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The genetics of Richter syndrome reveals disease heterogeneity and predicts survival after transformation

The genetics of Richter syndrome reveals disease heterogeneity and predicts survival after transformation
The genetics of Richter syndrome reveals disease heterogeneity and predicts survival after transformation
Richter syndrome (RS) represents the development of diffuse large B-cell lymphoma in the context of chronic lymphocytic leukemia. The scarcity of biologic information about RS has hampered the identification of molecular predictors of RS outcome. We addressed this issue by performing a comprehensive molecular characterization of 86 pathologically proven RS. TP53 disruption (47.1%) and c-MYC abnormalities (26.2%) were the most frequent alterations, whereas common genetic lesions of de novo diffuse large B-cell lymphoma were rare or absent. By multivariate analysis, lack of TP53 disruption (hazard ratio, 0.43; P = .003) translated into significant survival advantage with 57% reduction in risk of death. An algorithm based on TP53 disruption, response to RS treatment, and Eastern Cooperative Oncology Group performance status had 80.9% probability of correctly discriminating RS survival (c-index = .809). RS that were clonally unrelated to the paired chronic lymphocytic leukemia phase were clinically and biologically different from clonally related RS because of significantly longer survival (median, 62.5 months vs 14.2 months; P = .017) and lower prevalence of TP53 disruption (23.1% vs 60.0%; P = .018) and B-cell receptor stereotypy (7.6% vs 50.0%; P = .009). The molecular dissection of RS into biologically distinct categories highlights the genetic heterogeneity of this disorder and provides clinically relevant information for refining the prognostic stratification of patients.
0006-4971
3391-3401
Rossi, Davide
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Spina, Valeria
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Deambrogi, Clara
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Rasi, Silvia
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Laurenti, Luca
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Stamatopoulos, Kostas
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Arcaini, Luca
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Lucioni, Marco
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Rocque, Gabrielle B.
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Xu-Monette, Zijun Y
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Visco, Carlo
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Chang, Julie
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Chigrinova, Ekaterina
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Forconi, Francesco
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Marasca, Roberto
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Besson, Caroline
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Papadaki, Theodora
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Paulli, Marco
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Larocca, Luigi M
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Pileri, Stefano A
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Gattei, Valter
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Bertoni, Francesco
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Foà, Robin
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Young, Ken H
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Gaidano, Gianluca
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Rossi, Davide
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Spina, Valeria
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Deambrogi, Clara
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Rasi, Silvia
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Laurenti, Luca
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Stamatopoulos, Kostas
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Arcaini, Luca
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Lucioni, Marco
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Rocque, Gabrielle B.
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Xu-Monette, Zijun Y
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Visco, Carlo
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Chang, Julie
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Chigrinova, Ekaterina
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Forconi, Francesco
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Marasca, Roberto
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Besson, Caroline
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Papadaki, Theodora
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Paulli, Marco
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Larocca, Luigi M
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Pileri, Stefano A
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Gattei, Valter
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Bertoni, Francesco
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Foà, Robin
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Young, Ken H
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Gaidano, Gianluca
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Rossi, Davide, Spina, Valeria, Deambrogi, Clara, Rasi, Silvia, Laurenti, Luca, Stamatopoulos, Kostas, Arcaini, Luca, Lucioni, Marco, Rocque, Gabrielle B., Xu-Monette, Zijun Y, Visco, Carlo, Chang, Julie, Chigrinova, Ekaterina, Forconi, Francesco, Marasca, Roberto, Besson, Caroline, Papadaki, Theodora, Paulli, Marco, Larocca, Luigi M, Pileri, Stefano A, Gattei, Valter, Bertoni, Francesco, Foà, Robin, Young, Ken H and Gaidano, Gianluca (2011) The genetics of Richter syndrome reveals disease heterogeneity and predicts survival after transformation. Blood, 117 (12), 3391-3401. (doi:10.1182/blood-2010-09-302174). (PMID:21266718)

Record type: Article

Abstract

Richter syndrome (RS) represents the development of diffuse large B-cell lymphoma in the context of chronic lymphocytic leukemia. The scarcity of biologic information about RS has hampered the identification of molecular predictors of RS outcome. We addressed this issue by performing a comprehensive molecular characterization of 86 pathologically proven RS. TP53 disruption (47.1%) and c-MYC abnormalities (26.2%) were the most frequent alterations, whereas common genetic lesions of de novo diffuse large B-cell lymphoma were rare or absent. By multivariate analysis, lack of TP53 disruption (hazard ratio, 0.43; P = .003) translated into significant survival advantage with 57% reduction in risk of death. An algorithm based on TP53 disruption, response to RS treatment, and Eastern Cooperative Oncology Group performance status had 80.9% probability of correctly discriminating RS survival (c-index = .809). RS that were clonally unrelated to the paired chronic lymphocytic leukemia phase were clinically and biologically different from clonally related RS because of significantly longer survival (median, 62.5 months vs 14.2 months; P = .017) and lower prevalence of TP53 disruption (23.1% vs 60.0%; P = .018) and B-cell receptor stereotypy (7.6% vs 50.0%; P = .009). The molecular dissection of RS into biologically distinct categories highlights the genetic heterogeneity of this disorder and provides clinically relevant information for refining the prognostic stratification of patients.

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More information

e-pub ahead of print date: 25 January 2011
Published date: 24 March 2011
Organisations: Cancer Sciences

Identifiers

Local EPrints ID: 358130
URI: http://eprints.soton.ac.uk/id/eprint/358130
ISSN: 0006-4971
PURE UUID: 30dea01c-7f64-4c95-a5e8-9e84a11e45d1
ORCID for Francesco Forconi: ORCID iD orcid.org/0000-0002-2211-1831

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Date deposited: 08 Oct 2013 10:27
Last modified: 15 Mar 2024 03:40

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Contributors

Author: Davide Rossi
Author: Valeria Spina
Author: Clara Deambrogi
Author: Silvia Rasi
Author: Luca Laurenti
Author: Kostas Stamatopoulos
Author: Luca Arcaini
Author: Marco Lucioni
Author: Gabrielle B. Rocque
Author: Zijun Y Xu-Monette
Author: Carlo Visco
Author: Julie Chang
Author: Ekaterina Chigrinova
Author: Roberto Marasca
Author: Caroline Besson
Author: Theodora Papadaki
Author: Marco Paulli
Author: Luigi M Larocca
Author: Stefano A Pileri
Author: Valter Gattei
Author: Francesco Bertoni
Author: Robin Foà
Author: Ken H Young
Author: Gianluca Gaidano

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