Riddle: What do aplastic anemia, acute promyelocytic leukemia, and chronic myeloid leukemia have in common?

Multifocal epithelial tumors and field cancerization: stroma as a primary determinant

“…Field effects have also been implicated in nonepithelial cancer types, such as melanoma (37) and brain tumors (38). Further, bone marrow field effects have been invoked to explain the development of secondary myelodysplastic syndrome and/or acute leukemia in patients initially diagnosed with severe aplastic anemia (39,40).…”

Severe Aplastic Anemia Manifesting After Complete Remission of Acute Promyelocytic Leukemia: Is it a Fortuitous Association?

“…The evolution of other clonal disorders such as PNH, MDS and AML in AA patients treated with immunosuppressive therapy has since been well recognized [3,4,6]. Similarly secondary MDS or AML developing following treatment of APL is also documented in the literature [10,14].…”

“…A primary insult to the bone marrow could simultaneously lead to several abnormal hematopoietic cell clones, with one dominating and others present below the threshold of detection. Brodsky and Jones [4] termed this phenomenon 'field leukemogenic effect'. Disease specific targeted therapy is ineffective in suppressing the other abnormal clones allowing them to expand and become detectable.…”

“…Acute leukemia, secondary myelodysplastic syndrome (MDS), and paroxysmal nocturnal hemoglobinuria (PNH) frequently evolve from severe aplastic anemia following immunosuppressive therapy [4].…”

Quantitative analysis of bone marrow CD34 cells in aplastic anemia and hypoplastic myelodysplastic syndromes

“…8,22,23 MDS also evolves out of AA in about 10-20% of patients. 20,24,25 Moreover, both diseases may have a similar pathophysiology, 5,8,26 and immunosuppressive therapy may benefit some patients with hMDS. 27,28 Despite the close relationship between AA and hMDS, there are important differences between the two diseases.…”