Search

Your search keyword '"Bénédicte Bruno"' showing total 10 results
Start Over Author "Bénédicte Bruno" Publication Year Range Last 3 years
10 results on '"Bénédicte Bruno"'

1. VZV Prophylaxis After Allogeneic Hematopoietic Stem Cell Transplantation in Children: When to Stop?

Author

Eva deBerranger, Anne‐Flore Derache, Nassima Ramdane, Julien Labreuche, Pauline Navarin, Fanny Gonzales, Wadih Abou‐Chahla, Brigitte Nelken, and Bénédicte Bruno

Subjects
acyclovir prophylaxis, allogeneic hematopoietic stem cell transplantation, children, herpes zoster, lymphocytes immunophenotyping, VZV infection, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

ABSTRACT Background Acyclovir treatment is an efficient prophylaxis to prevent varicella‐zoster virus (VZV) reactivation after allogeneic hematopoietic stem cell transplantation (HSCT). Aims This single center retrospective study tried to determine if the lymphocytes immunophenotyping could help to determine the duration of prophylaxis, and evaluated complications, and associated risk factors for VZV infection. Methods and Results Eighty‐four children underwent an allogeneic HSCT, in which 77 received an acyclovir prophylaxis. Twenty‐one of the 77 had a VZV infection with an incidence rate of 1.30 per 100 patients‐months (exact 95% CI, 0.81 to 2.01). Among these 21 patients with VZV infection, 16 had an infection after withdrawing acyclovir prophylaxis within a median of 49 days (range, 11 days–5.8 months). Thirty‐five percent of the VZV infected patients were hospitalized, 9% had a visceral dissemination, and 9% had postherpetic neuralgia. In multivariate analysis, higher VZV infection rate was associated with conditioning regimen with total body irradiation, immunoglobulin substitution, and antithymocyte globulin. The incidence of VZV infection increased significantly when patients had a CD4+ lymphocytes count below 23% (cHR 3.28 [95% CI, 1.09–9.81]; p = 0.03) or a CD4+/CD8+ ratio less than 0.9 (cHR 3.13 [95% CI, 1.04–9.36]; p = 0.04) at the time of stopping acyclovir prophylaxis. Conclusion After cessation of acyclovir prophylaxis, VZV reactivation can occur and be responsible for morbidity after allogeneic HSCT. This study suggests that the proportion of CD4+ lymphocytes and the CD4+/CD8+ ratio can inform decisions about the duration of acyclovir prophylaxis after allogeneic HSCT to prevent VZV reactivation.

Published
2024
Full Text
View/download PDF

2. Childhood myelodysplastic syndromes: Is cytoreductive therapy useful before allogeneic hematopoietic stem cell transplantation?

Author

Baptiste Le Calvez, Maxime Jullien, Jean H. Dalle, Cécile Renard, Charlotte Jubert, Arthur Sterin, Catherine Paillard, Anne Huynh, Sarah Guenounou, Bénédicte Bruno, Virginie Gandemer, Nimrod Buchbinder, Pauline Simon, Cécile Pochon, Anne Sirvent, Dominique Plantaz, Justyna Kanold, Marie C. Béné, Fanny Rialland, Audrey Grain, and Société Francophone de Greffe de Moelle et de Thérapie Cellulaire (SFGM‐TC)

