acute myeloid leukaemia


Also found in: Dictionary, Thesaurus, Financial, Encyclopedia.
Related to acute myeloid leukaemia: Chronic myeloid leukaemia, Acute lymphoblastic leukaemia

acute myeloid leukaemia

A rapidly progressing form of leukaemia characterised by the proliferation of immature WBCs (blasts in peripheral circulation).
 
Epidemiology
Primarily in adults or infants under age 1; 2,000 new cases are diagnosed/year, UK.
 
Clinical findings
Fatigue, weight-loss, fever, weakness, pallor, bone and joint pain, bleeding gums, nosebleeds, bruising, lymphadenopathy.
 
Complications
Bleeding, increased infections.
 
Management
Chemotherapy, bone marrow transplantation.

FAB classification, acute leukaemias
Acute myeloid leukaemia (AML) 
M0—Myeloblasts with minimal differentiation.
M1—Myeloblasts without maturation.
M2—Myeloblasts with maturation (best AML prognosis).
M3—Hypergranular promyelocytic leukaemia (faggot cells).
M3V—Variant, microgranular promyelocytic leukaemia.
M4—Myelomonocytic leukocytes.
M5—Monocytic, subtype: 
  a. Poorly differentiated monocytic leukaemia. 
  b. Well-differentiated monocytic leukaemia.
M6—Erythroleukaemia/DiGuglielmo syndrome.
M7—Megakaryocytic leukaemia—pleomorphic undifferentiated cells with cytoplasmic blebs; myelofibrosis or increased marrow reticulin; positive for platelet peroxidase antifactor VIII. 

WHO classification
AML with recurrent cytogenetic abnormalities.
AML with multi-lineage dysplasia (as a precursor to myelodysplastic syndrome).
AML related to therapy.
AML NOS.

AML variants
AML with recurrent cytogenetic abnormalities.
AML with t(8;21)(q22;q22).
AML with inv(16)(p13q22).
AML with t(15;17)(q22;q12).
AML with 11q23 (MLL) abnormalities.
AML with multilineage dysplasia.
AML (and MDS), therapy-related:
• Alkylating agent related;
• Topoisomerase-II inhibitor related.
AML, not otherwise categorised.

acute myeloid leukaemia

A form of LEUKAEMIA in which the cells present in abnormal numbers are derived from primitive precursors, in the bone marrow, of the white blood cells. The median age of presentation is 70. Genetic defects and age-related factors are thought to be the principal determinants of lack of success of chemotherapy in elderly patients.
References in periodicals archive ?
Acute Myeloid Leukaemia Phase 2 Clinical Trial Pipeline Insights
Acute Myeloid Leukaemia Phase 1 Clinical Trial Pipeline Insights
Acute Myeloid Leukaemia Preclinical Research Pipeline Insights
Acute Myeloid Leukaemia Discovery Stage Pipeline Insights
The new research has shown that mutation in NPM1 is a key event in the development of a large proportion of cases of acute myeloid leukaemia and that it exerts its effect by helping cells to self-renew, a process that can be thought of as the first step towards leukaemia.
We have used targeted gene disruption to look at the way acute myeloid leukaemia develops in mice and have found critical steps that take place when the cancer develops.
The team started by developing a strain of mice that contained a 'control switch', that allowed the researchers to turn on mutations in the acute myeloid leukaemia gene Npm1.
DNA repair contributes to the drug-resistant phenotype of primary acute myeloid leukaemia cells with FLT3 internal tandem duplications and is reversed by the FLT3 inhibitor PKC412.
Bioenvision is currently conducting further clinical studies with clofarabine throughout Europe, in refractory/relapsed paediatric acute leukaemia and in adult acute myeloid leukaemia.

Full browser ?