11q deletions in hematological malignancies

Citation
O. Monni et S. Knuutila, 11q deletions in hematological malignancies, LEUK LYMPH, 40(3-4), 2001, pp. 259-266
Citations number
61
Categorie Soggetti
Hematology,"Onconogenesis & Cancer Research
Journal title
LEUKEMIA & LYMPHOMA
ISSN journal
10428194 → ACNP
Volume
40
Issue
3-4
Year of publication
2001
Pages
259 - 266
Database
ISI
SICI code
1042-8194(200101)40:3-4<259:1DIHM>2.0.ZU;2-B
Abstract
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.