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Abstract For most patients with childhood myelodysplastic syndrome (cMDS), allogeneic hematopoietic stem cell transplantation (allo‐HSCT) remains the only curative option. In the case of increased blasts (cMDS‐IB), the benefit of pretransplant cytoreductive therapy remains controversial. In this multicenter retrospective study, the outcomes of all French children who underwent allo‐HSCT for cMDS reported in the SFGM‐TC registry between 2000 and 2020 were analyzed (n = 84). The median age at transplantation was 10.2 years. HSCT was performed from matched sibling donors (MSD) in 29% of the cases, matched unrelated donors (MUD) in 44%, haploidentical in 6%, and cord blood in 21%. Myeloablative conditioning was used in 91% of cases. Forty‐eight percent of patients presented with cMDS‐IB at diagnosis (median BM blasts: 8%). Among them, 50% received pretransplant cytoreductive therapy. Five‐year overall survival (OS), cumulative incidence of nonrelapse mortality (NRM), and relapse were 67%, 26%, and 12%, respectively. Six‐month cumulative incidence of grade II–IV acute graft‐versus‐host disease was 46%. Considering the whole cohort, age under 12, busulfan/cyclophosphamide/melphalan conditioning or MUD were associated with poorer 5‐year OS. In the cMDS‐IB subgroup, pretransplant cytoreductive therapy was associated with a better OS in univariate analysis. This seems to be mainly due to a decreased NRM since no impact on the incidence of relapse was observed. Overall, those data may argue in favor of cytoreduction for cMDS‐IB. They need to be confirmed on a larger scale and prospectively.

Published
2024
Full Text
View/download PDF

3. A predictive classifier of poor prognosis in transplanted patients with juvenile myelomonocytic leukemia: a study on behalf of the Société Francophone de Greffe de Moelle et de Thérapie Cellulaire

Author

Déborah Meyran, Chloé Arfeuille, Sylvie Chevret, Quentin Neven, Aurélie Caye-Eude, Elodie Lainey, Arnaud Petit, Fanny Rialland, Gérard Michel, Dominique Plantaz, Charlotte Jubert, Alexandre Theron, Virginie Gandemer, Marie Ouachée-Chardin, Catherine Paillard, Bénédicte Bruno, Nimrod Buchbinder, Cécile Pochon, Charlotte Calvo, Mony Fahd, André Baruchel, Hélène Cavé, Jean-Hugues Dalle, and Marion Strullu

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Juvenile myelomonocytic leukemia (JMML) is an aggressive pediatric myeloproliferative neoplasm requiring hematopoietic stem cell transplantation (HSCT) in most cases. We retrospectively analyzed 119 JMML patients who underwent first allogeneic HSCT between 2002 and 2021. The majority (97%) carried a RAS-pathway mutation, and 62% exhibited karyotypic alterations or additional mutations in SETBP1, ASXL1, JAK3 and/or the RAS pathway. Relapse was the primary cause of death, with a 5-year cumulative incidence of 24.6% (95%CI: 17.1-32.9). Toxic deaths occurred in 12 patients, resulting in treatmentrelated mortality (TRM) of 9.0% (95%CI: 4.6-15.3). The 5-year overall (OS) and event-free survival were 73.6% (95%CI: 65.7-82.4) and 66.4% (95%CI: 58.2-75.8), respectively. Four independent adverse prognostic factors for OS were identified: age at diagnosis >2 years, time from diagnosis to HSCT >6 months, monocyte count at diagnosis >7.2x109/L, and the presence of additional genetic alterations. Based on these factors, we proposed a predictive classifier. Patients with three or more predictors (21% of the cohort) had a 5-year OS of 34.2%, whereas those with none (7%) had a 5-year OS of 100%. Our study demonstrates improved transplant outcomes compared to prior published data, which can be attributed to the synergistic impacts of a low TRM and a reduced yet still substantial relapse incidence. By integrating genetic information with clinical and hematological features, we have devised a predictive classifier. This classifier effectively identifies a subgroup of patients who are at a heightened risk of unfavorable post-transplant outcomes who would benefit novel therapeutic agents and post-transplant strategies.

