The frequently occurring T-cell receptor delta (TCRD) deletions in
precursor-B-acute lymphoblastic leukemia (precursor-B-ALL) are assumed to
be mainly caused by Vdelta2-Jalpha rearrangements. We designed a multiplex
polymerase chain reaction tified clonal Vdelta2-Jalpha rearrangements in
141 of 339 (41%) childhood and 8 of 22 (36%) adult precursor-B-ALL. A
significant proportion (44%) of Vdelta2-Jalpha rearrangements in childhood
precursor-B-ALL were oligoclonal. Sequence analysis showed preferential
usage of the Jalpha29 gene segment in 54% of rearrangements. The remaining
Vdelta2-Jalpha rearrangements used 26 other Jalpha segments, which
included 2 additional clusters, one involving the most upstream Jalpha
segments (ie, Jalpha48 to Jalpha61; 23%) and the second cluster located
around the Jalpha9 gene segment (7%). Real-time quantitative PCR studies
of normal lymphoid cells showed that Vdelta2 rearrangements to upstream
Jalpha segments occurred at low levels in the thymus (10(-2) to 10(-3))
and were rare (generally below 10(-3)) in B-cell precursors and mature T
cells. Vdelta2-Jalpha29 rearrangements were virtually absent in normal
lymphoid cells. The monoclonal Vdelta2-Jalpha rearrangements in
precursor-B-ALL may serve as patient-specific targets for detection of
minimal residual disease, because they show high sensitivity (10(-4) or
less in most cases) and good stability (88% of rearrangements preserved at
relapse)