Can BCAT1 Expression Level Help Predict Disease Progression in Chronic Lymphocytic Leukaemia

Chronic lymphocytic leukaemia (CLL) is the most common blood
cancer in the UK, with an incidence of >3500 newly diagnosed
cases per year resulting in >1000 deaths. Disease prevalence
increases with age, where the majority of patients are >65 years
old [1]. CLL is a largely indolent disease and is routinely staged
according to the Binet system as follows; stage A (involving
0-2 lymphoid sites), stage B (involving 2-5 lymphoid cites) and
stage C (platelets < 1x1011/L or haemoglobin <10g/dL), the
latter stage reflecting loss of bone marrow function [2]. Whilst
for some stage A patients, the disease may remain stable for
many decades (median life expectancy of 13 years), for others
the disease progresses more rapidly [3]. This observation likely
reflects the genetic and molecular heterogeneity of CLL. As such
there are several prognostic risk factors used to stratify newly
diagnosed patients, which include; trisomy-12, 13q/17p/11q23
deletion, advanced stage, males>females, unmutated VH Ig
genes, raised lactate dehydrogenase activity and expression
of Zap70 and CD38 [4]. CLL is traditionally treated with a
combination of chemotherapeutic reagents, namely, Fludarabine/
Cyclophosphamide/Rituximab (FCR), however treatment remains
challenging within the elderly population [1]. Lately the Brutan’s
tyrosine kinase inhibitor, Ibrutinib, has shown great promise for
the treatment of CLL [5]. However, exceptions are identified as
well as treatment resistance prompting further research into CLL
treatment strategies [6].