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In 2008 the first evidence-based Canadian consensus guideline addressing the diagnosis, monitoring and management of transfusional iron overload in patients with myelodysplastic syndromes (MDS) was published. The Canadian Consortium on MDS, comprised of hematologists from across Canada with a clinical and academic interest in MDS, reconvened to update these guidelines. A literature search was updated in 2017; topics reviewed include mechanisms of iron overload induced cellular damage, evidence for clinical endpoints impacted by iron overload including organ dysfunction, infections, marrow failure, overall survival, acute myeloid leukemia progression, and endpoints around hematopoietic stem-cell transplant. Evidence for an impact of iron reduction on the same endpoints is discussed, guidelines are updated, and areas identified where evidence is suboptimal. The guidelines address common questions around the diagnosis, workup and management of iron overload in clinical practice, and take the approach of who, when, why and how to treat iron overload in MDS. Practical recommendations for treatment and monitoring are made. Evidence levels and grading of recommendations are provided for all clinical endpoints examined.

In December 2005, 11 Canadian hematologists met to develop an evidence-based clinical practice guideline that would address the diagnosis, monitoring, management, and rationale for the treatment of transfusional iron overload in patients with myelodysplastic syndromes (MDS). This Expert Panel consisted of hematologists from across Canada, each with an active practice in a major population centre or a rural area. Based on an extensive literature search and years of clinical experience, their mandate was to address common clinical practice questions, particularly why treat, whom to treat, when to initiate treatment, and how to treat iron overload in patients with MDS.

Two of 19 B-cell non-Hodgkin's lymphoma (NHL) were found to have clonally rearranged T-cell receptor (TCR) beta chain genes with a germline TCR-gamma gene configuration. The inappropriate rearrangements had a similar structure to the TCR-beta rearrangements described in B-cell chronic lymphocytic leukemia. All cases analysed displayed a consistent germline transcription of TCR-beta and alpha chain genes which was independent of rearrangement. Consistent with this, all cases showed some degree of hypomethylation of the TCR-beta chain locus similar though distinguishable from the pattern seen in mature T cells, but quite different from that seen in normal mature B cells. Taken together, these data suggest that most NHL's arise from an immature B-lymphocyte precursor at a stage of differentiation where lineage commitment is incomplete.

Non-random rearrangement of genes encoding the gamma chain of the T-cell antigen receptor is known to occur in a developmentally regulated fashion during thymocyte differentiation. We show here that peripheral blood T lymphocytes from patients with B-cell chronic lymphocytic leukemia display marked abnormalities in the spectrum of gamma variable region gene rearrangements compared with normal peripheral blood. Of seven patients studied, all displayed a reduction of rearrangements into V9 (subgroup V II), while two cases had, in addition, over-representation of specific rearrangements involving subgroup V I; one V 2/4, the other V 5. These observations have a number of implications relevant to mechanisms of disease pathogenesis, and may provide new insight into the basis of T-cell dysfunction that is frequently associated with this condition.