scholarly journals T cell gamma gene rearrangements in hematologic neoplasms

Blood ◽  
1987 ◽  
Vol 69 (3) ◽  
pp. 968-970 ◽  
Author(s):  
N Asou ◽  
M Matsuoka ◽  
T Hattori ◽  
F Kawano ◽  
S Maeda ◽  
...  
Keyword(s):  
T Cell ◽  
Gene Rearrangement ◽  
Cell Receptor ◽  
Gene Rearrangements ◽  
Hematologic Neoplasms ◽  
Cellular Origin ◽  
Immature B Cells ◽  
T Cell Receptor Beta ◽  
Potential Tool ◽  
Receptor Beta

Abstract Rearrangements of the T cell gamma (T gamma) gene were studied in primary neoplastic cells from 75 patients with leukemia or lymphoma. T gamma gene rearrangements were observed in 19 of 21 T cell neoplasms; 14 of 21 immature B cell leukemias, including 4 out of 5 patients with rearrangements of both immunoglobulin heavy-chain (JH) and T cell receptor beta chain (T beta) genes; none out of 16 nonlymphoid leukemias. Thus, T gamma gene rearrangement is frequently found in immature B cells and is not always found in T cells showing T beta gene rearrangement, but it is not detected in nonlymphoid cells. Furthermore, T gamma gene rearrangement in cells with the germline configuration of the JH and T beta genes was observed. These results indicate that the detection of T gamma gene rearrangement does not allow a clear assignment to a particular lineage. However, an analysis of T gamma gene rearrangement provides a further potential tool to establish the lymphoid cellular origin and clonality of hematologic neoplasms and identify the normal stages of lymphocyte differentiation.

scholarly journals T cell gamma gene rearrangements in hematologic neoplasms

Blood ◽  
1987 ◽  
Vol 69 (3) ◽  
pp. 968-970
Author(s):  
N Asou ◽  
M Matsuoka ◽  
T Hattori ◽  
F Kawano ◽  
S Maeda ◽  
...  
Keyword(s):  
T Cell ◽  
Gene Rearrangement ◽  
Cell Receptor ◽  
Gene Rearrangements ◽  
Hematologic Neoplasms ◽  
Cellular Origin ◽  
Immature B Cells ◽  
T Cell Receptor Beta ◽  
Potential Tool ◽  
Receptor Beta

Rearrangements of the T cell gamma (T gamma) gene were studied in primary neoplastic cells from 75 patients with leukemia or lymphoma. T gamma gene rearrangements were observed in 19 of 21 T cell neoplasms; 14 of 21 immature B cell leukemias, including 4 out of 5 patients with rearrangements of both immunoglobulin heavy-chain (JH) and T cell receptor beta chain (T beta) genes; none out of 16 nonlymphoid leukemias. Thus, T gamma gene rearrangement is frequently found in immature B cells and is not always found in T cells showing T beta gene rearrangement, but it is not detected in nonlymphoid cells. Furthermore, T gamma gene rearrangement in cells with the germline configuration of the JH and T beta genes was observed. These results indicate that the detection of T gamma gene rearrangement does not allow a clear assignment to a particular lineage. However, an analysis of T gamma gene rearrangement provides a further potential tool to establish the lymphoid cellular origin and clonality of hematologic neoplasms and identify the normal stages of lymphocyte differentiation.

scholarly journals Anaplastic large-cell lymphomas of T-cell and null-cell phenotype express cytotoxic molecules

Blood ◽  
1996 ◽  
Vol 88 (10) ◽  
pp. 4005-4011 ◽  
Author(s):  
HD Foss ◽  
I Anagnostopoulos ◽  
I Araujo ◽  
C Assaf ◽  
G Demel ◽  
...  
Keyword(s):  
T Cell ◽  
Granzyme B ◽  
Large Cell ◽  
Cell Receptor ◽  
Null Cell ◽  
Cellular Origin ◽  
T Cell Receptor Beta ◽  
Cytotoxic Molecules ◽  
Beta Chain Genes ◽  
Receptor Beta

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.

