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1. Prognostic impact of translocation t(14;16) in multiple myeloma according to the presence of additional genetic lesions

Author

Schavgoulidze, Anaïs, Perrot, Aurore, Cazaubiel, Titouan, Leleu, Xavier, Montes, Lydia, Jacquet, Caroline, Belhadj, Karim, Brechignac, Sabine, Frenzel, Laurent, Chalopin, Thomas, Rey, Philippe, Schiano de Collela, Jean-Marc, Dib, Mamoun, Caillot, Denis, Macro, Margaret, Fontan, Jean, Buisson, Laure, Pavageau, Luka, Roussel, Murielle, Manier, Salomon, Mohty, Mohamad, Martinet, Ludovic, Avet-Loiseau, Hervé, and Corre, Jill

Published
2023
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2. Biallelic deletion of 1p32 defines ultra-high-risk myeloma, but monoallelic del(1p32) remains a strong prognostic factor

Author

Schavgoulidze, Anaïs, Talbot, Alexis, Perrot, Aurore, Cazaubiel, Titouan, Leleu, Xavier, Manier, Salomon, Buisson, Laure, Mahéo, Sabrina, Do Souto Ferreira, Laura, Pavageau, Luka, Hulin, Cyrille, Marolleau, Jean-Pierre, Voillat, Laurent, Belhadj, Karim, Divoux, Marion, Slama, Borhane, Brechignac, Sabine, Macro, Margaret, Stoppa, Anne-Marie, Sanhes, Laurence, Orsini-Piocelle, Frédérique, Fontan, Jean, Chretien, Marie-Lorraine, Demarquette, Hélène, Mohty, Mohamad, Avet-Loiseau, Hervé, and Corre, Jill

Published
2023
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3. Primary plasma cell leukemias displaying t(11;14) have specific genomic, transcriptional, and clinical features

Author

Cazaubiel, Titouan, Leleu, Xavier, Perrot, Aurore, Manier, Salomon, Buisson, Laure, Maheo, Sabrina, Do Souto Ferreira, Laura, Lannes, Romain, Pavageau, Luka, Hulin, Cyrille, Marolleau, Jean-Pierre, Voillat, Laurent, Belhadj, Karim, Divoux, Marion, Slama, Borhane, Brechignac, Sabine, Macro, Margaret, Stoppa, Anne-Marie, Sanhes, Laurence, Orsini-Piocelle, Frédérique, Fontan, Jean, Chretien, Marie-Lorraine, Demarquette, Hélène, Mohty, Mohamad, Schavgoulidze, Anais, Avet-Loiseau, Herve, and Corre, Jill

Published
2022
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7. del(17p) without TP53 mutation confers a poor prognosis in intensively treated newly diagnosed patients with multiple myeloma

Author

Corre, Jill, Perrot, Aurore, Caillot, Denis, Belhadj, Karim, Hulin, Cyrille, Leleu, Xavier, Mohty, Mohamad, Facon, Thierry, Buisson, Laure, Do Souto, Laura, Lannes, Romain, Dufrechou, Stephanie, Prade, Naïs, Orsini-Piocelle, Frederique, Voillat, Laurent, Jaccard, Arnaud, Karlin, Lionel, Macro, Margaret, Brechignac, Sabine, Dib, Mamoun, Sanhes, Laurence, Fontan, Jean, Clement-Filliatre, Lauriane, Marolleau, Jean-Pierre, Minvielle, Stephane, Moreau, Philippe, and Avet-Loiseau, Hervé

Published
2021
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8. Del17p without TP53 mutation confers poor prognosis in intensively treated newly diagnosed multiple myeloma patients