Published
2024
Full Text
View/download PDF

4. Interactions médicamenteuses et incompatibilités physico-chimiques en phase aiguë post-allogreffe : quelle influence des médicaments de support ? Recommandations de la SFGM-TC

Author

Bénédicte Bruno, Lucie Capelle, Virginie Denis, Olivier Duval, Sorea Selmouni, Alban Villate, Delphine Cabelguenne, Valérie Coiteux, Tiphaine Lachner-Gaubert, Ibrahim Yakoub-Agha, and Nicolas Simon

Subjects
Cancer Research, Oncology, Radiology, Nuclear Medicine and imaging, Hematology, General Medicine
Published
2023
Full Text
View/download PDF

5. Ruxolitinib in Pediatric Patients with Treatment-Naïve or Steroid-Refractory Acute Graft-Versus-Host Disease: Primary Findings from the Phase I/II REACH4 Study

Author

Franco Locatelli, Hyoung Jin Kang, Bénédicte Bruno, Virginie Gandemer, Fanny Rialland, Maura Faraci, Yoshiyuki Takahashi, Katsuyoshi Koh, Henrique Bittencourt, Grace Cleary, Christine Rosko, Pantelia Roussou, Annie St. Pierre, Anirudh Prahallad, and Cristina Díaz-de-Heredia

Subjects
Immunology, Cell Biology, Hematology, Biochemistry
Published
2022
Full Text
View/download PDF

6. Inotuzumab Ozogamicin (InO) Combined with UKALL-R3 Modified Chemotherapy in Pediatric Patients with B-Cell Precursor CD22+ Acute Lymphoblastic Leukemia (BCP-ALL) - Results from the ITCC-059 Phase 1B Trial

Author

Edoardo Pennesi, Erica Brivio, Anneke C.J. Ammerlaan, Yilin Jiang, Vincent H.J. van der Velden, Berna Beverloo, Barbara Sleight, Susana Rives, Cristina Díaz de Heredia Rubio, Francisco J. Bautista Sirvent, Alba Rubio-San-Simón, Fanny Rialland, Carmelo Rizzari, Bella Bielorai, Arnaud Petit, Bénédicte Bruno, Ingrid Øra, Anna Nilsson, Gernot Engstler, Claudia Rossig, Benoit Brethon, Franco Locatelli, and Christian M. Zwaan

Subjects
Immunology, Cell Biology, Hematology, Biochemistry
Published
2022
Full Text
View/download PDF

7. Population Pharmacokinetics of Inotuzumab Ozogamicin (InO) As Single Agent in Pediatric Relapsed/Refractory Acute Lymphoblastic Leukemia - Results from the ITCC-059 Phase IA and Phase II Trial

Author

Edoardo Pennesi, Erica Brivio, Kathleen B. Pelletier, Ying Chen, Alwin D.R. Huitema, Yilin Jiang, Anneke C.J. Ammerlaan, Barbara Sleight, Franco Locatelli, Inge M. Van Der Sluis, Claudia Rossig, Christiane Chen-Santel, Bella Bielorai, Arnaud Petit, Jan Stary, Lucie Sramkova, Cristina Díaz de Heredia Rubio, Susana Rives, Aengus O'Marcaigh, Carmelo Rizzari, Gernot Engstler, Karsten Nysom, Alba Rubio-San-Simón, Francisco J. Bautista Sirvent, Bénédicte Bruno, Yives Bertrand, Benoit Brethon, Fanny Rialland, Genevieve Plat, Uta Dirksen, May Garrett, and Christian M. Zwaan

Subjects
Immunology, Cell Biology, Hematology, Biochemistry
Published
2022
Full Text
View/download PDF

