Abstract |
Inversion of chromosome 16, inv(16)(p13q22), juxtaposes the core binding factor beta (CBFB) and myosin heavy chain 11 (MYH11) genes, resulting in a myeloid leukemic disease phenotype characterized by increased bone marrow and peripheral blood blasts with myelomonocytic antigen expression and an accompanying eosinophilia. This cytogenetic abnormality has been reported in a variety of other neoplasms, in which it generally occurs as part of a complex karyotype, including rare B-lineage non-Hodgkin lymphomas. We report a case of clinically, morphologically, and immunologically typical lymphoplasmacytic lymphoma/Waldenström macroglobulinemia in which a majority of the malignant cells had an inv(16)(p13q22) as a sole abnormality. We review the literature and discuss the possible role of this genetic lesion in B-cell neoplasia.
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Authors | John L Frater, Mona Mirkhaef, Jacqueline R Batanian |
Journal | Cancer genetics and cytogenetics
(Cancer Genet Cytogenet)
Vol. 174
Issue 2
Pg. 161-5
(Apr 15 2007)
ISSN: 0165-4608 [Print] United States |
PMID | 17452259
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- Antibodies, Monoclonal
- Antibodies, Monoclonal, Murine-Derived
- Antineoplastic Agents
- Rituximab
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Topics |
- Aged, 80 and over
- Antibodies, Monoclonal
(therapeutic use)
- Antibodies, Monoclonal, Murine-Derived
- Antineoplastic Agents
(therapeutic use)
- Chromosome Banding
- Chromosome Inversion
- Chromosomes, Human, Pair 16
- Fatal Outcome
- Humans
- In Situ Hybridization, Fluorescence
- Karyotyping
- Leukemia, Lymphocytic, Chronic, B-Cell
(drug therapy, genetics, pathology)
- Male
- Rituximab
- Waldenstrom Macroglobulinemia
(drug therapy, genetics, pathology)
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