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Rearrangement of the TCR-delta gene was studied using J delta, C delta, and V delta probes in 61 cases of acute lymphoblastic leukemia (ALL) and several cases of chronic lymphoid neoplasms to define the specificity and the diversity of rearrangements occurring at the delta locus. TCR-delta rearrangements or deletions were found in all T (33 cases) and B lineage (28 cases) ALL but not in any case of B cell chronic proliferations (13 cases). The restriction patterns of rearrangement were clearly distinct between T and B ALL and use of one V delta probe showed that rearrangement of the V delta IDP2 gene segment which is also productively rearranged in the Peer cell line, occurred frequently in T-ALL but never in B lineage ALL. Studies of WT31 and delta TCS1 antibody reactivity showed that at least 4 of 13 CD3+ T-ALL cases expressed the delta protein. CD4 and/or CD8 Ag expression were observed in some of the gamma delta expressing T-ALL. These data show that particular TCR-delta gene rearrangements occur in neoplastic early B cells and that the combinatorial diversity of TCR-delta rearrangements in T cells is higher than initially expected. In addition this study shows that an important proportion of CD3 positive T-ALL cases express the gamma delta heterodimer.

A 75 year old woman with a 13 year history of classical chronic lymphatic leukaemia (CLL) developed hypercalcaemia. Unlike previous reports, this was not associated with blastic transformation, hyperparathyroidism or features of multiple myeloma, but was due to classical CLL per se.

The polymerase chain reaction was used to amplify rearrangements of T-cell receptor gamma genes from 2 leukemic DNA samples involving the same variable segment. One V-J junction was sequenced and an anti-junctional oligonucleotide synthesized. This oligonucleotide was used as probe on in vitro amplified DNA. We show that this strategy allows the detection of the corresponding clonal DNA at dilutions of up to 10(6) fold in germline DNA. Moreover we demonstrate that it is possible to differentiate this clone from the second leukemic clone and from polyclonal T-cells.

Moscovici, Carlo (University of Colorado Medical Center, Denver), and E. H. Macintyre. Effect of avian myeloblastosis virus in the Japanese quail. J. Bacteriol. 92:1141-1149. 1966.-Avian myeloblastosis virus (AMV) induced a spectrum of neoplasms in Japanese quail (Coturnix coturnix japonica) which was similar to that observed in the chicken, with one exception: the total absence of acute myeloblastic leukemia in quail. Studies in vivo as well as in vitro suggested that the cause for this difference may be ascribed to the heterogeneity of AMV and to the genetic makeup of the quail cell.