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Atypical (7;19) translocation in acute myelomonocytic leukemia
M E Sherer1, S Shekhter-Levin, J R Krause
1Department of Human Genetics, Univeristy of Pittsburgh, Pennsylvania.
Cancer Genetics and Cytogenetics
|December 1, 1991
Summary
A novel chromosome rearrangement, t(7;19)(q22;p13.3), was identified in a patient with acute myelomonocytic leukemia. This specific genetic alteration has not been previously reported as the sole clonal rearrangement in myeloid disorders.
Area of Science:
- Cytogenetics
- Hematologic Oncology
- Molecular Biology
Background:
- Acute myelomonocytic leukemia (FAB M4) is a subtype of myeloid leukemia characterized by the proliferation of myeloid and monocytic precursors.
- Chromosome abnormalities are common in acute myeloid leukemia and play a crucial role in diagnosis, prognosis, and treatment strategies.
Observation:
- Chromosome analysis of bone marrow aspirate from a 75-year-old male with acute myelomonocytic leukemia revealed a mosaic pattern with two cell lines.
- The observed mosaicism included a specific translocation: 46,XY/46,XY,t(7;19)(q22;p13.3).
Findings:
- The reciprocal translocation t(7;19)(q22;p13.3) was identified as the sole specific clonal chromosome rearrangement.
- This particular translocation has not been previously documented as the primary genetic abnormality in myeloid neoplasia.
- Genes located at the breakpoints, including those for plasminogen activator inhibitor type I, multi-drug resistance, erythropoietin (7q22), and the insulin receptor (19p13.3), are situated at fragile site loci.
Implications:
- The identification of this novel translocation may contribute to a better understanding of the genetic landscape of acute myelomonocytic leukemia.
- Further research is warranted to investigate the functional significance of the t(7;19)(q22;p13.3) rearrangement and its potential role in leukemogenesis.
- The involvement of fragile sites and specific genes at the translocation breakpoints suggests potential mechanisms underlying this chromosomal abnormality.
