10 results on '"Sabine Khalife‐Hachem"'
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2. When monoclonal gammopathy‐associated chronic neutrophilic leukemia is a reactive process distinct from a clonal myeloproliferative neoplasm: Lessons from mistakes
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Christophe Willekens, Claude Chahine, Matteo Dragani, Sabine Khalife‐Hachem, Camille Bigenwald, Julien Rossignol, Cristina Castilla‐Llorente, Alina Danu, Jean‐Marie Michot, Veronique Saada, Sophie Cotteret, Christophe Marzac, Aline Renneville, Isabelle Plo, Sophie Broutin, Nelly Bosselut, Bruno Cassinat, Julien Lazarovici, Nathalie Droin, and Stephane De Botton
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chronic neutrophilic leukemia ,leukemoid reaction ,leukocytosis ,MGUS ,proteasome inhibitor ,Diseases of the blood and blood-forming organs ,RC633-647.5 - Published
- 2023
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3. Molecular Landscape of Therapy-related Myeloid Neoplasms in Patients Previously Treated for Gynecologic and Breast Cancers
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Sabine Khalife-Hachem, Khalil Saleh, Florence Pasquier, Christophe Willekens, Anthony Tarabay, Leony Antoun, Thomas Grinda, Cristina Castilla-Llorente, Matthieu Duchmann, Cyril Quivoron, Nathalie Auger, Veronique Saada, Suzette Delaloge, Alexandra Leary, Aline Renneville, Ileana Antony-Debre, Filippo Rosselli, Stéphane De Botton, Flore Salviat, Christophe Marzac, and Jean-Baptiste Micol
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Diseases of the blood and blood-forming organs ,RC633-647.5 - Abstract
Definition of therapy-related myeloid neoplasms (TRMN) is only based on clinical history of exposure to leukemogenic therapy. No specific molecular classification combining therapy-related acute myeloid leukemia and therapy-related myelodysplastic syndromes has been proposed. We aimed to describe the molecular landscape of TRMN at diagnosis, among 77 patients with previous gynecologic and breast cancer with a dedicated next-generation sequencing panel covering 74 genes. We investigated the impact of clonal hematopoiesis of indeterminate potential-associated mutations (CHIP-AMs defined as presence at TRMN stage of mutations described in CHIP with a frequency >1%) on overall survival (OS) and the clinical relevance of a modified genetic ontogeny-based classifier that categorized patients in 3 subgroups. The most frequently mutated genes were TP53 (31%), DNMT3A (19%), IDH1/2 (13%), NRAS (13%), TET2 (12%), NPM1 (10%), PPM1D (9%), and PTPN11 (9%). CHIP-AMs were detected in 66% of TRMN patients, with no impact on OS. Yet, patients with CHIP-AM were older and had a longer time interval between solid tumor diagnosis and TRMN. According to our modified ontogeny-based classifier, we observed that the patients with TP53 or PPM1D mutations had more treatment lines and complex karyotypes, the “MDS-like” patients were older with more gene mutations, while patients with “De novo/pan-AML” mutations were younger with more balanced chromosomal translocations. Median OS within each subgroup was 7.5, 14.5, and 25.2 months, respectively, with statistically significant difference in multivariate analysis. These results support the integration of cytogenetic and molecular markers into the future TRMN classification to reflect the biological diversity of TRMN and its impact on outcomes.
