Academic literature on the topic 'Intraepithelial lymphoma'
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Journal articles on the topic "Intraepithelial lymphoma":
Rebollada-Merino, Agustín, Néstor Porras, Andrés Calvo-Ibbitson, Fernando Rodríguez-Franco, and Antonio Rodríguez-Bertos. "Bcl-2 Immunoexpression in Feline Epitheliotropic Intestinal T-Cell Lymphomas." Veterinary Sciences 9, no. 4 (March 31, 2022): 168. http://dx.doi.org/10.3390/vetsci9040168.
Attygalle, Ayoma D., Hongxiang Liu, Sima Shirali, Timothy C. Diss, Christoph Loddenkemper, Harald Stein, Ahmet Dogan, Ming-Qing Du, and Peter G. Isaacson. "Atypical marginal zone hyperplasia of mucosa-associated lymphoid tissue: a reactive condition of childhood showing immunoglobulin lambda light-chain restriction." Blood 104, no. 10 (November 15, 2004): 3343–48. http://dx.doi.org/10.1182/blood-2004-01-0385.
Muram-Zborovski, Talia, Danielle Loeb, and Tsieh Sun. "Primary Intestinal Intraepithelial Natural Killer–like T-Cell Lymphoma: Case Report of a Distinct Clinicopathologic Entity." Archives of Pathology & Laboratory Medicine 133, no. 1 (January 1, 2009): 133–37. http://dx.doi.org/10.5858/133.1.133.
Heo, Mi Hwa, Hye Ra Jung, Young Rok Do, Jung-Sook Ha, Hyera Kim, Do-Hoon Kim, and Jin Young Kim. "Intraepithelial Lymphocytosis of the Resection Margin in the Monomorphic Epitheliotropic Intestinal T-Cell Lymphoma." Blood 132, Supplement 1 (November 29, 2018): 5317. http://dx.doi.org/10.1182/blood-2018-99-115639.
Yuan, Constance M., Steven Stein, John H. Glick, and Mariusz A. Wasik. "Natural Killer–like T-Cell Lymphoma of the Small Intestine With a Distinct Immunophenotype and Lack of Association With Gluten-Sensitive Enteropathy." Archives of Pathology & Laboratory Medicine 127, no. 3 (March 1, 2003): e142-e146. http://dx.doi.org/10.5858/2003-127-e142-nktlot.
Kojima, Kazuhiro, James K. Chambers, Ko Nakashima, Yuko Goto-Koshino, and Kazuyuki Uchida. "Immunophenotyping of intraepithelial lymphocytes in canine chronic enteropathy and intestinal T-cell lymphoma using endoscopic samples." Veterinary Pathology 59, no. 2 (November 18, 2021): 227–35. http://dx.doi.org/10.1177/03009858211057220.
Nijeboer, Petula, Roy L. J. van Wanrooij, Greetje J. Tack, Chris J. J. Mulder, and Gerd Bouma. "Update on the Diagnosis and Management of Refractory Coeliac Disease." Gastroenterology Research and Practice 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/518483.
Hue, Susan Swee-Shan, Siok-Bian Ng, Shi Wang, and Soo-Yong Tan. "Cellular Origins and Pathogenesis of Gastrointestinal NK- and T-Cell Lymphoproliferative Disorders." Cancers 14, no. 10 (May 18, 2022): 2483. http://dx.doi.org/10.3390/cancers14102483.
de Baaij, Laura R., Marijn Radersma, Jolanda MW van de Water, Kim BJ Groot, Nathalie J. Hijmering, Laura M. Moesbergen, Otto J. Visser, et al. "Bortezomib Restores Defective Apoptosis by Upregulation of Noxa in Enteropathy-Associated T-Cell Lymphoma." Blood 118, no. 21 (November 18, 2011): 2722. http://dx.doi.org/10.1182/blood.v118.21.2722.2722.
Tjon, Jennifer M. L., Wieke H. M. Verbeek, Yvonne M. C. Kooy-Winkelaar, Binh H. Nguyen, Arno R. van der Slik, Allan Thompson, Mirjam H. M. Heemskerk, et al. "Defective synthesis or association of T-cell receptor chains underlies loss of surface T-cell receptor–CD3 expression in enteropathy-associated T-cell lymphoma." Blood 112, no. 13 (December 15, 2008): 5103–10. http://dx.doi.org/10.1182/blood-2008-04-150748.
Dissertations / Theses on the topic "Intraepithelial lymphoma":
Berrabah, Sofia. "Etude de nouvelles cibles thérapeutiques dans les lymphomes compliquant la maladie cœliaque." Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5201.
