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Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders

Based on the concept that the tumorogenesis in chronic lymphocytic leukaemia comprises both an initial, inherited mutation and subsequent somatic mutations, the pleiotypic diversity of familial chronic lymphocytic leukaemia and related malignant lymphoproliferative disorders is generally explained b...

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Autores principales: Jønsson, Viggo, Tjønnfjord, Geir E., Johannesen, Tom B., Samuelsen, Sven Ove, Ly, Bernt
Formato: Texto
Lenguaje:English
Publicado: Libertas Academica 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022357/
https://www.ncbi.nlm.nih.gov/pubmed/21566740
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author Jønsson, Viggo
Tjønnfjord, Geir E.
Johannesen, Tom B.
Samuelsen, Sven Ove
Ly, Bernt
author_facet Jønsson, Viggo
Tjønnfjord, Geir E.
Johannesen, Tom B.
Samuelsen, Sven Ove
Ly, Bernt
author_sort Jønsson, Viggo
collection PubMed
description Based on the concept that the tumorogenesis in chronic lymphocytic leukaemia comprises both an initial, inherited mutation and subsequent somatic mutations, the pleiotypic diversity of familial chronic lymphocytic leukaemia and related malignant lymphoproliferative disorders is generally explained by a repertoire of monoallelic polygenes in the initial mutation. Epigenetic genomic imprinting is a likely mechanism behind of the asynchroneous replicating monoallelic polygenes which is discussed in the light of pleiotrophy and birth order effect. Furthermore, it is discussed that one possible mechanism available for the epigenetic transfer of these genes could be the physiological pregnancy-related microchimerism between mother and fetus.
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spelling pubmed-30223572011-05-12 Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders Jønsson, Viggo Tjønnfjord, Geir E. Johannesen, Tom B. Samuelsen, Sven Ove Ly, Bernt Transl Oncogenomics Debate Based on the concept that the tumorogenesis in chronic lymphocytic leukaemia comprises both an initial, inherited mutation and subsequent somatic mutations, the pleiotypic diversity of familial chronic lymphocytic leukaemia and related malignant lymphoproliferative disorders is generally explained by a repertoire of monoallelic polygenes in the initial mutation. Epigenetic genomic imprinting is a likely mechanism behind of the asynchroneous replicating monoallelic polygenes which is discussed in the light of pleiotrophy and birth order effect. Furthermore, it is discussed that one possible mechanism available for the epigenetic transfer of these genes could be the physiological pregnancy-related microchimerism between mother and fetus. Libertas Academica 2008-02-10 /pmc/articles/PMC3022357/ /pubmed/21566740 Text en © 2008 The authors. http://creativecommons.org/licenses/by/3.0 This article is published under the Creative Commons Attribution By licence. For further information go to: http://creativecommons.org/licenses/by/3.0. (http://creativecommons.org/licenses/by/3.0)
spellingShingle Debate
Jønsson, Viggo
Tjønnfjord, Geir E.
Johannesen, Tom B.
Samuelsen, Sven Ove
Ly, Bernt
Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders
title Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders
title_full Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders
title_fullStr Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders
title_full_unstemmed Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders
title_short Possible Imprinting and Microchimerism in Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders
title_sort possible imprinting and microchimerism in chronic lymphocytic leukemia and related lymphoproliferative disorders
topic Debate
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022357/
https://www.ncbi.nlm.nih.gov/pubmed/21566740
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