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- 2021
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4. Germline RUNX1 Intragenic Deletion: Implications for Accurate Diagnosis of FPD/AML
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Nicolas Duployez, Jean-Edouard Martin, Sabine Khalife-Hachem, Ryane Benkhelil, Véronique Saada, Christophe Marzac, Nathalie Auger, Alice Marceau-Renaut, Rémi Favier, Paola Ballerini, Olivier Caron, André Baruchel, Stéphane de Botton, Claude Preudhomme, Jean-Baptiste Micol, Hana Raslova, and Iléana Antony-Debré
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Diseases of the blood and blood-forming organs ,RC633-647.5 - Published
- 2019
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5. Reduced Venetoclax Exposition to Seven Days of Azacitidine Is Efficient in Treatment-Naïve Patients with Acute Myeloid Leukemia
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Christophe Willekens, Samy Chraibi, Justine Decroocq, Benjamin Carpentier, Delphine Lebon, Sarah Bonnet, Nicolas Gauthier, Arnaud Pagès, Matteo Dragani, Sabine Khalife-Hachem, Jean-Baptiste Micol, Florence Pasquier, Stefan Wickenhauser, Véronique Saada, Véronique Vergé, Ahmadreza Arbab, Christophe Marzac, Laurent Pascal, Damien Roos-Weil, Eric Jourdan, Didier Bouscary, Stéphane de Botton, Cellules souches hématopoïétiques et développement des hémopathies myéloïdes (CSHMyelo), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Amiens-Picardie, HEMATIM - Hématopoïèse et immunologie - UR UPJV 4666 (HEMATIM), Université de Picardie Jules Verne (UPJV)-CHU Amiens-Picardie-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Montpellier, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Commissariat à l'énergie atomique et aux énergies alternatives - Laboratoire d'Electronique et de Technologie de l'Information (CEA-LETI), Direction de Recherche Technologique (CEA) (DRT (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), INSERM UMR 1287 Département d'hématologie, Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Dynamique moléculaire de la transformation hématopoïétique (Dynamo), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut Gustave Roussy (IGR), Département de biologie et pathologie médicales [Gustave Roussy], Université Grenoble Alpes - UFR Médecine (UGA UFRM), Université Grenoble Alpes (UGA), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université (SU), and Université de Montpellier (UM)
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Immunology ,Cell Biology ,Hematology ,Biochemistry ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology - Abstract
International audience
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- 2022
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6. ATG2B/GSKIP in de novo acute myeloid leukemia (AML): high prevalence of germline predisposition in French West Indies
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Jean-Edouard Martin, Christine Bellanné-Chantelot, Olivier Caron, Pascal Fuseau, Nathalie Auger, Barbara Schmaltz-Panneau, Sophie Cotteret, Stéphane de Botton, Christophe Willekens, Florence Pasquier, Christophe Marzac, Jean-Baptiste Micol, Jean Pegliasco, Maureen Lopez, William Vainchenker, Adel Ben-Ali, Véronique Saada, Carole Bourdin, Flore Salviat, Odile Bera, Sabine Khalife-Hachem, Isabelle Plo, Cristina Castilla-Llorent, Philippe Helias, Jean-Côme Meniane, Samy Chraibi, and Raouf Ben-Abdelali
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Cancer Research ,High prevalence ,Adult patients ,business.industry ,De novo acute ,Myeloid leukemia ,Hematology ,Germline ,Oncology ,hemic and lymphatic diseases ,Immunology ,Genetic predisposition ,Medicine ,business ,West indies - Abstract
Genetic predisposition to acute myeloid leukemia (AML) concerns a minority of adult patients. Development of high-throughput sequencing technologies over the last ten years allowed identification o...
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- 2021
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7. Therapy-related myeloid neoplasms following treatment with PARP inhibitors: new molecular insights
