath

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19

Marselli, L., L. Trincavelli, C. Santangelo, R. Lupi, S. Del Guerra, U. Boggi, A. Falleni, et al. "The role of peripheral benzodiazepine receptors on the function and survival of isolated human pancreatic islets." European Journal of Endocrinology, August 1, 2004, 207–14. http://dx.doi.org/10.1530/eje.0.1510207.

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OBJECTIVE: Peripheral benzodiazepine receptors (PBRs) are part of the mitochondrial permeability transition pore, and their activation may induce cell death. PBRs are expressed in human pancreatic islets, and cytokine-induced damage is accompanied by changes in their properties. We hypothesized that PBRs can have a role in human islet physiopathology, and evaluated the effects of prolonged exposure to two specific PBR ligands, PK11195 and Ro5-4864 on the function and survival of isolated human islets. DESIGN: Isolated human islets were prepared from the pancreas of 25 multiorgan cadaveric dono

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