Literatura científica selecionada sobre o tema "Maladie cœliaque réfractaire de type 2"
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Artigos de revistas sobre o assunto "Maladie cœliaque réfractaire de type 2"
Sahel, N., Z. El Bougrini, M. Zaizaa, B. Talamoussa, O. Jamal, N. Bahadi, A. Rkiouak e Y. Sekkach. "Maladie cœliaque compliquée de sprue réfractaire type 1 : à propos d’un cas". La Revue de Médecine Interne 45 (junho de 2024): A289—A290. http://dx.doi.org/10.1016/j.revmed.2024.04.293.
Texto completo da fonteMedhioub, M., O. Gannay, M. L. Hamzaoui, F. Trabelssi e M. M. Azzouz. "Maladie cœliaque compliquée de sprue réfractaire type 1 : à propos de deux cas". La Revue de Médecine Interne 36 (dezembro de 2015): A186. http://dx.doi.org/10.1016/j.revmed.2015.10.181.
Texto completo da fonteMalamut, G., O. Hermine e C. Cellier. "Structuration nationale pour la prise en charge des lymphomes à petites (sprue réfractaire de type II) et grandes cellules associés à la maladie cœliaque". Oncologie 10, n.º 6 (junho de 2008): 421–24. http://dx.doi.org/10.1007/s10269-008-0890-7.
Texto completo da fonteBel Feki, N., I. Ben Ghorbel, T. Ben Salem, A. Hamzaoui, M. Khanfir, M. Lamloum e M. H. Houman. "Une polyendocrinopathie autoimmune de type 2 associée à une maladie cœliaque compliquée d’un syndrome coronarien aigu". Annales d'Endocrinologie 75, n.º 5-6 (outubro de 2014): 508. http://dx.doi.org/10.1016/j.ando.2014.07.812.
Texto completo da fonteBeltran, S., H. Bony-Trifunovic, V. Gouilleux-Gruart, D. Djeddi, I. Dadamessi, J. L. Dupas e B. Boudailliez. "Prévalence des marqueurs biologiques de la maladie cœliaque dans une cohorte d’enfants et d’adolescents diabétiques de type I". Annales d'Endocrinologie 65, n.º 2 (abril de 2004): 131–35. http://dx.doi.org/10.1016/s0003-4266(04)95661-2.
Texto completo da fonteAdmin - JAIM. "Résumés des conférences JRANF 2021". Journal Africain d'Imagerie Médicale (J Afr Imag Méd). Journal Officiel de la Société de Radiologie d’Afrique Noire Francophone (SRANF). 13, n.º 3 (17 de novembro de 2021). http://dx.doi.org/10.55715/jaim.v13i3.240.
Texto completo da fonteTeses / dissertações sobre o assunto "Maladie cœliaque réfractaire de type 2"
Guégan, Nicolas. "Étude du rôle des mutations de la voie JAK-STAT dans la lymphomagenèse associée à la maladie cœliaque". Electronic Thesis or Diss., Université Paris Cité, 2024. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=6776&f=79039.
Texto completo da fonteRefractory celiac disease type 2 (RCD2) is a low-grade intraepithelial lymphoma complicating celiac disease (CD) and is a frequent initial step toward invasive lymphoma, specifically enteropathy-associated T-cell lymphoma (EATL). RCD2 cells originate from a small subpopulation of intraepithelial lymphocytes (IELs) called innate iCD3+ IELs, which are present in normal intestine. These cells, lacking CD3 on their surface (sCD3-), display characteristics of both T and NK cells and differentiate in the intestine from a hematopoietic precursor in response to a NOTCH signals and IL-15. RCD2 is characterized by the malignant transformation and accumulation of sCD3-iCD3+ IELs that harbor numerous somatic mutations. The most recurrent (>80%) include a JAK1 variant at position 1097 or variants in the SH2 domain of STAT3, which increase their response to inflammatory cytokines, as IL-15, which is overexpressed in the celiac intestine. These variants and other co-recurrent somatic genetic events are also present in EATL, whether they complicate RCD2 or occur de novo in celiac patients, indicating a shared mechanism of lymphomagenesis. One primary objective of this thesis was to evaluate the driver role, in lymphomagenesis, of the GdF JAK1 p.G1096D mutations (analogous to p.G1097D in humans) or STAT3 p.D661V in the context of IL-15 overexpression. I demonstrated that these mutations confer a selective advantage to murine innate iCD3+ cells differentiated in vitro in the presence of IL-15. Adoptive transfer of sCD3-iCD3+ cells carrying the JAK1 p.G1096D mutation into IL-15-overexpressing immunodeficient mice did not induce lymphoproliferation, suggesting the importance of additional genetic events. However, this transfer induced a hypereosinophilic syndrome (HSE) mimicing one of HSE discribed in humans with blood lymphoproliferative disorders of sCD3-CD4+ lymphocytes. A second objective was to assess, using a xenograft model, the efficacy of ruxolitinib (a JAK1 and JAK2 inhibitor) in treating RCD2. A 21-day treatment, initiated 14 days after the transfer of a cell line derived from RCD2 IELs, reduced tumor expansion, but this quickly reexpanded when the treatment was stopped. Data generated in vitro shown the genomic heterogeneity of the RCD2 cell line, allowing for the derivation of 6 ruxolitinib-resistant lines, which exhibited new mutations, including a common mutation in the tumor suppressor gene CDK13. These results suggest a risk of selecting ruxolitinib-resistant cells