Immunoglobulin gene rearrangements in acute lymphoblastic leukemia with the 9;II translocation

Abstract

The recurring chromosomal 9;11 translocation [t(9;11) (p22;q23)] typically is associated with acute monoblastic leukemia, but a number of patients with acute lymphoblastic leukemia also have been reported to have the t(9;11). To investigate the cell lineage in the latter cases, we analyzed DNA from the leukemic cells of an 8-year-old girl with acute lymphoblastic leukemia and a t(9;11) for rearrangements of the immunoglobulin and T-cell receptor genes. Rearrangements of both immunoglobulin heavy-chain loci and of one lambda light-chain gene were detected, as well as deletions affecting both alleles of the kappa light-chain genes; T-cell receptor genes were in germline configuration. These results provide further evidence that the 9;11 translocation is not limited to myeloid lineage leukemia and may be observed in acute lymphoblastic leukemia.

Post‐transplant lymphoproliferative disorder subtypes correlate with different recurring chromosomal abnormalities

“…The karyotypes are described according to the International System for Human Cytogenetic Nomenclature (Mitelman, 1995). Analysis of immunoglobulin heavy-chain gene (IGH) and T-cell receptor (TCR) rearrangements were performed on fresh or deparaffinized tissue by Southern blot analysis with probes for the IGH JH region and the TCRb Jb1 and Jb2 regions (Lorenzana et al, 1991). Alternatively, the B & T Cell Clonality Assay (IVS Technologies, Carlsbad, CA) was used.…”

Mature B-cell acute lymphoblastic leukemia with t(9;11) translocation: a distinct subset of B-cell acute lymphoblastic leukemia

“…9 These cases can show non-FAB-L3 morphology with sIg expression and MYC rearrangement, [7][8][9] L3 morphology with sIg expression but no MYC rearrangement, 19 and rare cases showing sIg expression with non-FAB-L3 morphology and no MYC rearrangement. [3][4][5][6][7][8][9] Some of these sIg þ B-ALL cases 20 These cases should probably be more appropriately named 'surface immunoglobulin-positive B-ALL. ' The most common cytogenetic abnormalities associated with mature B-ALL are translocations involving the MYC gene, including t(8;14), t(2;8), and t (8;22).…”

“…Literature review reveals four cases of MLL þ mature B-ALL. [3][4][5][6] Two additional cases are identified, one of ALL and the other of lymphoblastic lymphoma 25 (both presented at an international meeting, cases #106 and #139, Society for Hematopathology/European Association of Hematopathology workshop, Pediatric Hematopathology, Memphis, TN, USA). a and b).…”

“…However, rare cases of B-ALL with non-FAB-L3 morphology and without MYC rearrangements have also been reported in both adult and pediatric patients as 'mature B-ALL'. [3][4][5][6][7][8][9] These cases may or may not express TdT and CD34, but uniformly express sIg to some degree.…”

der(11)t(1;11)(q11-23;q14-25)

“…Among them, 4 cases were identified as secondary diseases (Muroi et al, 1996;Archimbaud et al, 1998;Harrison et al, 1998). There were 6 patients with ALL (Kaneko et al, 1982;Mamaeva et al, 1983;Lorenzana et al, 1991;Harrison et al, 1998;Betts et al, 2001;Wan et al, 2004), one of them was a secondary leukaemia (Harrison et al, 1998) and there were 3 biphenotypic leukaemias (Hayhashi et al, 1990;Forrest et al, 1998;Jarvis et al, 1999). Chronic lymphocytic leukemia was diagnosed in 2 patients (Qian et al, 1999;Travella et al, 2013), one of them transformed to Non hodgkin's lymphoma (Qian et al, 1999).…”