Publication: Tumour morphology - interplay between chromosome aberrations and founder cell differentiation
Authors
Gisselsson, D.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
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 selfreplicative
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.
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