The PLZF (promyelocytic leukemia zinc finger) transcriptional repressor, when fused to retinoic acid receptor alpha (RARalpha), causes a refractory form of acute promyelocytic leukemia. The highly conserved N-terminal BTB (bric a brac, tramtrack, broad complex)/POZ domain of PLZF plays a critical role in this disease, since it is required for transcriptional repression by the PLZF-RARalpha fusi...

BACKGROUND Acute promyelocytic leukemia (APL) accounts for less than 10% of pediatric AML. Cases of APL in Down syndrome (DS) have been described in the literature rarely and it is rarer still to find the microgranular variant (M3v) of APL in trisomy 21 patients. CASE PRESENTATION We present a case of a five-year-old female with Down syndrome diagnosed with acute promyelocytic leukemia (APL)....

Absent or diminished HLA-Dr antigen representation on the cell surface of both normal and leukemic promyelocytes is a hallmark of this stage of myeloid maturation. In order to document the specificity of this finding for acute promyelocytic leukemia, flow cytometric analysis of leukemic blasts was utilized on 36 cases of acute non-lymphocytic leukemia. All 15 of the promyelocytic leukemias (FAB...

Acute promyelocytic leukemia is characterized by gene rearrangements that always involve the retinoic acid receptor alpha on chromosome 15. In the majority of patients t(15;17) is detected, which generates the promyelocytic leukemia gene/retinoic acid receptor alpha rearrangement. This rearrangement interacts with several proteins, including the native promyelocytic leukemia gene, thus causing ...

background: acute renal failure describes as a syndrome by rapid decline in the ability of the kidney to eliminate waste products, regulate acid–base balance, and manage water homeostasis. when this impairment is prolonged and entered chronic phase, erythropoietin secretion by this organ is decreasing and toxic metabolic accumulates and causes hematological changes include decrease of hct, mcv ...

Briefly, the important clinical findings were as follows: A 10 year old white girl, acutely ill, febrile and showing disseminated skin purpura. There was no visceromegaly. The disease had apparently started 3 weeks before, with epistaxis and other purpuric manifestations. Laboratory findings showed severe anemia and thrombocytopenia with a leukocyte count of 3500 per cu. mm. The differential co...