8. Clonal hematopoiesis driven by chromosome 1q/MDM4 trisomy defines a canonical route toward leukemia in Fanconi anemia

Author

Marie Sebert, Stéphanie Gachet, Thierry Leblanc, Alix Rousseau, Olivier Bluteau, Rathana Kim, Raouf Ben Abdelali, Flore Sicre de Fontbrune, Loïc Maillard, Carèle Fedronie, Valentine Murigneux, Léa Bellenger, Naira Naouar, Samuel Quentin, Lucie Hernandez, Nadia Vasquez, Mélanie Da Costa, Pedro H. Prata, Lise Larcher, Marie de Tersant, Matthieu Duchmann, Anna Raimbault, Franck Trimoreau, Odile Fenneteau, Wendy Cuccuini, Nathalie Gachard, Nathalie Auger, Giulia Tueur, Maud Blanluet, Claude Gazin, Michèle Souyri, Francina Langa Vives, Aaron Mendez-Bermudez, Hélène Lapillonne, Etienne Lengline, Emmanuel Raffoux, Pierre Fenaux, Lionel Adès, Edouard Forcade, Charlotte Jubert, Carine Domenech, Marion Strullu, Bénédicte Bruno, Nimrod Buchbinder, Caroline Thomas, Arnaud Petit, Guy Leverger, Gérard Michel, Marina Cavazzana, Eliane Gluckman, Yves Bertrand, Nicolas Boissel, André Baruchel, Jean-Hugues Dalle, Emmanuelle Clappier, Eric Gilson, Ludovic Deriano, Sylvie Chevret, François Sigaux, Gérard Socié, Dominique Stoppa-Lyonnet, Hugues de Thé, Christophe Antoniewski, Dominique Bluteau, Régis Peffault de Latour, Jean Soulier, Institut de Recherche Saint-Louis - Hématologie Immunologie Oncologie (Département de recherche de l’UFR de médecine, ex- Institut Universitaire Hématologie-IUH) (IRSL), Université Paris Cité (UPCité), Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Génomes, biologie cellulaire et thérapeutiques (GenCellDi (U944 / UMR7212)), Collège de France (CdF (institution))-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), AP-HP Hôpital universitaire Robert-Debré [Paris], Recherche clinique appliquée à l'hématologie (URP_3518), Intégrité du génome, immunité et cancer - Genome integrity, Immunity and Cancer, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CHU Limoges, Institut Gustave Roussy (IGR), Unité de génétique et biologie des cancers (U830), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de Recherche en Génomique Humaine (CNRGH), Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Hématopoïèse normale et pathologique : émergence, environnement et recherche translationnelle [Paris] ((UMR_S1131 / U1131)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Centre d'Ingénierie génétique murine - Mouse Genetics Engineering Center (CIGM), Institut Pasteur [Paris] (IP), Institut de Recherche sur le Cancer et le Vieillissement (IRCAN), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), CHU Nice [Cimiez], Hôpital Cimiez [Nice] (CHU), CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Hôpitaux universitaires Est parisien [AP-HP], CHU Bordeaux [Bordeaux], Hospices Civils de Lyon (HCL), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), CHU Rouen, Normandie Université (NU), Centre hospitalier universitaire de Nantes (CHU Nantes), Centre d'études et de recherche sur les services de santé et la qualité de vie (CEReSS), Aix Marseille Université (AMU), Hôpital de la Timone [CHU - APHM] (TIMONE), CIC NECKER BT (CIC 1416), Immunologie humaine, physiopathologie & immunothérapie (HIPI (UMR_S_976 / U976)), Collège de France (CdF (institution)), École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL), This study received support from the European Research Council (ERC) Consolidator Grant to J.S. (CEVAL-311660), the FP7 Eurofancolen program (HEALTH-F5-2012-305421), the ANR program PACRI (Projet alliance parisienne des instituts de recherche en cancérologie), the CONECT-AML (Collaborative Network for Children and Teenagers with Acute Myeloid Leukemia) program supported by a grant from the Institut National du Cancer (INCa), Fondation ARC, Ligue nationale contre le cancer, and Laurette Fugain (INCa-ARC-LIGUE_11905) to J.S. and C.A., and the Association Française pour la Maladie de Fanconi (AFMF) grants 'Histoire naturelle de la maladie de Fanconi' to R.P.L. and J.S., 'Modélisation de la transformation leucémique dans la maladie de Fanconi' to D.B., and 'Cribles fonctionnels à haut débit de gènes modificateurs de la maladie de Fanconi' to C.G. M.S. was supported by the AVIESAN-INCa Program 'Formation à la Recherche Translationnelle,' and A.R. by a grant from the Fondation ARC. The work in E.G.’s lab is supported by Fondation ARC and ANR Telochrom. The work in L.D.’s lab is supported by INCa (PLBIO16-181) and ERC (310917)., ANR-11-PHUC-0002,PACRI,Alliance Parisienne des Instituts de Recherche en Cancérologie(2011), European Project: 311660,EC:FP7:ERC,ERC-2012-StG_20111109,CEVAL(2013), and European Project: 305421,EC:FP7:HEALTH,FP7-HEALTH-2012-INNOVATION-1,EUROFANCOLEN(2013)

