All-trans retinoic acid therapy induces maturation in acute promyelocytic leukaemia. We document in vivo evidence of differentiation by all-trans retinoic acid in a case of acute promyelocytic leukaemia which was characterized by cytoplasmic vacuolations.
The variant form of acute promyelocytic leukaemia (AML-M3) possesses its own characteristic morphology, although usually a few of the cells may have cytoplasmic features of typical AML-M3. In contrast to typical AML-M3, this M3-variant form commonly presents with hyperleucocytosis. As in typical AML-M3, disseminated intravascular coagulopathy (DIVC) occurs in the M3-variant. A boy with this morphological variant of AML-M3 is described. Uncharacteristically, his presenting white blood count was low, and DIVC was present before treatment was started. Six days into intensive chemotherapy his coagulopathy worsened and he subsequently died of intracranial haemorrhage. An alternative approach to the treatment of AML-M3, with the use of retinoids, is discussed.
Intense myelofibrosis is rarely associated with de novo acute myeloid leukaemia (AML) except in acute megakaryoblastic leukaemia (AML-M7) where there is diffuse marrow fibrosis as a consequence of proliferation of neoplastic myeloid cells. AML associated with significant myelofibrosis developing both de novo or secondary to primary (idiopathic) myelofibrosis is characterised by a fulminant course and extremely poor prognosis, primarily due to treatment-resistant disease. The prognostic value of degree of marrow fibrosis in de novo AML has been poorly investigated. We describe a case of extensive myelofibrosis associated with acute erythroblastic leukaemia (AML-M6) that responded to induction therapy of the leukaemia.
The growth inhibiting potential of andrographolide was evaluated in three acute promyelocytic leukaemia cell line models (HL-60, NB4 and all-trans retinoic acid (ATRA)-resistant NB4-R2).