5 research outputs found
Recommended from our members
Identification of a 6-cM Minimal Deletion at 11q23.1–23.2 and Exclusion of PPP2R1B Gene as a Deletion Target in Cervical Cancer
Previous functional and deletion mapping studies on cervical cancer (CC) have implicated one or more tumor suppressor genes (TSGs) on chromosome 11 at q13 and q22–24 regions. Of these, the 11q22–24 region exhibits frequent allelic deletions in a variety of solid tumor types, sug- gesting the presence of critical genes for tumor suppression in this region. However, the precise region of deletion on 11q is not clearly defined in CC. In an attempt to accurately map the deleted region, we performed an extensive loss of heterozygosity (LOH) mapping in 58 tumors using 25 polymorphic loci on both the short and long arms. The pattern of LOH identified three sites of deletions, two on 11p (p15.11–p15.3 and p12–13), and one on 11q (q23.1–q23.2). The 11q23.1–q23.2 exhibited highest fre- quency (60.6%) of deletions, suggesting that this could be the site of a candidate TSG in CC. The minimal deletion at 11q23.1–23.2 was re- stricted to a 6-cM region between 123.5 and 129.5 cM genetic distance on chromosome 11, identifying the site of a potential TSG important in the pathogenesis of CC. At least five known genes and 28 UniGene clusters were mapped to the present commonly deleted region. In addition, we have excluded a previously known TSG PPP2R1B at 11q23 as a deletion target in CC. The definition of the minimal deletion and the availability of expressed sequence resources should facilitate the identification of the candidate TSG
Recommended from our members
Lack of BCL10 mutations in germ cell tumors and B cell lymphomas
The BCL10 gene has recently been cloned from the chromosomal translocation t(1;14)(p22;q32) in a low-grade mucosa-associated lymphoid tissue (MALT) lymphoma, and was implicated in the pathogenesis of this and several other tumor types (Willis et al. 1999). BCL10 is a cellular homolog of the equine herpesvirus-2 E10 gene, which contains an amino-terminal caspase recruitment domain (CARD) and plays a role in apoptosis. Willis et al. 1999 also showed that BCL10 exhibits hypermutations in MALT lymphomas with t(1;14) as well as frequent mutations in 45% of B and T cell lineage lymphomas without the 1p22 chromosomal rearrangements. In addition, they reported BCL10 mutations in cell lines derived from several solid tumor types including three each of male germ cell tumors (GCTs) and mesotheliomas, suggesting that it may be commonly involved in the pathogenesis of many human malignancies. The 1p22 region is affected by frequent deletions in male GCTs (Mathew et al. 1994) and mesotheliomas (Lee et al. 1996), suggesting that inactivation of a critical gene in this region may play a role in the genesis of these tumors