Multiple deleted regions on the long arm of chromosome 6 in astrocytic tumours

Abstract

Summary Chromosome 6 deletions are common in human neoplasms including gliomas. In order to study the frequency and identify commonly deleted regions of chromosome 6 in astrocytomas, 159 tumours (106 glioblastomas, 39 anaplastic astrocytomas and 14 astrocytomas malignancy grade II) were analysed using 31 microsatellite markers that span the chromosome. Ninety-five per cent of cases with allelic losses had losses affecting 6q. Allelic losses were infrequent in astrocytomas malignancy grade II (14%) but more usual in anaplastic astrocytomas (38%) and glioblastomas (37%). Evidence for clonal heterogeneity in the astrocytomas and anaplastic astrocytomas was frequently observed (i.e. co-existence of subpopulations with and without chromosome 6 deletions). Clonal heterogeneity was less common in glioblastomas. Five commonly deleted regions were identified on 6q. These observations suggest that a number of tumour suppressor genes are located on 6q and that these genes may be involved in the progression of astrocytic tumours.

Mutations in Rb1 pathway-related genes are associated with poor prognosis in Anaplastic Astrocytomas

“…This was confirmed by the genetic analysis of the tumour tissue which, when compared with the individual patients' white blood cell DNA, showed genetic abnormalities in all cases (e.g. loss of heterozygosity (LOH) at a number of sites in addition to point mutations) (Ichimura et al, 1998;Miyakawa et al, 2000). The age range of the patients and the location of the tumours are comparable to similar studies, while the sex distribution is slightly unusual showing comparatively high number of female subjects (Kleihues and Cavanee, 2000).…”

Expression of Hqk Encoding a KH RNA Binding Protein Is Altered in Human Glioma

“…However, a high incidence of chromosomal aberrations at 6q23.3 to 26 in astrocytic tumors has been reported. [35][36][37] Introduction of a fragment of normal chromosome 6 into a tumor cell line with 6q deletion resulted in suppression of tumorigenicity, suggesting the presence of tumor suppressor gene(s) on the corresponding chromosomal region. 38) On the other hand, a null mutation in the gld-1 gene, a C. elegans homolog of qkI, leads to excessive oocyte growth, and partial loss-of-function mutation in gld-1 causes oocytes to arrest at the pachytene stage.…”

“…For all the human samples used in this study, informed consents were obtained. Tumor tissues were taken from surgical operations conducted at the Kumamoto University Hospital and processed by the standard methods as described by Miyakawa et al 35) Each tumor specimen was first examined pathologically, and the specimens containing a high percentage of tumor cells, generally more than 95%, were used for the subsequent molecular studies. DNA extraction from the tumor tissues was performed as described by Liang et al 36) Peripheral blood samples were obtained from patients with glial tumors, and DNAs were extracted with the DNA Extractor WB Kit (Nippon Gene, Toyama) according to the protocol provided by the supplier.…”

“…[35][36][37] To investigate whether Hqk is involved in tumor formation, we first looked for genomic deletion of Hqk in tumor samples including twenty gliomas, eight meningiomas and three schwannomas. PCR primer pairs that flank each exon were used to detect homozygous genomic deletions, but no such deletions were found in the tumor samples tested.…”

High-resolution genome-wide allelotype analysis identifies loss of chromosome 14q as a recurrent genetic alteration in astrocytic tumours

“…In low-grade astrocytic tumours, chromosomal regions with frequent loss have been identified on 6q, 10p, 13q, 17p and 22q (Tsuzuki et al, 1996;Ino et al, 1999;Miyakawa et al, 2000). Mutation of the TP53 gene, which is located on 17p, is the most common genetic alteration detected in 460% tumours (von Deimling et al, 1992a).…”