Subjects
MDM4, Fanconi anemia, precision medicine, [SDV]Life Sciences [q-bio], Genetics, leukemia, clonal hematopoiesis, Molecular Medicine, Cell Biology, TP53, mutational signature, genomic instability, BRCA2
Abstract

International audience; Fanconi anemia (FA) patients experience chromosome instability, yielding hematopoietic stem/progenitor cell (HSPC) exhaustion and predisposition to poor-prognosis myeloid leukemia. Based on a longitudinal cohort of 335 patients, we performed clinical, genomic, and functional studies in 62 patients with clonal evolution. We found a unique pattern of somatic structural variants and mutations that shares features of BRCA-related cancers, the FA-hallmark being unbalanced, microhomology-mediated translocations driving copy-number alterations. Half the patients developed chromosome 1q gain, driving clonal hematopoiesis through MDM4 trisomy downmodulating p53 signaling later followed by secondary acute myeloid lukemia genomic alterations. Functionally, MDM4 triplication conferred greater fitness to murine and human primary FA HSPCs, rescued inflammation-mediated bone marrow failure, and drove clonal dominance in FA mouse models, while targeting MDM4 impaired leukemia cells in vitro and in vivo. Our results identify a linear route toward secondary leukemogenesis whereby early MDM4-driven downregulation of basal p53 activation plays a pivotal role, opening monitoring and therapeutic prospects.

Published
2023
Full Text
View/download PDF

9. Drug-drug interactions and physicochemical incompatibilities during acute phase after allo-SCT: Guidelines from the Francophone Society of Bone Marrow Transplantation and Cellular Therapy (SFGM-TC)

Author

Bénédicte, Bruno, Lucie, Capelle, Virginie, Denis, Olivier, Duval, Sorea, Selmouni, Alban, Villate, Delphine, Cabelguenne, Valérie, Coiteux, Tiphaine, Lachner-Gaubert, Ibrahim, Yakoub-Agha, Nicolas, Simon, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institute for Translational Research in Inflammation - U 1286 (INFINITE (Ex-Liric)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Lille Inflammation Research International Center - U 995 (LIRIC), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Groupe de Recherche sur les formes Injectables et les Technologies Associées - ULR 7365 (GRITA), and Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)

