Academic literature on the topic 'Syndrome paranéoplasique'
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Journal articles on the topic "Syndrome paranéoplasique"
Charrit, M., Q. Thiebault, K. Mohabeer, A. Riche, and Q. Bodard. "Syndrome d’hyperleucocytose paranéoplasique." La Revue de Médecine Interne 43 (June 2022): A183. http://dx.doi.org/10.1016/j.revmed.2022.03.101.
Full textHounkpati, A., I. Marie, D. Paillotin, J. F. Muir, and A. Cuvelier. "Syndrome sclérodermiforme paranéoplasique." Revue des Maladies Respiratoires 27, no. 3 (March 2010): 251–56. http://dx.doi.org/10.1016/j.rmr.2009.09.005.
Full textBlanche, P., P. Beuzeboc, and D. Sicard. "Syndrome lupique paranéoplasique." La Revue de Médecine Interne 17 (January 1996): 461s. http://dx.doi.org/10.1016/s0248-8663(97)81073-9.
Full textMarcq, L., P. Y. Jeandel, E. Rosenthal, and J. G. Fuzibet. "Un syndrome pseudo paranéoplasique." La Revue de Médecine Interne 30 (June 2009): S133. http://dx.doi.org/10.1016/j.revmed.2009.03.295.
Full textPasquet, F., L. Karkowski, V. Hajek, L. Guilloton, P. Debourdeau, and M. Pavic. "Un syndrome cérébelleux paranéoplasique." La Revue de Médecine Interne 31 (June 2010): S181. http://dx.doi.org/10.1016/j.revmed.2010.03.313.
Full textKompé, A., J. Constans, S. Bakhach, and C. Conri. "Vitiligo: un nouveau syndrome paranéoplasique ?" La Revue de Médecine Interne 20 (June 1999): s153. http://dx.doi.org/10.1016/s0248-8663(99)80365-8.
Full textZenone, Thierry, Rawan Ghabdan, Céline Leveque-Michaud, and Victor Chan. "Myosite focale : un syndrome paranéoplasique." Revue du Rhumatisme 78, no. 5 (October 2011): 486–87. http://dx.doi.org/10.1016/j.rhum.2011.05.001.
Full textDauendorffer, J. N., and C. Bourgeois-Droin. "Acrokératose paranéoplasique (syndrome de Bazex)." Annales de Dermatologie et de Vénéréologie 133, no. 12 (December 2006): 1032–33. http://dx.doi.org/10.1016/s0151-9638(06)71097-3.
Full textHerson, S. "Dermatomyosite-polymyosite et syndrome paranéoplasique." La Revue de Médecine Interne 8, no. 3 (May 1987): 245–46. http://dx.doi.org/10.1016/s0248-8663(87)80225-4.
Full textBen Mahmoud, N., A. Ltaief, E. Ismail, and N. Ben Dhia. "Un syndrome paranéoplasique révélant d’autres." Annales d'Endocrinologie 78, no. 4 (September 2017): 392. http://dx.doi.org/10.1016/j.ando.2017.07.574.
Full textDissertations / Theses on the topic "Syndrome paranéoplasique"
Viaud, Jean-François. "Le syndrome de Cushing paranéoplasique à propos de 12 cas." Bordeaux 2, 1995. http://www.theses.fr/1995BOR23075.
Full textMestre, Claire. "Pachydermie plicaturée frontale, syndrome paranéoplasique accompagnant une tumeur carcinoi͏̈de bronchique métastasée." Bordeaux 2, 1991. http://www.theses.fr/1991BOR23095.
Full textPicon, Aline. "Syndrome de Cushing paranéoplasique et tumeurs neuro-endocrines pulmonaires : pièges et difficultés diagnostiques à propos de trois cas." Montpellier 1, 1996. http://www.theses.fr/1996MON11143.
Full textFaure, Catherine. "Traitement par le kétoconazole (Nizoral*) d'un syndrome de cushing paranéoplasique dû à une sécrétion ectopique d'ACTH par une tumeur carcinoi͏̈de thymique : à propos d'un cas." Bordeaux 2, 1992. http://www.theses.fr/1992BOR2M097.
Full textVillagrán-García, Macarena. "Clinical-immunological characterization and immune tolerance breakdown in paraneoplastic neurological syndromes associated with Hu antibodies." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10259.
