Statements in which the resource exists as a subject.
PredicateObject
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
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