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

Research output: Contribution to journalArticlepeer-review

Abstract

Secondary myelodysplastic syndrome (MDS)/acute leukemia frequently evolves from severe aplastic anemia (SAA) following immunosuppressive therapy. Secondary clonal cytogenetic abnormalities have now been reported after noncytotoxic therapy in two additional settings: all trans retinoic acid (ATRA) treatment of acute promyelocytic leukemia (APL) and imatinib for chronic myeloid leukemia (CML). We propose that SAA, APL, CML, and MDS represent different manifestations of generalized insults to the bone marrow. In SAA, the insult to hematopoietic progenitors leads to an immune attack, while in APL, CML, and MDS, it gives rise to the malignant clones. A primary insult to bone marrow could simultaneously lead to several abnormal hematopoietic cell clones, with one dominating and the others present but below the level of detection. Such a 'field leukemogenic effect' would be analogous to the 'field cancerization effect' described in solid tumors. Nonspecific cytotoxic therapies, including antileukemic chemotherapy and allogeneic transplantation, have broad activity that could inhibit both the overt disease and other undetectable coexistent abnormal clones. In contrast, disease-specific targeted therapy such as immunosuppressive therapy in aplastic anemia, ATRA in APL, or imatinib in CML would have no activity against other abnormal clones, allowing them to expand and become detectable as the dominant clone declines.

Original languageEnglish (US)
Pages (from-to)1740-1742
Number of pages3
JournalLeukemia
Volume18
Issue number10
DOIs
StatePublished - Oct 2004

Keywords

  • Acute promyelocytic leukemia
  • Aplastic anemia
  • Chronic myeloid leukemia
  • Paroxysmal nocturnal hemoglobinuria

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Riddle: What do aplastic anemia, acute promyelocytic leukemia, and chronic myeloid leukemia have in common?'. Together they form a unique fingerprint.

Cite this