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A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia
The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the...
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1970
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2008513/ https://www.ncbi.nlm.nih.gov/pubmed/4913770 |
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author | Spiers, A. S. D. Baikie, A. G. |
author_facet | Spiers, A. S. D. Baikie, A. G. |
author_sort | Spiers, A. S. D. |
collection | PubMed |
description | The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the frequency of these aberrations and their nature make them most unlikely to be due to chance. They appear to be non-random, often occurring in every cell of a tumour, and like the Ph(1) anomaly in chronic granulocytic leukaemia, mightpossess aetiological significance. The Ep- and Eqchromosomal anomalies resemble the Ph(1) in being fine structural modifications, which occur as acquired lesions only in neoplasms, often in tumour cells with otherwise normal karyotypes. Aberration of the group 17,18 chromosomes may sometimes be secondary to neoplasia but nevertheless of evolutionary significance for the tumour cells. Changes leading to relative or absolute excess of long-arm material of chromosome 18 may confer survival advantage upon cells, particularly if a normal complement of short-arm material is simultaneously retained. However, specific deletion of the distal part of the long arms of No. 18 may also favour cell survival. The short arms of chromosome 18 may carry genes limiting cell reproduction, while the long arms carry material promoting proliferation. More distally on the long arms, there may be genes which also limit reproduction. Disturbances affecting the balance between these components of the genome may be important in inception of neoplasia or subsequent evolution of tumour cell lines. |
format | Text |
id | pubmed-2008513 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1970 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20085132009-09-10 A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia Spiers, A. S. D. Baikie, A. G. Br J Cancer Articles The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the frequency of these aberrations and their nature make them most unlikely to be due to chance. They appear to be non-random, often occurring in every cell of a tumour, and like the Ph(1) anomaly in chronic granulocytic leukaemia, mightpossess aetiological significance. The Ep- and Eqchromosomal anomalies resemble the Ph(1) in being fine structural modifications, which occur as acquired lesions only in neoplasms, often in tumour cells with otherwise normal karyotypes. Aberration of the group 17,18 chromosomes may sometimes be secondary to neoplasia but nevertheless of evolutionary significance for the tumour cells. Changes leading to relative or absolute excess of long-arm material of chromosome 18 may confer survival advantage upon cells, particularly if a normal complement of short-arm material is simultaneously retained. However, specific deletion of the distal part of the long arms of No. 18 may also favour cell survival. The short arms of chromosome 18 may carry genes limiting cell reproduction, while the long arms carry material promoting proliferation. More distally on the long arms, there may be genes which also limit reproduction. Disturbances affecting the balance between these components of the genome may be important in inception of neoplasia or subsequent evolution of tumour cell lines. Nature Publishing Group 1970-03 /pmc/articles/PMC2008513/ /pubmed/4913770 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Articles Spiers, A. S. D. Baikie, A. G. A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia |
title | A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia |
title_full | A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia |
title_fullStr | A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia |
title_full_unstemmed | A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia |
title_short | A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia |
title_sort | special role of the group 17,18 chromosomes in reticuloendothelial neoplasia |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2008513/ https://www.ncbi.nlm.nih.gov/pubmed/4913770 |
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