Author

Corre, Jill, Perrot, Aurore, Caillot, Denis, Belhadj, Karim, Hulin, Cyrille, Leleu, Xavier, Mohty, Mohamad, Facon, Thierry, Buisson, Laure, Do Souto, Laura, Lannes, Romain, Dufrechou, Stephanie, Prade, Nais, Orsini-Piocelle, Frédérique, Voillat, Laurent, Jaccard, Arnaud, Karlin, Lionel, Macro, Margaret, Brechignac, Sabine, Dib, Mamoun, Sanhes, Laurence, Fontan, Jean, Filliatre‐Clement, Lauriane, Marolleau, Jean Pierre, Minvielle, Stephane, Moreau, Philippe, Avet-Loiseau, Hervé, Institut Universitaire du Cancer de Toulouse - Oncopole (IUCT Oncopole - UMR 1037), Université Toulouse III - Paul Sabatier (UT3), 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), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), CHU Dijon, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Hôpital Henri Mondor, Hôpital Haut-Lévêque [CHU Bordeaux], CHU Bordeaux [Bordeaux], Institut François Magendie, Hôpital de la Milétrie, Centre hospitalier universitaire de Poitiers (CHU Poitiers), Université Sorbonne Paris Cité (USPC), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service des Maladies du Sang [CHU Lille] (SMS), Hôpital Claude Huriez [Lille], CHU Lille-CHU Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre Hospitalier Annecy-Genevois [Saint-Julien-en-Genevois], Centre Hospitalier Chalon-sur-Saône William Morey, CHU Limoges, Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hospices Civils de Lyon (HCL), CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Hôpital Avicenne [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Centre Hospitalier Saint Jean de Perpignan, Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), CHU Amiens-Picardie, Integrative Oncogenomics of Multiple Myeloma Pathogenesis and Progression (CRCINA-ÉQUIPE 11), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Centre hospitalier universitaire de Nantes (CHU Nantes), Bernardo, Elizabeth, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Toulouse [Toulouse], Service des Maladies du Sang [CHRU Lille], Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)

Subjects
[SDV.CAN] Life Sciences [q-bio]/Cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer
Abstract

International audience; Despite tremendous improvements in the outcome of patients with multiple myeloma (MM) in the past decade, high-risk patients have not benefited from the approval of novel drugs. The most important prognostic factor is the loss of parts of the short arm of chromosome 17, known as deletion 17p (del(17p)). A recent publication (on a small number of patients) suggested that these patients are at very high-risk only if del(17p) is associated with TP53 mutations, the so-called "double-hit" population. To validate this finding, we designed a much larger study on 121 patients presenting del(17p) in >55% of their plasma cells, and homogeneously treated by an intensive approach. For these 121 patients, we performed deep next generation sequencing targeted on TP53. The outcome was then compared to a large control population (2505 patients lacking del(17p)). Our results confirmed that the "double hit" situation is the worst (median survival = 36 months), but that del(17p) alone also confers a poor outcome compared with the control cohort (median survival = 52.8 months vs 152.2 months, respectively). In conclusion, our study clearly confirms the extremely poor outcome of patients displaying "double hit", but also that del(17p) alone is still a very high-risk feature, confirming its value as a prognostic indicator for poor outcome.

Published
2020
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9. Eomes-Dependent Loss of the Co-activating Receptor CD226 Restrains CD8+ T Cell Anti-tumor Functions and Limits the Efficacy of Cancer Immunotherapy

