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Year : 2012  |  Volume : 37  |  Issue : 2  |  Page : 129-134

Molecular detection of 6q deletion in Egyptian patients with B-cell chronic lymphoproliferative disorders

1 Department of Clinical and Chemical Pathology, Faculty of Medicine, National Cancer Institute, Cairo University, Cairo, Egypt
2 Department of Clinical and Chemical Pathology, National Cancer Institute, Cairo University, Cairo, Egypt

Correspondence Address:
Dalia G. Amin
Department of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Cairo
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Source of Support: None, Conflict of Interest: None

DOI: 10.7123/01.EJH.0000415294.38654.88

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Deletions of the long arm of chromosome 6 (6q) are among the most frequent chromosome aberrations in multiple human tumors, including acute lymphocytic leukemia and non-Hodgkin’s lymphoma (NHL). The accurate characterization of the 6q deletions is of clinical significance in lymphoid malignancies because they are related to the prognosis. The aim of this study was to evaluate the frequency of 6q21 deletion in B-cell chronic lymphoproliferative disorders (BCLPDs) and to evaluate the association of this deletion with other prognostic criteria.

Patients and methods

A fluorescence in-situ hybridization probe set on chromosome 6q21 was used to evaluate 6q21 deletion in 63 patients with different BCLPDs, they were 30 patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL), 21 patients with NHL, four patients with Waldenström macroglobulinemia, and eight patients with multiple myeloma.


6q21 deletion was detected in 20% of CLL/SLL (6/30), (40%) of diffuse large B-cell lymphoma (2/6), 33.3% of follicular lymphoma (2/6), and 20% of mantle cell lymphoma (1/5), 25% of multiple myeloma (2/8), and in 50% of Waldenström macroglobulinemia (2/4) patients. None of the two patients with splenic lymphoma or the three patients with unclassifiable B-NHL showed 6q21 deletion. The median percentage of clonal lymphoid cells with deletion (6q21) was 45% (33–88%). CLL/SLL patients with 6q21 deletion had a significantly lower hemoglobin concentration (P=0.006); a significantly higher mean age (P=0.009); percent of peripheral blood prolymphocytes (P=0.001); and level of serum lactate dehydrogenase (P=0.009) compared with those without the deletion. All CLL/SLL patients (100%) with 6q deletion were allocated to stage C and stages III and IV of Binet and Rai staging systems, respectively, whereas only (58.3%) of those without 6q deletion were allocated to the same advanced stages; however, this was not statistically significant. Among NHL patients, 6q deletion was associated with older age (>60 years, P=0.01), lower hemoglobin concentration (P=0.003), higher level of β2-microglobulin (β2M) and lactate dehydrogenase (P=0.01 and 0.00, respectively), and higher incidence of splenomegaly (P=0.003). All NHL patients with 6q deletion were stratified into a high-risk group according to the International Prognostic Index, whereas those without 6q deletion, approximately 44%, were classified as a high-risk group (P=0.02). Staging of NHL patients according to the Ann Arbor system showed no significant difference between patients with 6q deletion and those without.


On the basis of the high frequency of deletion (6q) in BCLPDs, we suggest a pathogenetic role of this deletion in BCLPDs. Our results support previous studies that have shown an impact of 6q deletion on prognosis in subtypes of BCLPDs.

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