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AML Atlas, Facts & Treatment

AML Atlas: Acute myeloblastic leukemia (M1)

M1 Leukemia

Classification of acute leukemias used to rely entirely on morphology and histochemical changes, but now information regarding cytogenetic patterns and correlations with immunophenotype, oncogene expression, and gene mutation has changed the biology of this disease.[5]

Type I blasts without granules and no Type II blasts.

(left) FISH analysis utilizing a cosmid probe for the translocation. (Near left) Translocation t(9;22)(q34;q11.2) leading to the formation of a Ph chromosome commonly seen in AML without maturation (M1). ABL and BCR genes are affected by this translocation. Arrows indicate breakpoints in chromosomes 9 and 22.

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"In summary, the data... suggest that idarubicin provides a distinct advantage over daunorubicin in untreated patients with AML."[11]

Acute myeloblastic leukemia (M1)

M1 Leukemia

Myeloblasts shown, some containing a few granules and some Auer rods. There are less than 10% maturing granulocytes.

Translocation t(9;22) (q34;q11) shown by chromosome painting utilizing probes specific for whole chromosomes 9 (pink) and 22 (green).

M1 Leukemia

"...[IDAMYCIN] seems to offer several advantages over [daunorubicin]. There is a more rapid uptake by the cells, probably because of its increased lipid solubility, the major metabolite is an active compound, the remission rate is higher,[*] and the toxicity is comparable."[12]
-W.R. Vogler, Journal of Clinical Oncology, 1992

*In two of three US studies.

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Type I blasts without granules and Type II blasts with occ granules and Auer rods, but without significant maturation.

Trisomy 1q shown by chromosome painting highlighting two normal chromosome number 1's and extra material on the long arm of chromosome 1.

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