Unexpected consistent involvement of V beta gene segments in inappropriate T-cell receptor beta gene rearrangements occurring in B- lineage acute lymphoblastic leukemias

Blood ◽  
1992 ◽  
Vol 80 (10) ◽  
pp. 2614-2621 ◽  
Author(s):  
H Dombret ◽  
P Loiseau ◽  
JC Bories ◽  
F Sigaux
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Genomic Library ◽  
Cell Receptor ◽  
Gene Rearrangements ◽  
Specific Pcr ◽  
T Cell Receptor Beta ◽  
B Lineage ◽  
Beta Gene ◽  
Receptor Beta

Abstract T-cell receptor beta (TCR beta) gene rearrangements occur in a third of early B-cell acute lymphoblastic leukemias (ALLs). V, D, and J segments involved in these inappropriate rearrangements remain unknown and are of interest, both because partial D beta J beta and complete V beta D beta J beta recombinations occur at distinct stages of thymic maturation and because these rearrangements are regulated differently. We have therefore studied in detail seven cases of B-lineage ALL that show inappropriate clonal TCR beta gene rearrangements. Analysis of genomic DNA by Southern hybridization with C beta, J beta 1, V beta 8, and V beta 11 probes suggested the involvement of V beta segment in tumor cell rearrangements. A complete genomic library constructed from one case was screened with a C beta probe, and the TCR beta gene rearrangement was cloned and fully sequenced to show an out of frame V beta 2.2-J beta 2.6 recombination. TCR beta gene rearrangements occurring in other cases were further analyzed by polymerase chain reaction (PCR) using J beta and V beta primers and the resulting specific PCR products were sequenced. Evidence of clonal V beta rearrangements was obtained in all cases. These unexpected findings represent the first definitive demonstration that complete V beta(D beta)J beta rearrangements can occur in B-lineage cells and contrast with the previously reported lack of V beta(D beta)J beta rearrangement in B cells from V beta-J beta-C beta-E mu transgenic mice. In the context of increasing evidence that rearrangements are linked to transcription of unrearranged gene segments, these data prompt a search in B-lineage ALL cells for the presence of germline V beta transcripts whose deregulated expression may be linked to early transforming events.

Dominant T-Cell Receptor beta-Chain Gene Rearrangements Indicate Clonal Expansion in the Rheumatoid Joint

1990 ◽  
Vol 31 (1) ◽  
pp. 121-125 ◽  
Author(s):  
A. M. M. MILTENBURG ◽  
J. M. LAAR ◽  
M. R. DAHA ◽  
R. R. P. VRIES ◽  
P. J. ELSEN ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Clonal Expansion ◽  
Cell Receptor ◽  
Chain Gene ◽  
Gene Rearrangements ◽  
Beta Chain ◽  
T Cell Receptor Beta ◽  
Receptor Beta

scholarly journals Unexpected consistent involvement of V beta gene segments in inappropriate T-cell receptor beta gene rearrangements occurring in B- lineage acute lymphoblastic leukemias

Blood ◽  
1992 ◽  
Vol 80 (10) ◽  
pp. 2614-2621
Author(s):  
H Dombret ◽  
P Loiseau ◽  
JC Bories ◽  
F Sigaux
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Genomic Library ◽  
Cell Receptor ◽  
Gene Rearrangements ◽  
Specific Pcr ◽  
T Cell Receptor Beta ◽  
B Lineage ◽  
Beta Gene ◽  
Receptor Beta

T-cell receptor beta (TCR beta) gene rearrangements occur in a third of early B-cell acute lymphoblastic leukemias (ALLs). V, D, and J segments involved in these inappropriate rearrangements remain unknown and are of interest, both because partial D beta J beta and complete V beta D beta J beta recombinations occur at distinct stages of thymic maturation and because these rearrangements are regulated differently. We have therefore studied in detail seven cases of B-lineage ALL that show inappropriate clonal TCR beta gene rearrangements. Analysis of genomic DNA by Southern hybridization with C beta, J beta 1, V beta 8, and V beta 11 probes suggested the involvement of V beta segment in tumor cell rearrangements. A complete genomic library constructed from one case was screened with a C beta probe, and the TCR beta gene rearrangement was cloned and fully sequenced to show an out of frame V beta 2.2-J beta 2.6 recombination. TCR beta gene rearrangements occurring in other cases were further analyzed by polymerase chain reaction (PCR) using J beta and V beta primers and the resulting specific PCR products were sequenced. Evidence of clonal V beta rearrangements was obtained in all cases. These unexpected findings represent the first definitive demonstration that complete V beta(D beta)J beta rearrangements can occur in B-lineage cells and contrast with the previously reported lack of V beta(D beta)J beta rearrangement in B cells from V beta-J beta-C beta-E mu transgenic mice. In the context of increasing evidence that rearrangements are linked to transcription of unrearranged gene segments, these data prompt a search in B-lineage ALL cells for the presence of germline V beta transcripts whose deregulated expression may be linked to early transforming events.

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