WorldCat Identities

Ferrand, Christophe

Overview
Works: 15 works in 21 publications in 2 languages and 28 library holdings
Roles: Thesis advisor, Opponent, Contributor, Author, Other
Publication Timeline
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Most widely held works by Christophe Ferrand
CONTRIBUTION A L'IDENTIFICATION MOLECULAIRE D'UN NEUROPEPTIDE REVELE PAR CERTAINS IMMUNSERUMS ANTI PROLACTINE DANS DES NEURONES DE L'HYPOTHALAMUS LATERAL DU RAT by CHRISTOPHE FERRAND( Book )

2 editions published in 1994 in French and held by 3 WorldCat member libraries worldwide

New CD20 alternative splice variants: molecular identification and differential expression within hematological B cell malignancies by Clémentine Gamonet( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

Potential added value of a RT-qPCR method of SOX 11 expression, in the context of a multidisciplinary diagnostic assessment of B cell malignancies by Julien Magne( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

Etude génomique de la cohorte nationale de leucémies dérivées de cellules dendritiques plasmacytoïdes et hémopathies apparentées by Florian Renosi( )

2 editions published in 2021 in French and held by 2 WorldCat member libraries worldwide

Neoplasms involving plasmacytoid dendritic cells (pDCs) include Blastic pDC Neoplasms (BPDCN) and mature pDC proliferations associated with myeloid malignancies, namely AML-pDC when the malignancy is an Acute Myeloid Leukemia (AML). The ontogeny of pDCs is complex: their myeloid and/or lymphoid origin is uncertain and they probably consist of several sub-populations including newly identified cells, the AXL+ SIGLEC6+ DCs (AS-DCs). Through the French BPDCN network, we studied BDPCN and AML-pDC at the genetic and phenotypic level, integrating new data on pDC ontogeny.We demonstrate the BPDCN heterogeneity, with sometimes diagnostic trap related to aberrant markers sometimes expressed by neoplastic cells. BPDCN are also characterized by numerous genetic deletions of oncogenes (ETV6, IKZF1, RB1 and NR3C1) and immune response genes (IFNR1, CLEC4C, IFNA cluster). This is associated with epigenetic (TET2, ASXL1) and splicing (ZRSR2) abnormalities. Various markers evoke an AS-DC origin but some of these abnormalities are related to leukemogenesis and not ontogenesis, such as the 9p deletion leading to decreased expression of genes encoding type I interferons. In addition, even if AS-DC or B lymphoid markers can be found, the AS-DC profile is only found in a subgroup of patients. The transcriptional program of BPDCN is also characterized by cell cycle and SOX4 transcription factor deregulation.The study of 15 cases of AML-pDC show an excess of myeloblasts (CD45low CD34+) associated with an excess of.pDC whose phenotype is close to physiological pDCs for expression levels of CD303, cTCL1, CD123 and particularly with the absence of CD56 expression. All this profile clearly distinguishes them from blasts in BPDCN. Moreover, there is a continuous maturation from blasts to pDCs (loss of CD34, progressive expression of CD45, CD123, CD303, CD304) and to monocytes, suggesting a common progenitor to these populations. We also confirm the neoplastic nature of pDCs and the common clonal origin of blasts, pDCs and monocytes in AML-pDC, with the same mutations in all cell types. RUNX1 is the most frequently mutated gene (11 cases out of 15), and most importantly, in all evaluated M0-AML, raising the hypothesis of a new subtype of RUNX1-mutated M0-AML associated with an excess of pDC, potentially related to a progenitor wit myeloid and pDC potential
Phase I study of OM-174, a lipid A analogue, with assessment of immunological response, in patients with refractory solid tumors by Nicolas Isambert( )

1 edition published in 2013 in English and held by 2 WorldCat member libraries worldwide

Constitutional and somatic deletions of the Williams-Beuren syndrome critical region in Non-Hodgkin Lymphoma by David Guenat( )

1 edition published in 2014 in English and held by 2 WorldCat member libraries worldwide

Erratum to: New CD20 alternative splice variants: molecular identification and differential expression within hematological B cell malignancies by Clémentine Gamonet( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

Post-Essential Thrombocythemia Myelofibrosis and Multiple Isodicentric Y Chromosomes: A Unique Case among a Rare Association by Eric Dahlén( )

1 edition published in 2020 in English and held by 2 WorldCat member libraries worldwide

Identification de nouveaux transcrits alternatifs du gène CD20 humain, différentiellement exprimés dans les hémopathies impliquant le lymphocyte B by Clémentine Gamonet( Book )

2 editions published in 2015 in French and held by 2 WorldCat member libraries worldwide

