Acute promyelocytic leukemia with additional chromosomal abnormalities and absence of Auer rods

Zahid Kaleem, Michael S. Watson, Mary M. Zutter, Morey A. Blinder, Jay L. Hess

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


We report 4 acute promyelocytic leukemia cases that demonstrated karyotypic abnormalities in addition to the classic t(15;17) translocation and did not contain any Auer rods in leukemic blasts and dysplastic promyelocytes, either in the peripheral blood or in the bone marrow. Morphologically, 2 cases were characterized as the common or hypergranular type, and 2 were otherwise typical of the microgranular variant. Three patients had typical clinical and laboratory signs of disseminated intravascular coagulation. Immunophenotypic analysis of the blasts and dysplastic promyelocytes by dual-color flow cytometry revealed an immunoprofile consistent with acute promyelocytic leukemia. Cytogenetic analysis of the bone marrow revealed the following karyotypes: case 1, [47,XY,t(15;17)(q22;q12),+21]; case 2, [47,XY,t(15;17)(q22;q12),-16,+2 mar]; case 3, [47,XX,t(15;17)(q22;q12)ider(17)(q10),+8]; and case 4, [47,XY,der(5)t(5;?9)(p15;q12),t(15;17)(q22;q12). Review of an additional 7 cases with t(15;17) as the sole cytogenetic abnormality revealed Auer rods in all cases. Our findings emphasize the importance of cytogenetics in evaluating acute myeloid leukemias. Acute promyelocytic leukemia without Auer rods, which may be morphologically confused with other types of leukemia (in particular, acute myeloblastic leukemia, type M2 or M5) or agranulocytosis with maturation arrest, appears to be associated with additional chromosomal abnormalities and possibly a poorer prognosis.

Original languageEnglish
Pages (from-to)113-118
Number of pages6
JournalAmerican journal of clinical pathology
Issue number1
StatePublished - 1999


  • (15
  • 17) translocation
  • Auer rods
  • Chromosomal abnormalities
  • Promyelocytic leukemia


Dive into the research topics of 'Acute promyelocytic leukemia with additional chromosomal abnormalities and absence of Auer rods'. Together they form a unique fingerprint.

Cite this