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Tumour morphology--interplay between chromosome aberrations and founder cell differentiation.

Gisselsson Nord, David LU (2002) In Histology and Histopathology 17(4). p.1207-1212
Abstract
Studies of haematological neoplasms have shown that alterations in structure and/or expression of transcription factor genes may play a crucial role for transforming stem cells or progenitor cells into malignant cells. These mutations typically arise through balanced translocations and appear to induce a block in cellular differentiation. The impact of the transforming mutation is highly dependent on the lineage of the founder cell and each specific translocation is limited to one or a few morphological subtypes. Originating from immature cells, these neoplasms have a high self-replicative capacity and are already before transformation protected from senescence by constitutive telomerase expression. Most solid tumours, on the other hand,... (More)
Studies of haematological neoplasms have shown that alterations in structure and/or expression of transcription factor genes may play a crucial role for transforming stem cells or progenitor cells into malignant cells. These mutations typically arise through balanced translocations and appear to induce a block in cellular differentiation. The impact of the transforming mutation is highly dependent on the lineage of the founder cell and each specific translocation is limited to one or a few morphological subtypes. Originating from immature cells, these neoplasms have a high self-replicative capacity and are already before transformation protected from senescence by constitutive telomerase expression. Most solid tumours, on the other hand, probably originate from cells at higher levels of differentiation and require multiple mutations in oncogenes and tumour suppressor genes for neoplastic transformation. Absence of telomerase activity in the tumour-founding cell line predisposes to abnormal shortening of telomeric repeats in these cells during early clonal expansion. In turn, this triggers chromosomal breakage-fusion-bridge events through which the tumour genome is constantly reorganised, resulting in a complex and heterogeneous pattern of chromosome aberrations in the tumour cell population; the abnormal mitotic processes also give rise to cellular pleomorphism and nuclear atypia. Tumour morphology thus appears to be determined not only by the lineage of the transformed cell but also by its propensity for chromosomal instability. (Less)
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in
Histology and Histopathology
volume
17
issue
4
pages
1207 - 1212
publisher
Histology and Histopathology
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  • pmid:12371148
  • wos:000178234100022
  • scopus:0036790748
ISSN
1699-5848
language
English
LU publication?
yes
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ee1bbbbc-0ddf-46ab-9364-d68caef39351 (old id 110707)
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http://www.hh.um.es/Abstracts/Vol_17/17_4/17_4_1207.htm
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12371148&dopt=Abstract
date added to LUP
2007-07-06 14:12:37
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2017-07-02 04:14:40
@article{ee1bbbbc-0ddf-46ab-9364-d68caef39351,
  abstract     = {Studies of haematological neoplasms have shown that alterations in structure and/or expression of transcription factor genes may play a crucial role for transforming stem cells or progenitor cells into malignant cells. These mutations typically arise through balanced translocations and appear to induce a block in cellular differentiation. The impact of the transforming mutation is highly dependent on the lineage of the founder cell and each specific translocation is limited to one or a few morphological subtypes. Originating from immature cells, these neoplasms have a high self-replicative capacity and are already before transformation protected from senescence by constitutive telomerase expression. Most solid tumours, on the other hand, probably originate from cells at higher levels of differentiation and require multiple mutations in oncogenes and tumour suppressor genes for neoplastic transformation. Absence of telomerase activity in the tumour-founding cell line predisposes to abnormal shortening of telomeric repeats in these cells during early clonal expansion. In turn, this triggers chromosomal breakage-fusion-bridge events through which the tumour genome is constantly reorganised, resulting in a complex and heterogeneous pattern of chromosome aberrations in the tumour cell population; the abnormal mitotic processes also give rise to cellular pleomorphism and nuclear atypia. Tumour morphology thus appears to be determined not only by the lineage of the transformed cell but also by its propensity for chromosomal instability.},
  author       = {Gisselsson Nord, David},
  issn         = {1699-5848},
  language     = {eng},
  number       = {4},
  pages        = {1207--1212},
  publisher    = {Histology and Histopathology},
  series       = {Histology and Histopathology},
  title        = {Tumour morphology--interplay between chromosome aberrations and founder cell differentiation.},
  volume       = {17},
  year         = {2002},
}