D393-CD20 is a protein encoded by an alternatively spliced transcript of human cd20 gene, expressed only on tumoralB lymphocyte (Henry et al, Blood2010). Based on this results, we decided to study the cd20 splicing in pathologies involving B cells. During this work, we identified 5 cd20 alternative transcripts, among them the D393-CD20 variant. The 4 others werenamed according to their size: D657-, D618-, D480- and D177-CD20.D657- and D618-CD20 are weakly expressed in healthy donor and overexpressed in pathologies involving Blymphocytes, whereas D393-CD20 is only expressed in B malignancies. Splicing pattern of patients suffering from pathologies involving B lymphocyte (cancers, auto-immune diseases, EBVinfection) were performed by quantitative PCR, and these patterns revealed a splicing deregulation in these pathologieswith a higher proportion of alternative variants compared with healthy dormors. The observation of a specifie expression of D393-CD20 in tumoral cells suggests a splicing deregulation associatedwith oncogenesis, particularly in lymphoma derived from germinal center. If in our in vitro models, no direct correlation between D393-CD20 expression and resistances to anti-CD20 antibodiestreatments hâve been observed, when shown that these antibodies induced cd20 splicing modulation. These results open the way to a deeper study to determine the interest ofcd20 splicing deregulation as a biomarker, andthe impact of theses deregulations on CD20 protein expression since these protein is a preponderant target of therapeuticstrategies used in pathologies involving B cells
Ciblage de la cellule souche leucémique exprimant la protéine lL-1RAP : Approche d'immunothérapie anti-tumorale utilisant des lymphocytes T génétiquement modifiés pour exprimer un récepteur chimérique à l'antigène(CAR) by Walid Warda( Book )

3 editions published in 2018 in French and held by 2 WorldCat member libraries worldwide

Nous avons produit des CART-cells et des LT-mock ont été produits ex-vivo. L'efficacité de transduction est mesuré par l'expression CD3+/CD19+ (82% en moyenne, n=S), en cytométrie en flux. L'expression protéique de CAR a été vérifiée par western blot et en cytométrie en flux attestant de son expression membranaire. Nous avons testé la fonctionnalité de la cassette suicide iCaspase9/ AP1903 sur CART-cells après 48h de traitement à I' AP1903. Nous avons montré que plus de 90% des CART-cells entrent en apoptose (Marquage 7-AAD en cytométrie en flux). Nous avons ensuite réalisé des tests fonctionnels in-vitro des CART-cells contre des lignées LMC exprimant naturellement IL-lRAP ou contre des lignées transfectées pour exprimer la forme membranaire d'IL-lRAP. Après coculture des CART-cells en présence des cellules cibles IL-lRAP+ nous avons montré qu'ils prolifèrent (test CFSE), qu'ils sécrètent de l'interféron y et des cytokines inflammatoires. Enfin, par marquage 7-AAD, nous avons démontré la cytotoxicité des CART-cells contre les cellules ILl-RAP+. Finalement, nous avons montré l'efficacité des CART-cells in vivo, dans un modèle de xénogreffe tumorales dans des souris immunodéficiences NSG greffées par la lignée K562-IL1RAP+ / Luciférase +. On constate une diminution de la masse tumorale 4 jours après injection des CART-cells, jusqu'à disparition totale. Cette preuve de concept laisse entrevoir des perspectives thérapeutiques alternatives dans le traitement de la LMC ou LAM, qui devront être optimiser dans des modèles murins (séquence et nombres d'injection, nombres de cellules, associations avec ITKS ou autres chimiothérapies) afin de conduire un essai clinique de phase I, pour démontrer la faisabilité et la sécurité de l'approche pour envisager une démonstration d'efficacité chez l'homme. La sécurisation par la cassette suicide permet d'envisager l'utilisation des CART-cells en situation autologue ou allogénique (Donor Lymphocytes infusion, DU)
Chimeric antigen receptor T cells targeting IL-1RAP : a promising new cellular immunotherapy to treat acute myeloid leukemia by Rim Trad( )

2 editions published in 2021 in English and held by 2 WorldCat member libraries worldwide

La leucémie aiguë myéloïde (LAM) est globalement une maladie rare affectant plus fréquemment les personnes âgées et chez les hommes que chez les femmes. Le taux de nouveaux cas de LAM était de 4,3 pour 100 000 hommes et femmes par an. La LAM reste une maladie très difficile à guérir en raison de la persistance des cellules souches leucémiques (CSL), qui sont une sous-population de cellules de la LAM avec un auto-renouvellement et une capacité chimioréfractaire. Les LSC de LAM sont à la base de la maladie réfractaire/en rechute (R/R) chez 80 % des patients atteints de LAM ne recevant pas de greffe allogénique de cellules souches hématopoïétiques (allo-CSH). Le traitement de la LAM en rechute et réfractaire reste un défi de taille et est associé à un mauvais pronostic et à de faibles chances de guérison, en particulier chez les patients âgés. D'où la nécessité de nouvelles alternatives robustes à l'activité anti-leucémique tout en évitant la cytotoxicité des lymphocytes T contre les tissus sains pour le traitement des patients atteints de LAM. Dans cette étude, selon ce qui a été publié, nous avons montré que la protéine IL-1RAP est surexprimée à la surface cellulaire des LSC dans tous les sous-types de LAM et l'avons confirmée comme une cible intéressante et prometteuse dans la LAM par rapport à la LAM potentielle la plus courante. cibles. Après avoir établi la preuve de concept de l'efficacité des cellules CART ciblant l'IL-1RAP dans la leucémie myéloïde chronique (LMC), nous avons émis l'hypothèse que les cellules CART IL-1RAP de troisième génération pourraient éliminer les LSC AML. Nous avons d'abord démontré que les cellules CART IL-1RAP pouvaient être produites à partir des cellules T de la LAM au moment du diagnostic mais aussi lors de la rechute. La caractérisation des cellules CART IL-1RAP a montré l'expression des marqueurs de point de contrôle à la fin du processus de production. In vitro et in vivo, nous avons montré l'efficacité des cellules CART IL-1RAP contre des lignées cellulaires AML exprimant différents niveaux d'IL-1RAP et la cytotoxicité des cellules CART autologues contre des cellules primaires de patients atteints de LAM au diagnostic ou à la rechute. Dans les modèles de xénogreffe de LAM (PDX) dérivés de patients, nous avons confirmé que les cellules CART sont capables de circuler dans le sang périphérique et de migrer dans la moelle osseuse et la rate et sont cytotoxiques contre les cellules primaires de la LAM
SALL4 oncogene is an immunogenic antigen presented in various HLA-DR contexts( )