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Sylvain Garciaz, Olivier Caron, Amine Belhabri, Norbert Vey, Jacques Vargaftig, Veronique Verge, Sophie Cotteret, S. de Botton, Flore Salviat, Suzette Delaloge, Iléana Antony-Debré, Patricia Pautier, Christophe Marzac, Sarah Bertoli, Florence Pasquier, Jean-Baptiste Micol, Sabine Khalife-Hachem, Alexandra Leary, Etienne Rouleau, A Renneville, M Kfoury, Filippo Rosselli, Thomas Grinda, Christian Recher, Madalina Uzunov, Jean-Edouard Martin, Gabriel Etienne, Institut Gustave Roussy (IGR), Université Paris-Saclay, Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Cellules souches hématopoïétiques et développement des hémopathies myéloïdes (CSHMyelo), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Institut Curie [Paris], CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Léon Bérard [Lyon], Institut Universitaire du Cancer de Toulouse - Oncopole (IUCT Oncopole - UMR 1037), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM), Intégrité du génome et cancers (IGC), École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Service de biostatistique et d'épidémiologie (SBE), Direction de la recherche clinique [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Département de médecine oncologique [Gustave Roussy], Oncologie gynécologique, Institut Bergonié [Bordeaux], UNICANCER, Hôpital Haut-Lévêque [CHU Bordeaux], CHU Bordeaux [Bordeaux], Biomarqueurs prédictifs et nouvelles stratégies moléculaires en thérapeutique anticancéreuse (U981), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département d'hématologie [Gustave Roussy], Institut Gustave Roussy (IGR)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Génétique (Biologie pathologie), Département de biologie et pathologie médicales [Gustave Roussy], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM), École pratique des hautes études (EPHE), and NUNES, Jacques A
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Myeloid ,DNA Repair ,Poly ADP ribose polymerase ,[SDV]Life Sciences [q-bio] ,MEDLINE ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,Poly(ADP-ribose) Polymerase Inhibitors ,Bioinformatics ,03 medical and health sciences ,0302 clinical medicine ,Text mining ,[SDV.CAN] Life Sciences [q-bio]/Cancer ,Neoplasms ,Humans ,Medicine ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,Ovarian Neoplasms ,0303 health sciences ,Therapy related ,business.industry ,Hematology ,3. Good health ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,Female ,Poly(ADP-ribose) Polymerases ,business - Abstract
International audience; No abstract available
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- 2021
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8. Therapy Related Myeloid Neoplasm Post PARP Inhibitors: Potential Clonal Selection
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Madalina Uzunov, Sarah Bertoli, Amine Belhabri, Iléana Antony-Debré, Véronique Saada, Nathalie Auger, Thomas Grinda, Sabine Khalife-Hachem, Olivier Caron, Alexandra Leary, Maria Kfoury, Christel Guillouf, Florence Pasquier, Filippo Rosselli, Stéphane de Botton, Sylvain Garciaz, Gabriel Etienne, Etienne Rouleau, Jacques Vargaftig, Patricia Pautier, Christophe Marzac, Jean-Baptiste Micol, Norbert Vey, Jean-Edouard Martin, and Flore Salviat
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Oncology ,medicine.medical_specialty ,Chemotherapy ,Myeloid ,business.industry ,medicine.medical_treatment ,Immunology ,Cell Biology ,Hematology ,Gene mutation ,Biochemistry ,Olaparib ,Targeted therapy ,Radiation therapy ,chemistry.chemical_compound ,medicine.anatomical_structure ,Germline mutation ,chemistry ,Internal medicine ,medicine ,Rucaparib ,business - Abstract
Introduction Clonal selection is one of the mechanisms leading to therapy-related myeloid neoplasms (TRMN). A preexisting somatic mutation in hematopoietic stem cell (defined as clonal hematopoiesis [CH]) emerges under pressure of chemotherapy or radiotherapy, leading to TRMN development. Most of these mutations belong to the DNA damage response (DDR) pathway as TP53 or PPM1D mutations and are known to confer a dismal prognosis. Recently authorized for the treatment of ovarian cancers (OC), the poly (ADP-ribose) polymerase inhibitors (PARPi) represent a promising targeted therapy. However, by inducing DNA damage and altering DNA repair process, PARP inhibition could represent a challenge for the genetic stability of the healthy tissues. Thus, we assessed the effect of PARP inhibition on the development of CH and TRMN after PARPi treatment for OC (TRMN-PARPi) in combination with chemotherapies. Methods Firstly, we performed a targeted 77 genes mutational analysis using Next Generation Sequencing (NGS) in 13 patients exposed to PARPi without TRMN. Secondly, we retrospectively identified, with the help of the UNIHEM group of Unicancer, 17 patients who experienced TRMN-PARPi. Clinical, biological and survival data were collected and compared to 23 OC patients with TRMN not treated with PARPi (Gustave Roussy institutional database). Lastly, NGS was performed for 3 patients with TRMN-PARPi with sequential sampling. Patient's samples were obtained with informed consent. Results Thirteen OC patients during maintenance treatment with PARPi without TRMN were explored by NGS. Median age at NGS was 64.5 years old (yo) (40.5-75.3). 