Discontinuous deletions at 11q23 in B cell chronic lymphocytic leukemia

The rewards and challenges of array-based karyotyping for clinical oncology applications

“…21 Other groups have reported data suggesting that there is a slightly more telomeric but overlapping region that does not include ATM. [21][22][23] This finding was corroborated by Lehmann et al 5 who also observed a second commonly deleted region at 11q that is telomeric to the ATM gene when they used SNP arrays to karyotype CLL samples. It is postulated that this region may harbor another TSG associated with the development of CLL, and that concurrent deletion of ATM and this other TSG may contribute to a poor prognosis.…”

The class II tumor-suppressor gene RARRES3 is expressed in B cell lymphocytic leukemias and down-regulated with disease progression

“…19 Aberrations at 11q regions are recurring abnormalities in various types of neoplasias including lymphoproliferative disorders. [24][25][26][27][28] In addition, previous studies have shown that loss of heterozygosity (LOH) at the genomic region 11q22-q23 is one of the most common structural chromosome aberrations in B-CLL, 5,[7][8][9][10] suggesting that a novel tumor suppressor gene may be located in this region. Because RARRES3 is mapped to this hot spot chromosome region and this gene has not been analyzed thus far in hematologic malignancies, we performed expression and mutational analyses to determine whether RARRES3 could play a role in B-CLL pathogenesis.…”

“…5,6 The most frequent abnormalities are deletions in chromosome bands 13q12-q14 (30-80% of cases), followed by trisomy 12 (15-35%) and deletions at 11q (20%). 5,[7][8][9][10] 11q deletions correlate with extensive nodal involvement, younger age incidence and more aggressive disease progression. 5,7,11 Some of the reported genetic aberrations in B-CLL affect interesting genes, such as LEU2B (located at 13q14.3) which is frequently deleted in B-CLL, 12 although its involvement in the disease has not been yet elucidated.…”

Surface antigen expression in chronic lymphocytic leukemia: clustering analysis, interrelationships and effects of chromosomal abnormalities

“…16 It is tempting to think that this kind of differential splicing existed in our cases, where 11q23 deletion has been carefully characterized. [33][34][35] Although chromosome 11q22-23 is a gene rich area, we are not aware of any gene which might change the CD45 splicing strategy.…”