Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
|
pubmed:dateCreated |
1996-12-17
|
pubmed:abstractText |
To further specify the cellular origin and nature of anaplastic large-cell lymphoma (ALCL) and its relationship to other lymphoid neoplasms, particularly Hodgkin's disease (HD), we investigated the presence of cytotoxic molecules in a large well-characterized series of these tumors. For expression of the cytotoxic molecules perforin and granzyme B, in situ hybridization (ISH) and immunohistology were used, respectively. Overall, 23 of 25 ALCLs of T/null phenotype and five (three mixed cellularity and two nodular sclerosis) of 57 HD cases showed the presence of perforin transcripts and/or granzyme B molecules in neoplastic cells. Polymerase chain reaction (PCR) analysis of ALCLs showed that most (10 of 11) cases of null-cell ALCL (null-ALCL) contained a clonal rearrangement of T-cell receptor beta-chain genes, as did T-cell ALCL (T-ALCL; 9 of 10 cases). However, both cytotoxic molecules and clonally rearranged T-cell receptor beta-chain genes were absent in seven of seven and eight of nine cases of B-cell ALCL (B-ALCL), respectively. These data show that all or nearly all T-ALCLs, irrespective of the clinical subform or the lack of T-cell-associated molecules, are derived from activated cytotoxic T cells. The same appears to be true for the neoplastic cells of rare HD cases. These findings indicate that T-ALCLs are different from B-ALCLs and the majority of HD cases, and suggest that some HD cases, especially those with T-cell antigen-positive tumor cells, may be closely related to T-ALCL, at least in terms of cellular origin.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/GZMB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Granzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Perforin,
http://linkedlifedata.com/resource/pubmed/chemical/Pore Forming Cytotoxic Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Endopeptidases
|
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
0006-4971
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
88
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
4005-11
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:8916967-Biological Markers,
pubmed-meshheading:8916967-Cell Differentiation,
pubmed-meshheading:8916967-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor,
pubmed-meshheading:8916967-Granzymes,
pubmed-meshheading:8916967-Hodgkin Disease,
pubmed-meshheading:8916967-Humans,
pubmed-meshheading:8916967-Lymph Nodes,
pubmed-meshheading:8916967-Lymphocyte Activation,
pubmed-meshheading:8916967-Lymphocytes, Null,
pubmed-meshheading:8916967-Lymphoma, B-Cell,
pubmed-meshheading:8916967-Lymphoma, Large B-Cell, Diffuse,
pubmed-meshheading:8916967-Lymphoma, T-Cell,
pubmed-meshheading:8916967-Lymphoma, T-Cell, Peripheral,
pubmed-meshheading:8916967-Membrane Glycoproteins,
pubmed-meshheading:8916967-Neoplasm Proteins,
pubmed-meshheading:8916967-Neoplastic Stem Cells,
pubmed-meshheading:8916967-Perforin,
pubmed-meshheading:8916967-Pore Forming Cytotoxic Proteins,
pubmed-meshheading:8916967-Reed-Sternberg Cells,
pubmed-meshheading:8916967-Serine Endopeptidases,
pubmed-meshheading:8916967-T-Lymphocytes, Cytotoxic
|
pubmed:year |
1996
|
pubmed:articleTitle |
Anaplastic large-cell lymphomas of T-cell and null-cell phenotype express cytotoxic molecules.
|
pubmed:affiliation |
Institute of Pathology, Klinikum Benjamin Franklin, Free University of Berlin, Germany.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|