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Clonal evolution in chronic lymphocytic leukemia: impact of subclonality on disease progression
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
2015 (English)In: Expert Review of Hematology, ISSN 1747-4086, E-ISSN 1747-4094, Vol. 8, no 1, 71-78 p.Article, review/survey (Refereed) Published
Abstract [en]

In recent years, next-generation sequencing has unraveled the molecular landscape in chronic lymphocytic leukemia with the discovery of a number of recurrently mutated genes. Mutations in several of these genes, such as NOTCH1, SF3B1 and BIRC3, are linked to a more aggressive disease with early disease progression, short time-to-first-treatment and even chemorefractoriness. Although in its infancy, we have also begun to understand the complex dynamics of subclonal diversity and its impact on disease outcome. From pioneering studies, we know that certain genetic events are found in the majority of chronic lymphocytic leukemia cells and are considered as 'clonal driver mutations' (e.g., +12, 13q-), whereas others, present only in a fraction of the tumor, are deemed to be 'subclonal driver mutations' for example, TP53 and SF3B1. Over the coming years, we need to gain a deeper insight into the dynamics of this subclonal architecture to understand how, at an individual level, chronic lymphocytic leukemia patients should be followed, which will be particularly relevant as novel targeted therapies begin to emerge.

Place, publisher, year, edition, pages
2015. Vol. 8, no 1, 71-78 p.
National Category
Hematology
Identifiers
URN: urn:nbn:se:uu:diva-239493DOI: 10.1586/17474086.2015.972930ISI: 000347716500008PubMedID: 25345442OAI: oai:DiVA.org:uu-239493DiVA: diva2:774749
Available from: 2014-12-29 Created: 2014-12-29 Last updated: 2017-12-05Bibliographically approved

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