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Sci Rep. 2019 Jan 30;9(1):975. doi: 10.1038/s41598-018-37389-7.

Clonal dynamics monitoring during clinical evolution in chronic lymphocytic leukaemia.

Author information

1
Lymphoma Research Group, Medical Oncology Department, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain.
2
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Madrid, Spain.
3
Pathology Department/Translational Hematopathology Group, Hospital Universitario Marqués de Valdecilla/IDIVAL, Santander, Spain.
4
Bioinformatics Unit, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
5
CNAG-CRG, Centre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
6
Universitat Pompeu Fabra (UPF), Barcelona, Spain.
7
Hematology Department, Hospital Universitario Puerta de Hierro-Majadahonda and Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain.
8
Pathology Department, Hospital Fundación Jiménez Díaz, Madrid, Spain.
9
Hematology Department, Hospital Universitario Puerta de Hierro-Majadahonda and Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. jagarciam@aehh.org.
10
Lymphoma Research Group, Medical Oncology Department, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. msbeato@idiphim.org.

Abstract

Chronic lymphocytic leukaemia is the most prevalent leukaemia in Western countries. It is an incurable disease characterized by a highly variable clinical course. Chronic lymphocytic leukaemia is an ideal model for studying clonal heterogeneity and dynamics during cancer progression, response to therapy and/or relapse because the disease usually develops over several years. Here we report an analysis by deep sequencing of sequential samples taken at different times from the affected organs of two patients with 12- and 7-year disease courses, respectively. One of the patients followed a linear pattern of clonal evolution, acquiring and selecting new mutations in response to salvage therapy and/or allogeneic transplantation, while the other suffered loss of cellular tumoral clones during progression and histological transformation.

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