Genome wide DNA-profiling of HIV-related B-cell lymphomas

Daniela Capello; Marta Scandurra; Giulia Poretti; Paola M.V. Rancoita; Michael Mian; Annunziata Gloghini; Clara Deambrogi; Maurizio Martini; Davide Rossi; Timothy C. Greiner; Wing C. Chan; Maurilio Ponzoni; Santiago M. Moreno; Miguel A. Piris; Vincenzo Canzonieri; Michele Spina; Umberto Tirelli; Giorgio Inghirami; Andrea Rinaldi; Emanuele Zucca; Riccardo D. Favera; Franco Cavalli; Luigi Maria Larocca; Ivo Kwee; Antonino Carbone; Gianluca Gaidano; Francesco Bertoni

doi:10.1111/j.1365-2141.2009.07943.x

Genome wide DNA-profiling of HIV-related B-cell lymphomas

Daniela Capello
, Marta Scandurra
, Giulia Poretti
, Paola M.V. Rancoita
, Michael Mian
, Annunziata Gloghini
, Clara Deambrogi
, Maurizio Martini
, Davide Rossi
, Timothy C. Greiner
, Wing C. Chan
, Maurilio Ponzoni
, Santiago M. Moreno
, Miguel A. Piris
, Vincenzo Canzonieri
, Michele Spina
, Umberto Tirelli
, Giorgio Inghirami
, Andrea Rinaldi
, Emanuele Zucca

Riccardo D. Favera, Franco Cavalli, Luigi Maria Larocca, Ivo Kwee, Antonino Carbone, Gianluca Gaidano, Francesco Bertoni

Department of Translational Medicine

Research output: Contribution to journal › Article › peer-review

Abstract

Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0·032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42·5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0·029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.

Original language	English
Pages (from-to)	245-255
Number of pages	11
Journal	British Journal of Haematology
Volume	148
Issue number	2
DOIs	https://doi.org/10.1111/j.1365-2141.2009.07943.x
Publication status	Published - Jan 2010

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Acquired immunodeficiency syndrome
Affymetrix
Diffuse large B-cell lymphoma
Fragile Histidine Triad
WW domain-containing Oxidoreductase

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10.1111/j.1365-2141.2009.07943.x

Cite this

Capello, D., Scandurra, M., Poretti, G., Rancoita, P. M. V., Mian, M., Gloghini, A., Deambrogi, C., Martini, M., Rossi, D., Greiner, T. C., Chan, W. C., Ponzoni, M., Moreno, S. M., Piris, M. A., Canzonieri, V., Spina, M., Tirelli, U., Inghirami, G., Rinaldi, A., ... Bertoni, F. (2010). Genome wide DNA-profiling of HIV-related B-cell lymphomas. British Journal of Haematology, 148(2), 245-255. https://doi.org/10.1111/j.1365-2141.2009.07943.x

@article{6f1343bdad2e46618a02ba6918253e21,

title = "Genome wide DNA-profiling of HIV-related B-cell lymphomas",

abstract = "Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0·032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42·5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0·029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.",

keywords = "Acquired immunodeficiency syndrome, Affymetrix, Diffuse large B-cell lymphoma, Fragile Histidine Triad, WW domain-containing Oxidoreductase",

author = "Daniela Capello and Marta Scandurra and Giulia Poretti and Rancoita, \{Paola M.V.\} and Michael Mian and Annunziata Gloghini and Clara Deambrogi and Maurizio Martini and Davide Rossi and Greiner, \{Timothy C.\} and Chan, \{Wing C.\} and Maurilio Ponzoni and Moreno, \{Santiago M.\} and Piris, \{Miguel A.\} and Vincenzo Canzonieri and Michele Spina and Umberto Tirelli and Giorgio Inghirami and Andrea Rinaldi and Emanuele Zucca and Favera, \{Riccardo D.\} and Franco Cavalli and Larocca, \{Luigi Maria\} and Ivo Kwee and Antonino Carbone and Gianluca Gaidano and Francesco Bertoni",

year = "2010",

month = jan,

doi = "10.1111/j.1365-2141.2009.07943.x",

language = "English",

volume = "148",

pages = "245--255",

journal = "British Journal of Haematology",

issn = "0007-1048",

publisher = "John Wiley and Sons Inc.",

number = "2",

}

Capello, D, Scandurra, M, Poretti, G, Rancoita, PMV, Mian, M, Gloghini, A, Deambrogi, C, Martini, M, Rossi, D, Greiner, TC, Chan, WC, Ponzoni, M, Moreno, SM, Piris, MA, Canzonieri, V, Spina, M, Tirelli, U, Inghirami, G, Rinaldi, A, Zucca, E, Favera, RD, Cavalli, F, Larocca, LM, Kwee, I, Carbone, A, Gaidano, G & Bertoni, F 2010, 'Genome wide DNA-profiling of HIV-related B-cell lymphomas', British Journal of Haematology, vol. 148, no. 2, pp. 245-255. https://doi.org/10.1111/j.1365-2141.2009.07943.x

TY - JOUR

T1 - Genome wide DNA-profiling of HIV-related B-cell lymphomas

AU - Capello, Daniela

AU - Scandurra, Marta

AU - Poretti, Giulia

AU - Rancoita, Paola M.V.

AU - Mian, Michael

AU - Gloghini, Annunziata

AU - Deambrogi, Clara

AU - Martini, Maurizio

AU - Rossi, Davide

AU - Greiner, Timothy C.

AU - Chan, Wing C.

AU - Ponzoni, Maurilio

AU - Moreno, Santiago M.

AU - Piris, Miguel A.

AU - Canzonieri, Vincenzo

AU - Spina, Michele

AU - Tirelli, Umberto

AU - Inghirami, Giorgio

AU - Rinaldi, Andrea

AU - Zucca, Emanuele

AU - Favera, Riccardo D.

AU - Cavalli, Franco

AU - Larocca, Luigi Maria

AU - Kwee, Ivo

AU - Carbone, Antonino

AU - Gaidano, Gianluca

AU - Bertoni, Francesco

PY - 2010/1

Y1 - 2010/1

N2 - Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0·032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42·5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0·029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.

AB - Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0·032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42·5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0·029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.

KW - Acquired immunodeficiency syndrome

KW - Affymetrix

KW - Diffuse large B-cell lymphoma

KW - Fragile Histidine Triad

KW - WW domain-containing Oxidoreductase

UR - https://www.scopus.com/pages/publications/72649089121

U2 - 10.1111/j.1365-2141.2009.07943.x

DO - 10.1111/j.1365-2141.2009.07943.x

M3 - Article

SN - 0007-1048

VL - 148

SP - 245

EP - 255

JO - British Journal of Haematology

JF - British Journal of Haematology

IS - 2

ER -

Genome wide DNA-profiling of HIV-related B-cell lymphomas

Abstract

UN SDGs

Keywords

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