Full textHu antibodies, the most common in paraneoplastic neurological syndromes (PNS), strongly indicate small-cell lung cancer (SCLC). The clinical spectrum of Hu-PNS is diverse, most patients develop multifocal central, peripheral, and/or autonomic nervous system dysfunction. Despite extensive research, questions remain, namely regarding the immunological basis of clinical heterogeneity and why only a minority of SCLC patients develop Hu-PNS. Our PhD project aims to phenotype Hu-PNS patients, explore the immunogenetics and humoral responses underlying neurological phenotypes, and the genomic and transcriptomic features of their SCLC. First, we described 466 Hu-PNS patients. Hierarchical clustering identified three groups: patients with central nervous system (CNS) involvement; isolated neuropathy; and mixed CNS/peripheral phenotypes. Overall survival was similar across groups, primarily determined by cancer, but dysautonomia, present in 26% of patients, significantly influenced neurological mortality. Prominent CNS dysfunction led to fatal cardiovascular dysautonomia or central hypoventilation, while peripheral involvement was associated with gastrointestinal or secretomotor alterations, without increased mortality risk. We also characterized patients who developed neurological syndromes with Hu antibodies after immune checkpoint inhibitor (ICI) treatment. These patients were clinically indistinguishable from spontaneous cases and shared a strong association with SCLC, suggesting ICIs may induce Hu-PNS. Second, we immunologically investigated neurological phenotypes using two approaches. HLA genotyping of 100 patients confirmed an association with the DR3~DQ2 haplotype, particularly in patients with sensory neuropathy, and absent in those with only CNS involvement. Phage immunoprecipitation sequencing was used to evaluate Hu antibody epitope reactivity and other autoantibodies in serum and/or CSF of 210 patients. We found no direct clinical association with the Hu dominant epitope, but epitope reactivity differed between serum and CSF in 75% of patients with paired samples. This variation correlated with sample timing and phenotype: CSF from patients with differing serum/CSF epitopes was collected later after PNS onset, while patients with serum/CSF consistent epitope reactivity always had CNS phenotypes. In addition, we identified reactivities to other proteins, some more specific to serum or CSF, and a subset linked to specific phenotypes. Third, we examined SCLC molecular features of Hu-, GABAbR-PNS and control patients. Next-generation sequencing, copy number variation analysis, and bulk-RNA sequencing revealed no mutations, gains, deletions, or overexpression in the Hu gene family of Hu-PNS SCLC. However, a distinct transcriptomic profile with upregulated genes largely related to immune system processes characterized these tumors. We also identified specific genes upregulated in the SCLC of patients with sensory neuropathy, some of which were linked to axonogenesis and neuropathy development. Our findings suggest multiple factors contribute to Hu-PNS clinical variability, particularly a broad range of additional autoantigens. These may be partly driven by gene expression patterns in SCLC, as some upregulated genes in patients with sensory neuropathy were linked to axonogenesis. Genetic predisposition may also favor specific phenotypes, as the DR3~DQ2 haplotype was associated with sensory neuropathy. Compartmentalization within the nervous system could further contribute, as most patients targeted different Hu epitopes in serum and CSF, and some autoantigens were more specific to CSF. Finally, Hu genes alterations in SCLC are unlikely causes of neoantigenicity, while a distinct immune-related gene profile and ICIs could contribute to immune tolerance breakdown. This work advances understanding of Hu-PNS complexity and paves the way for further studies into the immunological and molecular drivers of paraneoplastic immunity
Mercié, Martial. "Syndromes paranéoplasiques oculaires." Bordeaux 2, 1997. http://www.theses.fr/1997BOR23016.
Full textCouillault, Coline. "Hétérogénéité et mécanismes d’initiation de la réponse humorale dans les tumeurs du sein et de l’ovaire." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1051/document.
Full textB and plasma cells are rising as crucial cells in the immune surveillance of tumors, even though their pro- or anti-tumor role is still debated. We argue that this dual functionality of B cells could depend on the identity of tumor-infiltrating B cell subsets and/or by the nature of the antibodies they produce. With that knowledge, we showed that breast and ovarian tumors are usually infiltrated by memory B cells and plasma cells that express and/or produce mainly IgG or IgA. This last class of Ig in highly enriched in in situ carcinomas of the breast, corresponding to earlier tumors, and in 15-20% of invasive tumors, suggesting a differential role of IgG and IgA in tumor progression. IgA, that can be monomeric or dimeric in tumors, often target antigens that differ from those targeted by IgG. We also show that antigens targeted by IgA and IgG in the tumor are often involved in functions related to the development of tissues and DNA interactions, and can be share amongst patients and between breast and ovarian tumors, suggesting their importance in the anti-tumor immune response. In parallel, using tumors from patients suffering from a paraneoplastic neurological syndrome, we established that the concomitant induction of IgG PC and CD8+ cytotoxic T cells in the tumor is associated wth amplifications and/or mutations in the genes of tumor antigens. These results highlight the importance of B cells and Ig in the anti-tumor immune response and give leads to look for new targets in immunotherapy
Damourette, Jacqueline. "Les syndromes paranéoplasiques chez les carnivores domestiques." Toulouse 3, 1985. http://www.theses.fr/1985TOU34139.
Full textDésirée, Colette. "Algodystrophie décalcifiante réflexe et tumeurs viscérales malignes : syndrôme paranéoplasique ?" Clermont-Ferrand 1, 1987. http://www.theses.fr/1987CLF13047.
Full textMartinez, Emmanuel. "Difficultés et pièges de l'exploration des syndromes de Cushing paranéoplasiques : à propos d'un cas non résolu suivi de janvier 1988 à octobre 1999." Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M150.
Full textBook chapters on the topic "Syndrome paranéoplasique"
Bessis, Didier. "Syndromes paranéoplasiques dermatologiques." In Manifestations dermatologiques des maladies du système hématopoïétique et oncologie dermatologique, 258–76. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-72092-5_21.
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