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Mutation of BAX occurs infrequently in acquired immunodeficiency syndrome-related non-Hodgkin's lymphomas

Mutation of BAX occurs infrequently in acquired immunodeficiency syndrome-related non-Hodgkin's lymphomas
Mutation of BAX occurs infrequently in acquired immunodeficiency syndrome-related non-Hodgkin's lymphomas
Acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin's lymphomas (AIDS-NHLs) consistently derive from B cells, are histologically heterogeneous, and are associated with distinct molecular pathways depending upon histology. Recently, it has been proposed that inactivating mutations of the bax death agonist may contribute to the pathogenesis of human tumors. In particular, among B-cell malignancies, BAX mutations have been detected at a certain frequency in Burkitt lymphomas. This study is aimed at defining the status of the BAX gene throughout the clinicopathologic spectrum of AIDS-NHL (n = 54), including AIDS-related Burkitt lymphoma (n = 14), AIDS-related Burkitt-like lymphoma (n = 8), AIDS-related diffuse large cell lymphoma (n = 15), AIDS-related primary central nervous system lymphoma (n = 6), and AIDS-related primary effusion lymphoma (n = 11). All 6 BAX exons and flanking sequences were subjected to mutational analysis by polymerase chain reaction-single strand conformation polymorphism followed by DNA direct sequencing of positive cases. Mutations of BAX among AIDS-NHL were restricted to a cell line of AIDS-related primary effusion lymphoma, which harbored a frameshift mutation causing the introduction of a proximal stop codon. All other AIDS-NHL displayed wild-type BAX alleles. In order to investigate whether BAX inactivation in AIDS-NHL may occur through mechanisms other than gene mutation, bax protein expression was investigated by Western blot analysis or immunohistochemistry in selected cases. All AIDS-NHL analyzed expressed normal bax proteins. Overall, this study indicates that deregulation of apoptotic control in AIDS-NHL is not caused by BAX alterations. Genes Chromosomes Cancer 27:177-182, 2000.
1045-2257
177-182
Gaidano, Gianluca
1a6a7107-107b-4891-82e0-5fedadd2f65a
Vivenza, Daniela
5895ef25-7092-4eb0-a93f-e897871d8b47
Forconi, Francesco
ce9ed873-58cf-4876-bf3a-9ba1d163edc8
Capello, Daniela
f4d381f4-aaa6-47ae-bebf-53b0aed65055
Gloghini, Annunziata
0190240b-12dd-41b1-ae0e-454effaf5393
Bhatia, Kishor
a0b4e0af-f51e-482f-a33e-2f3af3e9d3c3
Gutierrez, Marina
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Gallicchio, Margherita
e6dbe17c-45fc-436f-8f9d-6bb37ae044ff
Avanzi, Gian Carlo
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Fassone, Lucia
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Ariatti, Cristiano
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Buonaiuto, Daniela
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Cingolani, Antonella
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Saglio, Giuseppe
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Tirelli, Umberto
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Larocca, Luigi M.
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Dalla-Favera, Riccardo
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Carbone, Antonino
ea9f50b5-0bd5-4429-b436-4ecb4471d1b6
Gaidano, Gianluca
1a6a7107-107b-4891-82e0-5fedadd2f65a
Vivenza, Daniela
5895ef25-7092-4eb0-a93f-e897871d8b47
Forconi, Francesco
ce9ed873-58cf-4876-bf3a-9ba1d163edc8
Capello, Daniela
f4d381f4-aaa6-47ae-bebf-53b0aed65055
Gloghini, Annunziata
0190240b-12dd-41b1-ae0e-454effaf5393
Bhatia, Kishor
a0b4e0af-f51e-482f-a33e-2f3af3e9d3c3
Gutierrez, Marina
90a9356b-67e8-4dd0-8460-73f96561509d
Gallicchio, Margherita
e6dbe17c-45fc-436f-8f9d-6bb37ae044ff
Avanzi, Gian Carlo
e8803fd6-24e8-4949-93c9-e2b4a96f6605
Fassone, Lucia
e49ae2bd-7f9a-46ad-8e84-769852b487d8
Ariatti, Cristiano
f635afe6-33de-401b-ab85-3cb5bbde2610
Buonaiuto, Daniela
20cfd1e7-ac34-4e4b-8ae1-d8e178193d62
Cingolani, Antonella
5c375a25-2d63-46b0-90ad-783a0fc9c689
Saglio, Giuseppe
46ec4e74-92c7-4459-ac47-0b10cbcd887e
Tirelli, Umberto
160cb63e-e240-4b49-ba50-24bccc6bd0fb
Larocca, Luigi M.
9429df66-edeb-46d4-b148-bb5137d91c63
Dalla-Favera, Riccardo
74900c86-4420-4aac-a60e-1103fb60182b
Carbone, Antonino
ea9f50b5-0bd5-4429-b436-4ecb4471d1b6

