File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Nasal T/natural killer (NK)-cell lymphomas are derived from epstein- barr virus-infected cytotoxic lymphocytes of both NK- and T-cell lineage

TitleNasal T/natural killer (NK)-cell lymphomas are derived from epstein- barr virus-infected cytotoxic lymphocytes of both NK- and T-cell lineage
Authors
Issue Date1997
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 1997, v. 73 n. 3, p. 332-338 How to Cite?
AbstractThe cellular nature of nasal T/natural killer (NK)-cell lymphomas (NLs) remains controversial. It is still debatable whether these represent T-cell lymphomas with extensive loss of surface antigens or are, in fact, true NK- cell lymphomas. They are associated closely with Epstein-Barr virus (EBV), to the extent that EBV-encoded small non-polyadenylated RNAs (EBER) expression can be used as a marker for the neoplastic cells. The cell lineage of this group of lymphomas was examined further by correlating immunophenotype, genotype and EBV status with the expression of cytotoxic granule-associated proteins, perforin and T-cell intracellular antigen-1 (TIA-1) in 13 cases of NL. Combined immunophenotypic and gene rearrangement analyses demonstrated that NLs can be identified clearly as either NK-cell or T-cell tumours. Nasal NK-cell lymphomas lacked clonal rearrangement of both T-cell receptor (TCR) γ and immunogloulin heavy chain (IgH) genes and were either CD3(Leu4)- CD56+ (8 cases) or CD3(Leu4)+CD56+ (2 cases), whereas nasal T-cell lymphomas had rearranged TCRγ and germ-line IgH genes and were either CD3(Leu4)+CD56+ (2 cases) or CD3(Leu4)+CD56- (I case). Immunohistochemical (IH) studies showed that both perforin and TIA-I were expressed universally in NL, irrespective of NK- or T-cell lineage. Dual labelling of TIA-I by IH and EBER by in situ hybridisation demonstrated that the granule proteins were expressed predominantly by the EBER+ tumour cells. Our results indicate that NLs are derived from EBV-infected cytotoxic lymphocytes of both NK- and T-cell lineage. We postulate that cytotoxic lymphocytes generated during the cellular immune response to EBV infection or re-activation at the nasal region themselves may become targets for EBV infection and subsequent transformation.
Persistent Identifierhttp://hdl.handle.net/10722/148067
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChiang, AKSen_HK
dc.contributor.authorChan, ACLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorHo, FCSen_HK
dc.date.accessioned2012-05-29T06:10:40Z-
dc.date.available2012-05-29T06:10:40Z-
dc.date.issued1997en_HK
dc.identifier.citationInternational Journal Of Cancer, 1997, v. 73 n. 3, p. 332-338en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148067-
dc.description.abstractThe cellular nature of nasal T/natural killer (NK)-cell lymphomas (NLs) remains controversial. It is still debatable whether these represent T-cell lymphomas with extensive loss of surface antigens or are, in fact, true NK- cell lymphomas. They are associated closely with Epstein-Barr virus (EBV), to the extent that EBV-encoded small non-polyadenylated RNAs (EBER) expression can be used as a marker for the neoplastic cells. The cell lineage of this group of lymphomas was examined further by correlating immunophenotype, genotype and EBV status with the expression of cytotoxic granule-associated proteins, perforin and T-cell intracellular antigen-1 (TIA-1) in 13 cases of NL. Combined immunophenotypic and gene rearrangement analyses demonstrated that NLs can be identified clearly as either NK-cell or T-cell tumours. Nasal NK-cell lymphomas lacked clonal rearrangement of both T-cell receptor (TCR) γ and immunogloulin heavy chain (IgH) genes and were either CD3(Leu4)- CD56+ (8 cases) or CD3(Leu4)+CD56+ (2 cases), whereas nasal T-cell lymphomas had rearranged TCRγ and germ-line IgH genes and were either CD3(Leu4)+CD56+ (2 cases) or CD3(Leu4)+CD56- (I case). Immunohistochemical (IH) studies showed that both perforin and TIA-I were expressed universally in NL, irrespective of NK- or T-cell lineage. Dual labelling of TIA-I by IH and EBER by in situ hybridisation demonstrated that the granule proteins were expressed predominantly by the EBER+ tumour cells. Our results indicate that NLs are derived from EBV-infected cytotoxic lymphocytes of both NK- and T-cell lineage. We postulate that cytotoxic lymphocytes generated during the cellular immune response to EBV infection or re-activation at the nasal region themselves may become targets for EBV infection and subsequent transformation.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.subject.meshGene Rearrangement, B-Lymphocyte, Heavy Chainen_US
dc.subject.meshGene Rearrangement, Gamma-Chain T-Cell Antigen Receptoren_US
dc.subject.meshGenotypeen_US
dc.subject.meshHerpesvirus 4, Humanen_US
dc.subject.meshHumansen_US
dc.subject.meshKiller Cells, Natural - Immunology - Pathologyen_US
dc.subject.meshLymphoma, T-Cell - Genetics - Immunology - Pathology - Virologyen_US
dc.subject.meshMembrane Glycoproteins - Analysisen_US
dc.subject.meshMembrane Proteins - Analysisen_US
dc.subject.meshNeoplasm Proteins - Analysisen_US
dc.subject.meshNose Neoplasms - Genetics - Immunology - Pathology - Virologyen_US
dc.subject.meshPerforinen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshPoly(A)-Binding Proteinsen_US
dc.subject.meshPore Forming Cytotoxic Proteinsen_US
dc.subject.meshProteinsen_US
dc.subject.meshRna-Binding Proteins - Analysisen_US
dc.subject.meshRibosomal Proteinsen_US
dc.subject.meshT-Lymphocytes, Cytotoxic - Immunology - Pathology - Virologyen_US
dc.titleNasal T/natural killer (NK)-cell lymphomas are derived from epstein- barr virus-infected cytotoxic lymphocytes of both NK- and T-cell lineageen_HK
dc.typeArticleen_HK
dc.identifier.emailChiang, AKS:chiangak@hkucc.hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.authorityChiang, AKS=rp00403en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/(SICI)1097-0215(19971104)73:3<332::AID-IJC5>3.0.CO;2-0en_HK
dc.identifier.pmid9359478-
dc.identifier.scopuseid_2-s2.0-0030663229en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030663229&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume73en_HK
dc.identifier.issue3en_HK
dc.identifier.spage332en_HK
dc.identifier.epage338en_HK
dc.identifier.isiWOS:A1997YE84900005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChiang, AKS=7101623534en_HK
dc.identifier.scopusauthoridChan, ACL=16047349300en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridHo, FCS=7103408147en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats