Myeloid & Lymphoid disorders in practice - 2012

Comment: Chimerism assays – the need for standardisation
John Reilly
pp 2-2
Cognoscenti of Greek mythology will know that the Khimaira, or Chimera, was a monstrous, fire-breathing beast that despoiled the countryside and ravaged the herds of Anatolia. This imaginary being was a composite creature, possessing the body and maned head of a lioness, the hindquarters of a dragon, a set of goat’s udders and a serpentine tail. More recently, however, geneticists have adopted the term chimera to indicate an organism composed of genetically distinct cell types. Such human chimeras were first discovered with the advent of blood typing, when it was appreciated that some individuals possessed more than one blood type.
MicroRNAs: back to basics
Charles H Lawrie
pp 3-5
Despite being only formally recognised for just over ten years, microRNAs (miRNAs) have emerged as one of the hottest subjects in biology in recent times. There is now overwhelming evidence that miRNAs play a fundamental role in many, if not all, physiological and disease processes, including myeloid disorders. This review will give a brief overview of this field, focusing on the involvement and potential clinical significance of miRNAs in the myeloid malignancies acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS).
Management of non-proliferative CMML
Moya E Young and Kavita Raj
pp 6-8
Chronic myelomonocytic leukaemia (CMML) is a haematological disorder characterised by features of both myeloproliferative neoplasms (MPNs) and myelodysplastic syndrome (MDS). Persistent monocytosis (>1.0 x 109/l) – often accounting for over 10% of total white cells – within the peripheral blood is the hallmark feature of this disease, along with myelodysplasia. In the absence of dysplasia, diagnosis may be made with the identification of cytogenetic abnormalities (about 40%) or mutations in associated genes such as TET2 and RUNX1.
The role of radiotherapy in the management of myeloproliferative neoplasms
Dan Smith and N George Mikhaeel
pp 9-12
The myeloproliferative neoplasms (MPNs) form a group of conditions in which excess clonal myeloid cells develop. The Philadelphia chromosome, which produces the BCR-ABL fusion gene, causes chronic myeloid leukaemia (CML) – characterised by a markedly elevated granulocyte count. Three diseases are associated with a mutation in JAK2: polycythaemia vera (PV), essential thrombocythaemia (ET) and myelofibrosis. PV and ET exhibit excess erythrocytes and platelets respectively, while the bone marrow in myelofibrosis demonstrates clonal stem cells and a typical fibrotic structure, either de novo (primary myelofibrosis [PMF]) or secondary to PV or ET.
What have we learned from randomised controlled trials in acute myeloid leukaemia?
Steven Knapper
pp 13-15
The last 30–40 years have seen a steady rise in long-term survival rates for younger acute myeloid leukaemia (AML) patients, usually defined as those below 60 years of age. Over most of this time, the combination of an anthracycline (usually daunorubicin) with cytarabine has remained the mainstay of initial therapy and much of the improvement in patient outcome has been attributable to advances in supportive care that have increased our ability to negotiate periods of pancytopenia that follow intensive chemotherapy.