Normal and malignant B-cell development with special reference to Hodgkin's disease
| ISSN: |
1569-8041
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|---|---|
| Keywords: |
germinal center ; Hodgkin's disease ; Ig gene rearrangement ; micromanipulation ; Reed–Sternberg cell ; single-cell PCR
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| Source: |
Springer Online Journal Archives 1860-2000
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| Topics: |
Medicine
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| Notes: |
Abstract During their development, B lymphocytes are repeatedly selected for theexpression of an appropriate surface receptor: the pre-B-cell receptor atthe pre-B-cell stage and surface immunoglobulin (Ig) at the transition froma pre-B cell to a mature B cell. Furthermore, stringent selection for Bcells expressing high affinity antibodies operates when antigen-activated Bcells proliferate within germinal centers (GC). Here, somatic pointmutations are introduced into rearranged V region genes at a high rate, andB cells acquiring favorable mutations are selected to differentiate intomemory B cells or plasma cells. In the frame of this developmental scheme, extending a recent analysis, weinvestigated 10 primary cases of Hodgkin's disease (HD) for B-lineage originand clonality [1]. Single Hodgkin and Reed–Sternberg (H-RS) cells weremicromanipulated from frozen tissue sections and analyzed by PCR forrearranged V genes. Clonal VH and/orV_κ/V_λ gene rearrangements wereobtained from 9 of the cases. This shows that H-RS cells represent a clonal,B-lineage-derived population of tumor cells. Somatic mutations were found inall clonal VH gene rearrangements. Interestingly, mutationsleading to stop codons in in-frame V gene rearrangements were detected in fourcases. Since GC B cells acquiring such crippling mutations are usuallyefficiently eliminated within the GC, the finding of those mutations indicatesthat H-RS cells are derived from precursors within the GC that escapedapoptosis by a transforming event.
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| Type of Medium: |
Electronic Resource
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| URL: |
| _version_ | 1798296354551758848 |
|---|---|
| autor | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. |
| autorsonst | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. |
| book_url | http://dx.doi.org/10.1023/A:1008294602841 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM192900552 |
| issn | 1569-8041 |
| journal_name | Annals of oncology |
| materialart | 1 |
| notes | Abstract During their development, B lymphocytes are repeatedly selected for theexpression of an appropriate surface receptor: the pre-B-cell receptor atthe pre-B-cell stage and surface immunoglobulin (Ig) at the transition froma pre-B cell to a mature B cell. Furthermore, stringent selection for Bcells expressing high affinity antibodies operates when antigen-activated Bcells proliferate within germinal centers (GC). Here, somatic pointmutations are introduced into rearranged V region genes at a high rate, andB cells acquiring favorable mutations are selected to differentiate intomemory B cells or plasma cells. In the frame of this developmental scheme, extending a recent analysis, weinvestigated 10 primary cases of Hodgkin's disease (HD) for B-lineage originand clonality [1]. Single Hodgkin and Reed–Sternberg (H-RS) cells weremicromanipulated from frozen tissue sections and analyzed by PCR forrearranged V genes. Clonal VH and/orV_κ/V_λ gene rearrangements wereobtained from 9 of the cases. This shows that H-RS cells represent a clonal,B-lineage-derived population of tumor cells. Somatic mutations were found inall clonal VH gene rearrangements. Interestingly, mutationsleading to stop codons in in-frame V gene rearrangements were detected in fourcases. Since GC B cells acquiring such crippling mutations are usuallyefficiently eliminated within the GC, the finding of those mutations indicatesthat H-RS cells are derived from precursors within the GC that escapedapoptosis by a transforming event. |
| package_name | Springer |
| publikationsjahr_anzeige | 1997 |
| publikationsjahr_facette | 1997 |
| publikationsjahr_intervall | 8004:1995-1999 |
| publikationsjahr_sort | 1997 |
| publisher | Springer |
| reference | 8 (1997), S. 79-81 |
| schlagwort | germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR |
| search_space | articles |
| shingle_author_1 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. |
| shingle_author_2 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. |
| shingle_author_3 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. |
| shingle_author_4 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. |
| shingle_catch_all_1 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. Normal and malignant B-cell development with special reference to Hodgkin's disease germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR Abstract During their development, B lymphocytes are repeatedly selected for theexpression of an appropriate surface receptor: the pre-B-cell receptor atthe pre-B-cell stage and surface immunoglobulin (Ig) at the transition froma pre-B cell to a mature B cell. Furthermore, stringent selection for Bcells expressing high affinity antibodies operates when antigen-activated Bcells proliferate within germinal centers (GC). Here, somatic pointmutations are introduced into rearranged V region genes at a high rate, andB cells acquiring favorable mutations are selected to differentiate intomemory B cells or plasma cells. In the frame of this developmental scheme, extending a recent analysis, weinvestigated 10 primary cases of Hodgkin's disease (HD) for B-lineage originand clonality [1]. Single Hodgkin and Reed–Sternberg (H-RS) cells weremicromanipulated from frozen tissue sections and analyzed by PCR forrearranged V genes. Clonal VH and/orV_κ/V_λ gene rearrangements wereobtained from 9 of the cases. This shows that H-RS cells represent a clonal,B-lineage-derived population of tumor cells. Somatic mutations were found inall clonal VH gene rearrangements. Interestingly, mutationsleading to stop codons in in-frame V gene rearrangements were detected in fourcases. Since GC B cells acquiring such crippling mutations are usuallyefficiently eliminated within the GC, the finding of those mutations indicatesthat H-RS cells are derived from precursors within the GC that escapedapoptosis by a transforming event. 1569-8041 15698041 Springer |
