Monosomy 20 as a pointer to dicentric (9;20) in acute lymphoblastic leukemia

Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization

“…The formation of dicentric chromosomes involving chromosome 9 usually leads to loss of 9p and 7p, 12p or 20q (Behrendt et al, 1995;Clark et al, 2000). Two patients with a dic(9;20)(p11B13;q11) were included in this study.…”

The frequency and prognostic impact of dic(9;20)(p13.2;q11.2) in childhood B-cell precursor acute lymphoblastic leukemia: results from the NOPHO ALL-2000 trial

“…2;q11.2) is a rare, but recurrent aberration in B-cell precursor acute lymphoblastic leukemia (BCP ALL); on the basis of G-banding analyses, the dic(9;20) has been reported to be present in 1-2% and 0.5% of childhood and adult BCP ALLs, respectively. [1][2][3][4][5][6][7][8] Since the dic(9;20) aberration was first described in 1995, (see refs. 1, 2) B130 dic(9;20)-positive ALL cases have been reported in the literature.…”

“…To date, only six studies have comprised 10 or more dic(9;20)-positive cases. 2,[4][5][6][7][8] Studies on pediatric cases have shown that dic(9;20) positive leukemias display consistent BCP immunophenotypic features, with positivity for HLA-DR, CD10, CD19, CD20 and CD22 and negativity for T cell and myeloid markers, show a female predominance, and have a significant age incidence peak at 3-4 years. Most patients are allocated to non-standard risk treatment arms because of high white blood cell (WBC) count and a relatively high frequency of central nervous system (CNS) disease or other types of extra-medullary leukemia at diagnosis.…”

“…Most patients are allocated to non-standard risk treatment arms because of high white blood cell (WBC) count and a relatively high frequency of central nervous system (CNS) disease or other types of extra-medullary leukemia at diagnosis. 2,[4][5][6] As regards, the prognostic implications and other clinical ramifications of dic (9;20), they remain to be clarified in detail. [5][6][7]10 Several studies have characterized the dic (9;20) at the cytogenetic and molecular genetic levels, revealing breakpoint heterogeneity on both chromosomes, albeit with clustering of breaks in sub-bands 9p13.2 and 20q11.2.…”

“…(see refs. [11][12][13][14][15][16] As this subtle abnormality easily escapes detection by conventional cytogenetics, being misclassified as monosomy 20 and/or deletion of 9p, [2][3][4][5] and that it may have a clinically important impact, other methods are definitely needed. As of yet, the dic(9;20) has not been shown to result in any gene fusion, rendering PCR-based methods unavailable for detection.…”