Author

Weulersse, Marianne, Asrir, Assia, Pichler, Andrea A.C., Lemaitre, Lea, Braun, Matthias, Carrié, Nadège, Joubert, Marie Véronique, Le Moine, Marie, Do Souto, Laura, Gaud, Guillaume, Das, Indrajit, Brauns, Elisa, Scarlata, Clara Maria, Morandi, Elena, Sundarrajan, Ashmitha, Cuisinier, Marine, Buisson, Laure, Maheo, Sabrina, Kassem, Sahar, Agesta, Arantxa, Pérès, Michaël, Verhoeyen, Els, Martinez, Alejandra, Mazieres, Julien, Dupré, Loïc, Gossye, Thomas, Pancaldi, Vera, Guillerey, Camille, Ayyoub, Maha, Dejean, Anne S., Saoudi, Abdelhadi, Goriely, Stanislas, Avet-Loiseau, Herve, Bald, Tobias, Smyth, Mark J., Martinet, Ludovic, Weulersse, Marianne, Asrir, Assia, Pichler, Andrea A.C., Lemaitre, Lea, Braun, Matthias, Carrié, Nadège, Joubert, Marie Véronique, Le Moine, Marie, Do Souto, Laura, Gaud, Guillaume, Das, Indrajit, Brauns, Elisa, Scarlata, Clara Maria, Morandi, Elena, Sundarrajan, Ashmitha, Cuisinier, Marine, Buisson, Laure, Maheo, Sabrina, Kassem, Sahar, Agesta, Arantxa, Pérès, Michaël, Verhoeyen, Els, Martinez, Alejandra, Mazieres, Julien, Dupré, Loïc, Gossye, Thomas, Pancaldi, Vera, Guillerey, Camille, Ayyoub, Maha, Dejean, Anne S., Saoudi, Abdelhadi, Goriely, Stanislas, Avet-Loiseau, Herve, Bald, Tobias, Smyth, Mark J., and Martinet, Ludovic

Abstract

info:eu-repo/semantics/published

Published
2020

11. Eomes-Dependent Loss of the Co-activating Receptor CD226 Restrains CD8+ T Cell Anti-tumor Functions and Limits the Efficacy of Cancer Immunotherapy

Author

Weulersse, Marianne, primary, Asrir, Assia, additional, Pichler, Andrea C., additional, Lemaitre, Lea, additional, Braun, Matthias, additional, Carrié, Nadège, additional, Joubert, Marie-Véronique, additional, Le Moine, Marie, additional, Do Souto, Laura, additional, Gaud, Guillaume, additional, Das, Indrajit, additional, Brauns, Elisa, additional, Scarlata, Clara M., additional, Morandi, Elena, additional, Sundarrajan, Ashmitha, additional, Cuisinier, Marine, additional, Buisson, Laure, additional, Maheo, Sabrina, additional, Kassem, Sahar, additional, Agesta, Arantxa, additional, Pérès, Michaël, additional, Verhoeyen, Els, additional, Martinez, Alejandra, additional, Mazieres, Julien, additional, Dupré, Loïc, additional, Gossye, Thomas, additional, Pancaldi, Vera, additional, Guillerey, Camille, additional, Ayyoub, Maha, additional, Dejean, Anne S., additional, Saoudi, Abdelhadi, additional, Goriely, Stanislas, additional, Avet-Loiseau, Hervé, additional, Bald, Tobias, additional, Smyth, Mark J., additional, and Martinet, Ludovic, additional

Published
2020
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13. Eomes-Dependent CD226 Loss Alters TCR Responsiveness and Restrains CD8+ T Lymphocyte Anti-Tumor Functions

Author

Weulersse, Marianne, primary, Asrir, Assia, additional, Pichler, Andrea Charlotte, additional, Braun, Matthias, additional, Joubert, Marie-Véronique, additional, Do Souto, Laura, additional, Gaud, Guillaume, additional, Das, Indrajit, additional, Scarlata, Clara Maria, additional, Sundarrajan, Ashmitha, additional, Carrié, Nadège, additional, Kassem, Sahar, additional, Cuisinier, Marine, additional, Buisson, Laure, additional, Maheo, Sabrina, additional, Pérès, Michaël, additional, Verhoeyen, Els, additional, Martinez, Alejandra, additional, Guillerey, Camille, additional, Agesta, Arantxa, additional, Saoudi, Abdelhadi, additional, Ayyoub, Maha, additional, Dejean, Anne, additional, Avet-Loiseau, Hervé, additional, Bald, Tobias, additional, Smyth, Mark John, additional, and Martinet, ludovic, additional