1 edition published in 2018 in English and held by 1 WorldCat member library worldwide

Identification d'un transcrit alternatif du gène CD20 dans les hémopathies B, codant pour une nouvelle protéine et impliqué dans les résistances au Rituximab : cible potentielle en immunothérapie anti-tumorale by Carole Henry-Dunand( Book )

1 edition published in 2010 in French and held by 1 WorldCat member library worldwide

Within the framework of the use of " the gene-suicide " system, the gene of susceptibility HSV-tk had been used to modulate alloreactivity after bone-marrow transplantation. This model showed its limits and our laboratory turned to the use of the CD20/Rituximab (RTX) system. Indeed, as a membrane protein, the molecule CD20 allows a cell sorting of the genetically modified cells ; furhtermore it is the target of a monoclonal antibody, the RTX, allowing the lysis of the cells expressing this antigen. In this context, we were interested in the existence of a population of T lymphocytes expressing the CD20 molecule. Indeed, the molecule CD20 normally expressed on B cells was described, in the litterature, as being present on a small contingent of T cells. We emitted the hypothesis that this population could be an artefact observed in flow cytometry. Secondly, an alternative splice of the CD20 gene was brought to light in the laboratory, coding a truncated mRNA called deltaCD20 (deltaCD20). This mRNA is connected to the activation and/or cellular transformation. This work thus consisted of the characterization of this mRNA deltaCD20 and in the revealing of the protein coded by this mRNA. CD20 being the target of the treatment by RTX, we also put in relation the presence of this mNRA with the RTX resistances in vitro and in vivo. The last part of the results concerns the exploration of an anti-tumoral immunotherapy approach targeting this protein deltaCD20, expressed in B cells malingnancies and potentially involved in RTX resistances. We so generated CD20 specific T cells. The long-term purpose of this strategy would be to improve the treatment of refractory patients and/or in relapse after RTX treatment
Decoding the cellular interactions regulating CAR T cell antitumor activity in vivo using two-photon intravital imaging by Marine Cazaux( )

1 edition published in 2020 in English and held by 1 WorldCat member library worldwide

Chimeric antigen receptor (CAR) T cells represent a potentially curative strategy for relapsed and refractory B cell malignancies. This strategy is based on the modification of the patient's T cells to express a chimeric antigen receptor that targets a tumor-associated marker, thus triggering tumor elimination. However, the outcome and dynamics of CAR T cell interactions in distinct anatomical sites are poorly understood. Also, whether CAR T cells act autonomously or require interactions with the tumor microenvironment (TME) is unclear. Using intravital imaging, we tracked interactions established by anti-CD19 CAR T cells in aggressive B cell lymphoma-bearing mice. Circulating targets trapped CAR T cells in the lungs, reducing their access to lymphoid organs. In the bone marrow, tumor apoptosis was largely due to CAR T cells that engaged, killed, and detached from their targets within 25 min. Notably, not all CAR T cell contacts elicited calcium signaling or killing while interacting with tumors, uncovering extensive functional heterogeneity. Mathematical modeling revealed that direct killing was sufficient for tumor regression. Also, antigen-loss variants emerged in the bone marrow, but not in lymph nodes, where CAR T cell cytotoxic activity was reduced, revealing underappreciated anatomical heterogeneity. Using single-cell RNA sequencing, we revealed profound modification of the TME during CAR T cell therapy. IFN-gamma production by CAR T cells and cytokine signaling in host cells not only enhanced endogenous T and NK cell activity but were also essential for sustaining CAR T cell cytotoxicity as revealed by intravital imaging. Compared to CD8+ CAR T cells, CD4+ CAR T cells were more efficient at host immune activation but less capable of tumor killing. In sum, CAR T cells are not acting alone in vivo but rely instead on a cytokine-mediated crosstalk with the TME for optimal activity. In sum, we have unraveled underappreciated anatomical and functional heterogeneity of CAR T cells, as well as essential crosstalks between CAR T cells and the TME. Identifying the strengths and the weaknesses of CAR T cells should help to design optimized CAR T cell strategies to limit relapses
 
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Languages
French (11)

English (10)