Subjects
[SDV]Life Sciences [q-bio]
Abstract

International audience; Since patients require multiple intravenous drugs, drug incompatibilities and drug interactions are frequent during the acute phase following hematopoietic cell transplantation. The risk of drug-drug interactions is increased in patients with several comorbidities. The goal of this workshop was to learn how to mitigate the risks of drug incompatibilities and interactions when their usage is therapeutically warranted. Our focus was on proton pump inhibitors and antiemetic drugs as they are routinely used in hematopoietic transplants and frequently lead to incompatibilities and interactions with other drugs such as immunosuppressives and antimicrobials. Routine procedures in transplantation such as the choice of vascular access devices, the setting of infusion lines, the scheduling of administration of drugs and their dilution volumes can be effective armaments to mitigate the risks of drug incompatibilities and interactions. In addition, a multidisciplinary concertation between clinicians, pharmacists and nurses is a key point in the success of patient's care.; Les interactions médicamenteuses et les incompatibilités physico-chimiques sont fréquentes durant la phase aiguë post-allogreffe chez des patients qui nécessitent plusieurs médicaments sous forme injectable. Le risque est accru chez les patients présentant plusieurs comorbidités. L’objectif de cet atelier était d’apprendre comment atténuer les risques d’incompatibilités et d’interactions médicamenteuses lorsque leur utilisation est justifiée sur le plan thérapeutique. Nous nous sommes concentrés sur les inhibiteurs de la pompe à protons et les antiémétiques, car ils sont couramment utilisés dans les greffes hématopoïétiques et entraînent fréquemment des incompatibilités et des interactions avec des médicaments essentiels tels que les immunosuppresseurs et les antimicrobiens. Notre atelier a conclu que les procédures de routine en greffe telles que le choix des dispositifs d’accès vasculaire, le montage des perfusions, le plan d’administration des médicaments et leur volume de dilution peuvent être des armes efficaces dans la lutte pour atténuer les risques d’incompatibilités et d’interactions médicamenteuses. Nous avons également exploré la valeur ajoutée d’une concertation multidisciplinaire entre cliniciens, pharmaciens et infirmières

Published
2023
Full Text
View/download PDF

10. Inotuzumab ozogamicin combined with chemotherapy in pediatric B-cell precursor CD22+ acute lymphoblastic leukemia: results of the phase IB ITCC-059 trial

Author

Edoardo Pennesi, Erica Brivio, Anneke C. J. Ammerlaan, Yilin Jiang, Vincent H. J. van der Velden, H. Berna Beverloo, Barbara Sleight, Franco Locatelli, Benoit Brethon, Claudia Rossig, Gernot Engstler, Anna Nilsson, Benedicte Bruno, Arnaud Petit, Bella Bielorai, Carmelo Rizzari, Fanny Rialland, Alba Rubio-San-Simón, Francisco J. Bautista Sirvent, Cristina Diaz-de-Heredia, Susana Rives, and Christian M. Zwaan

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Abstract

Inotuzumab Ozogamicin (InO) is a CD22-directed antibody conjugated with calicheamicin. The Phase 1B of the ITCC-059 trial tested InO combined with chemotherapy in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Relapsed /refractory CD22+ BCP-ALL pediatric patients were enrolled. The primary objective was to establish the Recommended Phase 2 Dose (RP2D). Secondary objectives included preliminary efficacy and tolerability. InO was combined with 1.5 mg/m2 of vincristine (days 3, 10, 17, 24), 20 mg/m2 of dexamethasone (two 5-day blocks, then amended), and intrathecal therapy. A rolling-6 design was used testing InO from 0.8 to 1.8 mg/m2/cycle. Between May-2020 and Apr-2022, 30 patients were treated, and 29 were evaluable for dose limiting toxicities (DLTs). At 1.1 mg/m2/cycle, two out of four patients had DLTs (liver toxicity). InO was de-escalated to 0.8 mg/m2/cycle (n=6) without DLTs while awaiting a protocol amendment to reduce dexamethasone dose to 10 mg/m2. Post amendment, InO was re-escalated to 1.1 mg/m2/cycle (n=6, 1 DLT), then to 1.4 mg/m2/cycle (n=3, no DLTs), and finally to 1.8 mg/m2/cycle (n=7, 1 DLT). Three additional patients were treated in an expansion cohort. The pooled response rate was 80% (24/30; 95%CI: 61.4% to 92.3%) and, among responders, 66.7% achieved minimal residual disease negativity. The RP2D of InO combined with vincristine, dexamethasone and IT therapy was declared at 1.8 mg/m2/cycle (1.5 mg/m2/cycle after remission) in a fractionated schedule. This combination showed an response rate similar to the single agent cohorts of this trial, with liver toxicity issues at the initial higher dexamethasone dose. #NTR5736

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results