Rearrangements between the immunoglobulin heavy chain gene JH and Cµ regions accompany normal B lymphocyte differentiation in vitro

Nature ◽  
1982 ◽  
Vol 299 (5885) ◽  
pp. 742-744 ◽  
Author(s):  
Julia L. Hurwitz ◽  
John J. Cebra
Keyword(s):  
Heavy Chain ◽  
B Lymphocyte ◽  
Immunoglobulin Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Lymphocyte Differentiation

The mouse immunoglobulin heavy-chain gene enhancer contains sequences that inhibit transcription in vitro in HeLa cell extracts

1986 ◽  
Vol 6 (11) ◽  
pp. 4117-4121
Author(s):  
J P Dougherty ◽  
P Augereau ◽  
P Chambon
Keyword(s):  
Heavy Chain ◽  
Simian Virus 40 ◽  
Immunoglobulin Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Cell Extracts ◽  
Mouse Immunoglobulin ◽  
Transcription In Vitro

The effect of the cell-specific mouse immunoglobulin heavy-chain gene (IgH) enhancer on transcription from heterologous promoter elements was studied in vitro with a HeLa whole-cell extract. No stimulation of transcription could be seen under conditions in which an activation was observed with the simian virus 40 enhancer. We found, however, that a specific segment of the IgH enhancer region contains sequences which inhibit transcription in vitro.

scholarly journals The mouse immunoglobulin heavy-chain gene enhancer contains sequences that inhibit transcription in vitro in HeLa cell extracts.

1986 ◽  
Vol 6 (11) ◽  
pp. 4117-4121 ◽  
Author(s):  
J P Dougherty ◽  
P Augereau ◽  
P Chambon
Keyword(s):  
Heavy Chain ◽  
Simian Virus 40 ◽  
Immunoglobulin Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Cell Extracts ◽  
Mouse Immunoglobulin ◽  
Transcription In Vitro

The effect of the cell-specific mouse immunoglobulin heavy-chain gene (IgH) enhancer on transcription from heterologous promoter elements was studied in vitro with a HeLa whole-cell extract. No stimulation of transcription could be seen under conditions in which an activation was observed with the simian virus 40 enhancer. We found, however, that a specific segment of the IgH enhancer region contains sequences which inhibit transcription in vitro.

scholarly journals Primary Malignant Lymphoma of the Brain: Mutation Pattern of Rearranged Immunoglobulin Heavy Chain Gene

2002 ◽  
Vol 93 (12) ◽  
pp. 1308-1316 ◽  
Author(s):  
Sumio Endo ◽  
Shu-Jing Zhang ◽  
Takafumi Saito ◽  
Mitsuo Kouno ◽  
Toshihiko Kuroiwa ◽  
...  
Keyword(s):  
Malignant Lymphoma ◽  
Heavy Chain ◽  
Immunoglobulin Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Mutation Pattern ◽  
The Brain

Can Polymerase Chain Reaction Help Distinguish Benign From Malignant Lymphoid Aggregates in Bone Marrow Aspirates?

2000 ◽  
Vol 124 (4) ◽  
pp. 511-515
Author(s):  
Jonathan Ben-Ezra ◽  
Kirk Hazelgrove ◽  
Andrea Ferreira-Gonzalez ◽  
Carleton T. Garrett
Keyword(s):  
Bone Marrow ◽  
Polymerase Chain Reaction ◽  
Heavy Chain ◽  
Immunoglobulin Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Lymphoid Aggregates

Abstract Objective.—Although morphologic and immunologic clues are helpful in distinguishing benign from malignant lymphoid aggregates in bone marrow biopsies, there remain some cases in which it is not possible to arrive at a definitive diagnosis. Since the malignant aggregates are monoclonal B-cell proliferations, we sought to determine whether performing polymerase chain reaction for the immunoglobulin heavy-chain locus would be helpful in distinguishing these 2 entities. Methods and Results.—Scrapings from unstained bone marrow aspirate smears or touch preparations of bone marrow biopsies from 15 patients with benign bone marrow lymphoid aggregates and 18 patients with malignant lymphoid infiltrates were analyzed for rearrangements of the FR3 region of the immunoglobulin heavy-chain gene locus by a heminested polymerase chain reaction procedure. All specimens had amplifiable DNA, as shown by amplification of the ras proto-oncogene. None of the 15 cases of benign bone marrow lymphoid aggregates demonstrated clonality upon amplification of the immunoglobulin heavy-chain gene locus. In contrast, 8 of the 18 malignant samples were positive (P = .01 by χ2 test; sensitivity, 44%; specificity, 100%; positive predictive value, 100%; negative predictive value, 60%). There was a tendency for there to be more lymphocytes in stained bone marrow aspirate smears from the cases of malignant lymphoid aggregates with a positive polymerase chain reaction result than in those without demonstrable clonality (36.0 ± 35.4% vs 9.8 ± 8.0%, P = .13). Conclusions.—Polymerase chain reaction for the immunoglobulin heavy-chain gene locus may help distinguish benign from malignant bone marrow lymphoid aggregates. Although the presence of false-negative samples may be related to the relative lack of lymphocytes in the bone marrow aspirates, other factors, such as the lack of amplification of the FR3 region of the immunoglobulin heavy-chain gene locus in particular tumors, cannot be ruled out with certainty.

scholarly journals The t(5;14) chromosomal translocation in a case of acute lymphocytic leukemia joins the interleukin-3 gene to the immunoglobulin heavy chain gene

Blood ◽  
1989 ◽  
Vol 73 (8) ◽  
pp. 2081-2085 ◽  
Author(s):  
JC Grimaldi ◽  
TC Meeker
Keyword(s):  
Heavy Chain ◽  
Acute Lymphocytic Leukemia ◽  
Chromosomal Translocation ◽  
Immunoglobulin Heavy Chain ◽  
Lymphocytic Leukemia ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Interleukin 3 ◽  
Chromosomal Breakpoints

Abstract Chromosomal translocations have proven to be important markers of the genetic abnormalities central to the pathogenesis of cancer. By cloning chromosomal breakpoints one can identify activated proto-oncogenes. We have studied a case of B-lineage acute lymphocytic leukemia (ALL) that was associated with peripheral blood eosinophilia. The chromosomal translocation t(5;14) (q31;q32) from this sample was cloned and studied at the molecular level. This translocation joined the immunoglobulin heavy chain joining (Jh) region to the promotor region of the interleukin-3 (IL-3) gene in opposite transcriptional orientations. The data suggest that activation of the IL-3 gene by the enhancer of the immunoglobulin heavy chain gene may play a central role in the pathogenesis of this leukemia and the associated eosinophilia.

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