2017
DOI: 10.1111/bjh.14719
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Chronic lymphocytic leukaemia genomics and the precision medicine era

Abstract: Massive genomic analyses have underscored the diversity of chronic lymphocytic leukaemia (CLL) between patients. Genetic heterogeneity of tumour clones within a patient may fuel tumour evolution. Several recurrently deregulated intra-cellular pathways are candidates for targeted therapies that are very promising and are dramatically changing clinical patients' perspectives. In this review we present an overview of the genetic and epigenetic features of CLL and their clinical and biological implications.

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Cited by 14 publications
(22 citation statements)
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References 175 publications
(309 reference statements)
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“…It is remarkable that the present proteome profiles revealed a rather consistent protein pattern across the individual donors as demonstrated in Fig. 1D, despite B-CLL is associated with a rather heterogeneous genotype (86).…”
Section: Discussionsupporting
confidence: 61%
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“…It is remarkable that the present proteome profiles revealed a rather consistent protein pattern across the individual donors as demonstrated in Fig. 1D, despite B-CLL is associated with a rather heterogeneous genotype (86).…”
Section: Discussionsupporting
confidence: 61%
“…Nevertheless, several questions remain unanswered, conclusive risk factors for the incidence of the disease could not yet be recognized, and the pathophysiology of the disease is still not fully understood. One of the reasons therefore may be that B-CLL represents a very heterogeneous disorder, associated with a multiplicity of possible genetic alterations (2), which is further strongly dependent on functional changes in the tumor microenvironment (3)(4)(5). Genetic as well as environmental factors may both be responsible for the considerably varying disease progression and individual therapeutic response, which are hardly predictable.…”
Section: B Cell Chronic Lymphocytic Leukemia (B-cll) the Most Commonmentioning
confidence: 99%
“…Nfkbie loss cooperates with MYD88 signaling MYD88 codes for an proximal signaling adaptor downstream of IL-1R and mammalian TLRs. Mutations in MYD88, essentially the missense p.L265P mutation, are observed in a wide range of B-cell malignancies 8,10,13,[35][36][37][38][39] . They have been shown to activate the JAK and NF-κB pathways 36 .…”
Section: These In Vitro Data Mirror the In Vivo Results And Indicate mentioning
confidence: 99%
“…Nfkbie-deficient mice develop several features of human lymphoproliferative B-cell disorders, in particular, MBL, a low-penetrance premalignant stage 13,56 . Firstly, Nfkbie deficiency in mice leads to the expansion of an oligoclonal CD19 +CD5+B-cell subset, and in humans, mature CD19+CD5 +B cells, show high transcriptional and functional similarity to CLL B cells and are candidate for being a normal cellular counterpart of CLL B cells 13,45,54 . Secondly, Nfkbie-deficient B1a cells exhibited increased survival, proliferation, and enhanced NF-κB activity in response to stimulation consistently with the observations made for NFKBIE-mutated human CLL B-cells 2 .…”
Section: Discussionmentioning
confidence: 99%
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