Armenian Hamster Anti-Mouse TCR Vγ1.1/Cr4 Monoclonal antibody, clone 2.11 Functional Grade

The presence of Ig and TCR gene rearrangement has been reported to occur in ANLL. However, most of the studies have been performed in short series of patients and, in general, not all rearranging genes have been included. We have investigated the configuration of immunoglobulin (Ig) and T-cell receptor loci (TCR) in a series of 160 untreated patients with de novo acute non-lymphoblastic leukaemia (ANLL) and correlated the results with the morphological and immunophenotypic characteristics of blast cells. IGH gene rearrangement was detected in 16/160 cases analysed (10%) and IGK was rearranged in half of them. The incidence of cases displaying TCRB, TCRG and TCRD rearrangements was 5.6%, 13.8% and 13%, respectively. Concomitant recombinatorial events including different Ig and/or TCR genes were frequently detected. Gene rearrangement was not related to the stage of cell differentiation within the myeloid lineage assessed both by morphological and immunophenotypic criteria. Regarding the correlation with the presence of lymphoid related markers, the only relevant association was between the expression of CD7 antigen and TCRG and TCRD gene rearrangement. Our results show that the incidence of gene rearrangement in ANLL may be slightly higher than previously suspected, and that it is not associated with early stages of cell differentiation nor to the expression of lymphoid markers.

Swine chromosome 18 (SSC18) has the poorest marker density in the USDA-MARC porcine linkage map. In order to increase the marker density, seven genes from human chromosome 7 (HSA7) expected to map to SSC18 were selected for marker development. The genes selected were: growth hormone releasing hormone receptor (GHRHR), GLI-Kruppel family member (GLI3), leptin (LEP), capping protein muscle Z-line alpha 2 subunit (CAPZA2), beta A inhibin (INHBA), T-cell receptor beta (TCRB) and T-cell receptor gamma (TCRG). Large-insert clones (YACs, BACs and cosmids) that contained these genes, as well as two previously mapped microsatellite markers (SW1808 and SW1984), were identified and screened for microsatellites. New microsatellite markers were developed from these clones and mapped. Selected clones were also physically assigned by fluorescence in situ hybridization (FISH). Fifteen new microsatellite markers were added to the SSC18 linkage map resulting in a map of 28 markers. Six genes have been included into the genetic map improving the resolution of the SSC18 and HSA7 comparative map. Assignment of TCRG to SSC9 has identified a break in conserved synteny between SSC18 and HSA7.