Refractory coeliac disease type II (RCDII), also called intraepithelial lymphoma, is a rare but severe complication of coeliac disease characterized by the clonal expansion of a small subset of innate intraepithelial lymphocytes (IEL), present in the normal human and murine intestine. Our lab has shown that this population displays shared features between T and natural killer (NK) cells. These so-called iCD3+ innate IEL are mainly characterized by intracellular expression of CD3, which is not detected at the cell surface, expression of NK receptors as well as DNA rearrangement of T cell receptor genes. Our lab has also shown that iCD3+ innate IEL originate from bone marrow precursors through coordinated NOTCH1 and interleukin (IL)-15 signals. During lymphomagenesis, iCD3+ innate IEL of most RCDII patients were shown to have acquired somatic gain-of-function mutations in JAK1 and/or STAT3 that confer increased sensitivity to interleukin-15, a cytokine overexpressed in the intestine of coeliac patients, thereby promoting their clonal expansion. Thus, our hypothesis is that JAK1/STAT3 mutations play a key role in initiating lymphomagenesis associated to coeliac disease in an IL-15-rich environment and that they could represent an attractive therapeutic target.The first objective of my thesis was to study the interest of JAK/STAT inhibitors for RCDII treatment. First, we have tested in vitro different JAK/STAT inhibitors on IL-15-dependent RCDII or normal IEL-T cell lines. We have shown that these inhibitors decrease the proliferation and phosphorylation of STAT3 and increase cellular apoptosis in both RCDII and normal T cell lines. Secondly, we have established a xenograft model based on the injection of cells derived from biopsy or blood from one RCDII patient into immunodeficient mice overexpressing the human IL-15 transgene in their gut epithelium (Rag-/-Gc-/- IL-15TgE; IRGC) to test the efficacy of JAK/STAT inhibitors in vivo. Treatment of xenografted mice with ruxolitinib, a potent inhibitor of JAK1/JAK2 decreased the frequency, number and cytotoxic potential of human tumoral cells and allowed clinical restoration. These preliminary results are encouraging but need to be confirmed. The second objective of my thesis was to test whether the Stat3 pD661V mutation is sufficient to induce the intraepithelial lymphoma in an IL-15-rich context in IRGC mice. We have successfully generated murine iCD3+ innate IEL in vitro, resembling their human counterparts from common lymphoid precursors by combining NOTCH and IL-15 signals. We then transduced CLP with a retroviral vector containing wild-type or mutated Stat3 pD661V. The transduced cells were injected into IRGC mice that subsequently were followed-up during a period of 8 weeks. In vitro generated iCD3+ innate IEL preferentially homed to the intestine. However, no development of intraepithelial lymphoma was observed suggesting that the Stat3 pD661V variant alone is not sufficient to induce the intraepithelial lymphoma. These preliminary results need to be reproduced and confirmed. The murine model used to test the role of STAT3 will now be used to evaluate the respective contribution of canonical mutations in JAK1 and STAT3 and of other recurrent mutations identified in RCDII
Castel-Branco, Inês Ferreira Ferrão. "Linfoma granular de células grandes em felinos." Master's thesis, 2021. http://hdl.handle.net/10400.26/38158.
Large granular lymphoma (LGL large granular lymphocytes) is classified by the World Health Organization (WHO) as a subtype of T-cell lymphoma associated with enteropathy type I, in which cells have azurophilic cytoplasmic granules visible on cytological examination. In most cases, LGL lymphoma develops in the mucosa of the small intestine, mainly in the jejunum, with posterior involvement of other organs and possible secondary LGL leukemia. These cats present a clinical signs of gastrointestinal (GI) disease, with segmental increase of the intestine, which over time evolves to an tumor mass easily detectable during clinical examination. However, there are cases reported without GI involvement. Feline LGL lymphoma is a rare lymphoma that exhibits a very aggressive biological behavior in mos cases, and is not commonly described in the literature. All published studies show lower survival rates compared to other lymphoma subtypes, having a very poor response to chemotherapy. However, sporadic cases present a better prognosis. Phenotypically both neoplasic LGL and intraepithelial lymphocytes (IEL Intra-epithelial lymphocytes) express CD103 (αEβ7) and CD8αα, suggesting that these lymphomas may arise from these cells. In addition, this subtype of lymphoma can develop from an inflammatory process that evolves into a chronic stage, in which the prolonged antigenic stimulation stimulates the intraepithelial T cells to go trought a clonal transformation. However, the origin of the chronic inflammation of the intestine remains unknown. Thus, the objective of this review was to describe this lymphoma in depth, discussing its possible origin and prognostic factors. This review also aims to contribute to future research to increase knowledge about this disease.
Book chapters on the topic "Intraepithelial lymphoma":
Viney, Jo, Karen Philpott, and Mike Owen. "Analysis of Intraepithelial Lymphocytes and Peyer’s Patch Lymphoid Tissue in TCR-Alpha Knockout Mice." In Advances in Experimental Medicine and Biology, 117–20. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1941-6_21.
Naresh, Kikkeri N. "Gastrointestinal lymphomas." In Oxford Textbook of Medicine, edited by Jack Satsangi, 2892–902. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0301.
J. Ciclitira, Paul, and Alastair Forbes. "Management of Patients with Refractory Coeliac Disease." In Celiac Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96231.
"Non-Inflammatory Pathologies of Conjunctiva." In Medical Atlas of Cornea and External Diseases in Middle Eastern Populations, 92–119. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-6937-5.ch004.