Published
2019
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14. Myeloma MRD by deep sequencing from circulating tumor DNA does not correlate with results obtained in the bone marrow

Author

Mazzotti, Céline, primary, Buisson, Laure, additional, Maheo, Sabrina, additional, Perrot, Aurore, additional, Chretien, Marie-Lorraine, additional, Leleu, Xavier, additional, Hulin, Cyrille, additional, Manier, Salomon, additional, Hébraud, Benjamin, additional, Roussel, Murielle, additional, Do Souto, Laura, additional, Attal, Michel, additional, Avet-Loiseau, Hervé, additional, and Corre, Jill, additional

Published
2018
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15. del(17p) without TP53mutation confers a poor prognosis in intensively treated newly diagnosed patients with multiple myeloma

Author

Corre, Jill, Perrot, Aurore, Caillot, Denis, Belhadj, Karim, Hulin, Cyrille, Leleu, Xavier, Mohty, Mohamad, Facon, Thierry, Buisson, Laure, Do Souto, Laura, Lannes, Romain, Dufrechou, Stephanie, Prade, Naïs, Orsini-Piocelle, Frederique, Voillat, Laurent, Jaccard, Arnaud, Karlin, Lionel, Macro, Margaret, Brechignac, Sabine, Dib, Mamoun, Sanhes, Laurence, Fontan, Jean, Clement-Filliatre, Lauriane, Marolleau, Jean-Pierre, Minvielle, Stephane, Moreau, Philippe, and Avet-Loiseau, Hervé

Abstract

Despite tremendous improvements in the outcome of patients with multiple myeloma in the past decade, high-risk patients have not benefited from the approval of novel drugs. The most important prognostic factor is the loss of parts of the short arm of chromosome 17, known as deletion 17p (del(17p)). A recent publication (on a small number of patients) suggested that these patients are at very high-risk only if del(17p) is associated with TP53mutations, the so-called “double-hit” population. To validate this finding, we designed a much larger study on 121 patients presenting del(17p) in > 55% of their plasma cells, and homogeneously treated by an intensive approach. For these 121 patients, we performed deep next generation sequencing targeted on TP53. The outcome was then compared with a large control population (2505 patients lacking del(17p)). Our results confirmed that the “double hit” situation is the worst (median survival = 36 months), but that del(17p) alone also confers a poor outcome compared with the control cohort (median survival = 52.8 months vs 152.2 months, respectively). In conclusion, our study clearly confirms the extremely poor outcome of patients displaying “double hit,“ but also that del(17p) alone is still a very high-risk feature, confirming its value as a prognostic indicator for poor outcome.

Published
2021
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17. Biallelic deletion of 1p32 defines ultra-high-risk myeloma, but monoallelic del(1p32) remains a strong prognostic factor

Author

Schavgoulidze, Anaïs, Talbot, Alexis, Perrot, Aurore, Cazaubiel, Titouan, Leleu, Xavier, Manier, Salomon, Buisson, Laure, Maheo, Sabrina, Ferreira, Laura Do Souto, Pavageau, Luka, Hulin, Cyrille, Marolleau, Jean-Pierre, Voillat, Laurent, Belhadj, Karim, Divoux, Marion, Slama, Borhane, Brechignac, Sabine, Macro, Margaret, Stoppa, Anne-Marie, Sanhes, Laurence, Orsini-Piocelle, Frédérique, Fontan, Jean, Chretien, Marie-Lorraine, Demarquette, Hélène, Mohty, Mohamad, Avet-Loiseau, Hervé, and Corre, Jill