4/13 (31%) patients harbored BRCA1/2 germline mutation. Time between OC diagnosis and NGS was 4.3 y (1-11.6). The median number of chemotherapy line at PARPi initiation was 2 (1-3). 7 received Olaparib, 5 Niraparib and 1 Rucaparib. The median duration of PARPi treatment before NGS was 4.7 months (1.1-25.1). 12/13 patients experienced hematological toxicities during the PARPi treatment. CH was found in 10/13 (77%) patients (Figure 1a), including mutations of DDR genes in 8/10 (80%). 6/8 (75%) patients had 2 or more gene mutations. Next we identified 17 cases of TRMN occurring during or after PARPi administration for OC (6/17 [35%] t-AML and 11/17 [65%] t-MDS). 12/17 (71%) patients had BRCA germline mutations (7 BRCA1 and 5 BRCA2). All received Olaparib with a median dose of 600mg/d (400-1200). Median duration of Olaparib treatment was 1.7 years (0.2-4.6). TRMN-PARPi were described 1.4 months (0-10.9) after the end of PARPi administration. We compared these patients to a cohort of TRMN post OC not treated by PARPi. Number of therapy lines for OC, time between TRMN and OC diagnosis, median age at TRMN, were, for TRMN-PARPi, 2 (1-8), 5.9 y (0.9-20.8), 64.4 yo (46-74); respectively, compared to 3 (1-8), 4.9 y (1.7-36.9), 59.3 yo (35.7-85.7); (p=ns). TRMN-PARPi cytogenetic was unfavorable for 16/17 (94%) (including 11/17 [65%] complex karyotype) compared to 16/23 (70%) (11/23 [48%] complex karyotype). C Median survival was significantly lower in the TRMN-PARPi group 3.9 months 95%CI [2.0-9.7] and 6.1 months 95%CI [4.1-15.8] respectively, p=0.046, Fig 1b). However, median survival from OC diagnosis was not different between the two groups 6.2 y 95%CI [5.6-NA] for TRMN-PARPi vs 5.6 y 95%CI [5.0-11.6]. NGS was available for 8/17 TRMN-PARPi and revealed mutations in DDR genes in 7/8 patients (6 patients with TP53 mutation, 2 with PPM1D mutation). For 3 patients, we had samples from OC stage, before PARPi administration. We found that mutations from TRMN stage were present at lower frequency, confirming clonal selection by PARPi treatment (Figure 1c). Conclusions Here we described, for the first time, a cohort of TRMN patients previously treated with PARPi for an OC. Intriguingly, most of these TRMN occurred with a short latency at the end of PARPi treatment, with unfavorable cytogenetic and very short OS. Moreover, we found a very high percentage of CH involved in the DDR pathway (62%) in patients under PARPi treatment without TRMN suggesting a potential clonal selection which could lead ultimately to TRMN. PARPi are now indicated in 1rst line high grade OC regardless of BRCA status, which should expand indications. Benefit for OC patients is not questionable; however, caution will be warranted for patients with CH before PARPi treatment, especially implicating DDR mutations. Disclosures Etienne: Incyte: Consultancy, Speakers Bureau; Pfizer: Consultancy, Speakers Bureau; Bristol-Myers Squibb: Consultancy, Research Funding, Speakers Bureau; Novartis: Consultancy, Research Funding, Speakers Bureau.
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- 2020
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9. Spontaneous molecular response of IDH2 acute myeloid leukemia
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Christophe Marzac, Jean-Baptiste Micol, Valerie Camara-Clayette, Eric Hernandez, Raouf Benabdelali, Stéphane de Botton, Sophie Cotteret, Jean Pegliasco, Véronique Saada, and Sabine Khalife-Hachem
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medicine.medical_specialty ,Hematology ,Fatal outcome ,business.industry ,Myeloid leukemia ,General Medicine ,medicine.disease ,IDH2 ,Neoplasm regression ,Leukemia ,Molecular Response ,Internal medicine ,Cancer research ,medicine ,business - Published
- 2019
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10. ANTIBIOSTOP, for all?
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Sabine Khalife-Hachem, Florence Pasquier, and Jean-Baptiste Micol
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Microbiology (medical) ,High rate ,Pediatrics ,medicine.medical_specialty ,Chemotherapy ,General Immunology and Microbiology ,business.industry ,Incidence (epidemiology) ,medicine.medical_treatment ,MEDLINE ,General Medicine ,Neutropenia ,medicine.disease ,03 medical and health sciences ,0302 clinical medicine ,Infectious Diseases ,hemic and lymphatic diseases ,030220 oncology & carcinogenesis ,medicine ,030212 general & internal medicine ,Complication ,business ,Febrile neutropenia - Abstract
Febrile neutropenia (FN) is a frequent complication of chemotherapy, responsible for high rates of morbidity and mortality [1]. The incidence of FN depends upon depth and duration of neutropenia. P...
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- 2018
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