| shingle_catch_all_2 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. Normal and malignant B-cell development with special reference to Hodgkin's disease germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR Abstract During their development, B lymphocytes are repeatedly selected for theexpression of an appropriate surface receptor: the pre-B-cell receptor atthe pre-B-cell stage and surface immunoglobulin (Ig) at the transition froma pre-B cell to a mature B cell. Furthermore, stringent selection for Bcells expressing high affinity antibodies operates when antigen-activated Bcells proliferate within germinal centers (GC). Here, somatic pointmutations are introduced into rearranged V region genes at a high rate, andB cells acquiring favorable mutations are selected to differentiate intomemory B cells or plasma cells. In the frame of this developmental scheme, extending a recent analysis, weinvestigated 10 primary cases of Hodgkin's disease (HD) for B-lineage originand clonality [1]. Single Hodgkin and Reed–Sternberg (H-RS) cells weremicromanipulated from frozen tissue sections and analyzed by PCR forrearranged V genes. Clonal VH and/orV_κ/V_λ gene rearrangements wereobtained from 9 of the cases. This shows that H-RS cells represent a clonal,B-lineage-derived population of tumor cells. Somatic mutations were found inall clonal VH gene rearrangements. Interestingly, mutationsleading to stop codons in in-frame V gene rearrangements were detected in fourcases. Since GC B cells acquiring such crippling mutations are usuallyefficiently eliminated within the GC, the finding of those mutations indicatesthat H-RS cells are derived from precursors within the GC that escapedapoptosis by a transforming event. 1569-8041 15698041 Springer |
| shingle_catch_all_3 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. Normal and malignant B-cell development with special reference to Hodgkin's disease germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR Abstract During their development, B lymphocytes are repeatedly selected for theexpression of an appropriate surface receptor: the pre-B-cell receptor atthe pre-B-cell stage and surface immunoglobulin (Ig) at the transition froma pre-B cell to a mature B cell. Furthermore, stringent selection for Bcells expressing high affinity antibodies operates when antigen-activated Bcells proliferate within germinal centers (GC). Here, somatic pointmutations are introduced into rearranged V region genes at a high rate, andB cells acquiring favorable mutations are selected to differentiate intomemory B cells or plasma cells. In the frame of this developmental scheme, extending a recent analysis, weinvestigated 10 primary cases of Hodgkin's disease (HD) for B-lineage originand clonality [1]. Single Hodgkin and Reed–Sternberg (H-RS) cells weremicromanipulated from frozen tissue sections and analyzed by PCR forrearranged V genes. Clonal VH and/orV_κ/V_λ gene rearrangements wereobtained from 9 of the cases. This shows that H-RS cells represent a clonal,B-lineage-derived population of tumor cells. Somatic mutations were found inall clonal VH gene rearrangements. Interestingly, mutationsleading to stop codons in in-frame V gene rearrangements were detected in fourcases. Since GC B cells acquiring such crippling mutations are usuallyefficiently eliminated within the GC, the finding of those mutations indicatesthat H-RS cells are derived from precursors within the GC that escapedapoptosis by a transforming event. 1569-8041 15698041 Springer |
| shingle_catch_all_4 | Rajewsky, K. Kanzler, H. Hansmann, M.-L. Küppers, R. Normal and malignant B-cell development with special reference to Hodgkin's disease germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR germinal center Hodgkin's disease Ig gene rearrangement micromanipulation Reed–Sternberg cell single-cell PCR Abstract During their development, B lymphocytes are repeatedly selected for theexpression of an appropriate surface receptor: the pre-B-cell receptor atthe pre-B-cell stage and surface immunoglobulin (Ig) at the transition froma pre-B cell to a mature B cell. Furthermore, stringent selection for Bcells expressing high affinity antibodies operates when antigen-activated Bcells proliferate within germinal centers (GC). Here, somatic pointmutations are introduced into rearranged V region genes at a high rate, andB cells acquiring favorable mutations are selected to differentiate intomemory B cells or plasma cells. In the frame of this developmental scheme, extending a recent analysis, weinvestigated 10 primary cases of Hodgkin's disease (HD) for B-lineage originand clonality [1]. Single Hodgkin and Reed–Sternberg (H-RS) cells weremicromanipulated from frozen tissue sections and analyzed by PCR forrearranged V genes. Clonal VH and/orV_κ/V_λ gene rearrangements wereobtained from 9 of the cases. This shows that H-RS cells represent a clonal,B-lineage-derived population of tumor cells. Somatic mutations were found inall clonal VH gene rearrangements. Interestingly, mutationsleading to stop codons in in-frame V gene rearrangements were detected in fourcases. Since GC B cells acquiring such crippling mutations are usuallyefficiently eliminated within the GC, the finding of those mutations indicatesthat H-RS cells are derived from precursors within the GC that escapedapoptosis by a transforming event. 1569-8041 15698041 Springer |
| shingle_title_1 | Normal and malignant B-cell development with special reference to Hodgkin's disease |
| shingle_title_2 | Normal and malignant B-cell development with special reference to Hodgkin's disease |
| shingle_title_3 | Normal and malignant B-cell development with special reference to Hodgkin's disease |
| shingle_title_4 | Normal and malignant B-cell development with special reference to Hodgkin's disease |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:50:45.877Z |
| titel | Normal and malignant B-cell development with special reference to Hodgkin's disease |
| titel_suche | Normal and malignant B-cell development with special reference to Hodgkin's disease |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM192900552 |