Abstract

Cytogenetics abnormalities (CAs) are known to be the preponderant prognostic factor in multiple myeloma. Our team has recently developed a prognostic score based on 6 CAs, with which del(1p32) appears to be the second worst abnormality after del(17p). This study aimed to confirm the adverse effect of 1p32 deletion in patients with newly diagnosed multiple myeloma (NDMM). Among 2551 patients with newly diagnosed multiple myeloma, 11% were harboring del(1p32). Their overall survival (OS) was significantly inferior compared with patients without del(1p32) (median OS: 49 months vs 124 months). Likewise, progression-free survival was significantly shorter. More importantly, biallelic del(1p32) conferred a dramatically poorer prognosis than a monoallelic del(1p32) (median OS: 25 months vs 60 months). As expected, the OS of patients with del(1p32) significantly decreased when this abnormality was associated with other high-risk CAs (del[17p], t([4;14], or gain[1q]). In the multivariate analysis, del(1p32) appeared as a negative prognostic factor; after adjustment for age and treatment, the risk of progression was 1.3 times higher among patients harboring del(1p32), and the risk of death was 1.9 times higher. At the dawn of risk-adapted treatment strategies, we have confirmed the adverse effect of del(1p32) in multiple myeloma and the relevance of its assessment at diagnosis.

Published
2022
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18. Eomes-Dependent Loss of the Co-activating Receptor CD226 Restrains CD8 + T Cell Anti-tumor Functions and Limits the Efficacy of Cancer Immunotherapy.

Author

Weulersse M, Asrir A, Pichler AC, Lemaitre L, Braun M, Carrié N, Joubert MV, Le Moine M, Do Souto L, Gaud G, Das I, Brauns E, Scarlata CM, Morandi E, Sundarrajan A, Cuisinier M, Buisson L, Maheo S, Kassem S, Agesta A, Pérès M, Verhoeyen E, Martinez A, Mazieres J, Dupré L, Gossye T, Pancaldi V, Guillerey C, Ayyoub M, Dejean AS, Saoudi A, Goriely S, Avet-Loiseau H, Bald T, Smyth MJ, and Martinet L

Subjects
Animals, Humans, Immune Checkpoint Inhibitors immunology, Immunotherapy methods, Mice, Mice, Inbred C57BL, Neoplasms therapy, Programmed Cell Death 1 Receptor immunology, Receptors, Antigen, T-Cell immunology, Signal Transduction immunology, Transcriptome immunology, Tumor Microenvironment immunology, Tumor Necrosis Factor Receptor Superfamily, Member 9 immunology, Antigens, Differentiation, T-Lymphocyte immunology, CD8-Positive T-Lymphocytes immunology, Neoplasms immunology, T-Box Domain Proteins immunology
Abstract

CD8 + T cells within the tumor microenvironment (TME) are exposed to various signals that ultimately determine functional outcomes. Here, we examined the role of the co-activating receptor CD226 (DNAM-1) in CD8 + T cell function. The absence of CD226 expression identified a subset of dysfunctional CD8 + T cells present in peripheral blood of healthy individuals. These cells exhibited reduced LFA-1 activation, altered TCR signaling, and a distinct transcriptomic program upon stimulation. CD226 neg CD8 + T cells accumulated in human and mouse tumors of diverse origin through an antigen-specific mechanism involving the transcriptional regulator Eomesodermin (Eomes). Despite similar expression of co-inhibitory receptors, CD8 + tumor-infiltrating lymphocyte failed to respond to anti-PD-1 in the absence of CD226. Immune checkpoint blockade efficacy was hampered in Cd226 -/- mice. Anti-CD137 (4-1BB) agonists also stimulated Eomes-dependent CD226 loss that limited the anti-tumor efficacy of this treatment. Thus, CD226 loss restrains CD8 + T cell function and limits the efficacy of cancer immunotherapy., Competing Interests: Declaration of Interests M.J.S. has research agreements with Bristol Myers Squibb and Tizona Therapeutics and is on the scientific advisory boards of Tizona Therapeutics and Compass Therapeutics. L.M. has research agreements with Bristol Myers Squibb, Sanofi-Aventis, and Roche., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Published
2020
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