Structural aberrations involving 11q are among the most common aberrations
in a number of hematological malignancies. Most of the aberrations, such as
translocations: and deletions, often harbor a breakpoint at 11q23, which s
uggests that this region might contain a tumor suppressor gene important fo
r the genesis of lymphoproliferative disorders. Interestingly, deletions ar
e concentrated only in some subtypes of hematological malignancies, where t
hey are detected at a relatively high frequency. In B-cell chronic lymphocy
tic leukemia (B-CLL), deletions have been detected in 20-30% of the cases,
whereas almost half of the mantle cell lymphomas (MCL) show deletion at 11q
23 in fluorescence in situ hybridization analysis. In T-cell prolymphocytic
leukemia (T-PLL) deletions involving the region 11q23.3-23.1 have also bee
n detected to be frequent. In B-cell chronic lymphocytic leukemia, 11q dele
tion is associated with more rapid disease progression and poor survival in
a younger subgroup of patients. The putative tumor suppressor genes have r
emained unrevealed until recently, when the ATM gene was found to carry mut
ations in cases with deletion in B-CLL, MCL and T-PLL. These data suggest t
hat 11q deletions and dysfunction of the ATM gene might have significance i
n the tumorigenesis of certain subsets of hematological malignancies. Impor
tance of 11q deletion as a diagnostic marker needs to be further studied in
a larger series of patients. Another issue that remains to be investigated
is the involvement of other target gents in the deletion.