Gaidano, Gianluca, Vivenza, Daniela, Forconi, Francesco, Capello, Daniela, Gloghini, Annunziata, Bhatia, Kishor, Gutierrez, Marina, Gallicchio, Margherita, Avanzi, Gian Carlo, Fassone, Lucia, Ariatti, Cristiano, Buonaiuto, Daniela, Cingolani, Antonella, Saglio, Giuseppe, Tirelli, Umberto, Larocca, Luigi M., Dalla-Favera, Riccardo and Carbone, Antonino (2000) Mutation of BAX occurs infrequently in acquired immunodeficiency syndrome-related non-Hodgkin's lymphomas. Genes, Chromosomes and Cancer, 27 (2), 177-182. (doi:10.1002/(SICI)1098-2264(200002)27:2<177::AID-GCC9>3.0.CO;2-O). (PMID:10612806)

Record type: Article

Abstract

Acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin's lymphomas (AIDS-NHLs) consistently derive from B cells, are histologically heterogeneous, and are associated with distinct molecular pathways depending upon histology. Recently, it has been proposed that inactivating mutations of the bax death agonist may contribute to the pathogenesis of human tumors. In particular, among B-cell malignancies, BAX mutations have been detected at a certain frequency in Burkitt lymphomas. This study is aimed at defining the status of the BAX gene throughout the clinicopathologic spectrum of AIDS-NHL (n = 54), including AIDS-related Burkitt lymphoma (n = 14), AIDS-related Burkitt-like lymphoma (n = 8), AIDS-related diffuse large cell lymphoma (n = 15), AIDS-related primary central nervous system lymphoma (n = 6), and AIDS-related primary effusion lymphoma (n = 11). All 6 BAX exons and flanking sequences were subjected to mutational analysis by polymerase chain reaction-single strand conformation polymorphism followed by DNA direct sequencing of positive cases. Mutations of BAX among AIDS-NHL were restricted to a cell line of AIDS-related primary effusion lymphoma, which harbored a frameshift mutation causing the introduction of a proximal stop codon. All other AIDS-NHL displayed wild-type BAX alleles. In order to investigate whether BAX inactivation in AIDS-NHL may occur through mechanisms other than gene mutation, bax protein expression was investigated by Western blot analysis or immunohistochemistry in selected cases. All AIDS-NHL analyzed expressed normal bax proteins. Overall, this study indicates that deregulation of apoptotic control in AIDS-NHL is not caused by BAX alterations. Genes Chromosomes Cancer 27:177-182, 2000.

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More information

Published date: 23 February 2000
Organisations: Cancer Sciences

Identifiers

Local EPrints ID: 358188
URI: http://eprints.soton.ac.uk/id/eprint/358188
ISSN: 1045-2257
PURE UUID: 54fe7778-9a0e-47d9-a768-56fe1fd30230
ORCID for Francesco Forconi: ORCID iD orcid.org/0000-0002-2211-1831

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Date deposited: 11 Oct 2013 11:35
Last modified: 15 Mar 2024 03:41

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Contributors

Author: Gianluca Gaidano
Author: Daniela Vivenza
Author: Daniela Capello
Author: Annunziata Gloghini
Author: Kishor Bhatia
Author: Marina Gutierrez
Author: Margherita Gallicchio
Author: Gian Carlo Avanzi
Author: Lucia Fassone
Author: Cristiano Ariatti
Author: Daniela Buonaiuto
Author: Antonella Cingolani
Author: Giuseppe Saglio
Author: Umberto Tirelli
Author: Luigi M. Larocca
Author: Riccardo Dalla-Favera
Author: Antonino Carbone

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