Loss of heterozygosity at chromosome 1p in different solid human tumours: association with survival.

The distal half of chromosome 1p was analysed with 15 polymorphic microsatellite markers in 683 human solid tumours at different locations. Loss of heterozygosity (LOH) was observed at least at one site in 369 cases or 54% of the tumours. LOHs detected ranged from 30-64%, depending on tumour location.

Mapping loss of heterozygosity at chromosome 13q: loss at 13q12-q13 is associated with breast tumour progression and poor prognosis.

Several chromosome regions exhibit loss of heterozygosity (LOH) in human breast carcinoma and are thought to harbour tumour suppressor genes (TSG). At chromosome 13q, two TSGs have been identified, RB1 at 13q14 and BRCA2 at 13q12-q13. In this study, 139 sporadic breast tumours were analysed with 18 polymorphic microsatellite markers for detailed mapping of LOH at chromosome 13q and evaluation of an association with known progression factors.

Replication error in human breast cancer: comparison with clinical variables and family history of cancer.

Replication errors (RER) at microsatellite repeats indicate genomic instability in hereditary nonpolyposis colorectal cancer (HNPCC) and in some sporadic cancers. We have studied genomic instability in 313 sporadic breast tumors and in 106 tumors from BRCA2, 999del5 carriers at 43 genomic loci on 13 chromosomes. RER was observed in 8/419 (1.

High frequency of LOH at chromosome 18q in human breast cancer: association with high S-phase fraction and low progesterone receptor content.

Human primary breast cancers were analysed for somatic loss of heterozygosity (LOH) at chromosome 18 with 15 polymorphic microsatellite markers. LOH was observed in 148 of the 228 cases analyzed, (65%). Three smallest common deletion regions (SCDR) were detected on the long arm of chromosome 18.

High incidence of loss of heterozygosity at chromosome 17p13 in breast tumours from BRCA2 mutation carriers.

Breast tumours from BRCA1 and BRCA2 mutation carriers are genetically instable and display specific patterns of chromosomal aberrations, suggestive of distinct genetic pathways in tumour progression. The frequency of abnormalities affecting chromosome 17p and the TP53 gene was determined in 27 breast tumours from 26 female patients carrying the Icelandic BRCA2 founder mutation (999del5). Loss of heterozygosity (LOH) was detected in 23 of the 27 tumours (85%).

Loss of heterozygosity at chromosome 7q in human breast cancer: association with clinical variables.

In this study 238 human primary breast cancers were analysed with 9 polymorphic microsatellite markers specific to region 7q21-q35 on chromosome 7. LOH was observed at one or more marker in 82 cases or (34%). The deletions were evenly distributed throughout the region.

Loss of heterozygosity on chromosome 9 in human breast cancer: association with clinical variables and genetic changes at other chromosome regions.

Primary breast tumors were tested for loss of heterozygosity (LOH), on chromosome 9p with microsatellite markers restricted to a 28 cM region including the MTS1 gene. LOH was found with at least 1 marker in 38% of the 201 cases analyzed. A high frequency of deletions was detected at the 9p23-p21 region, indicating a tumor suppressor gene(s) important for breast cancer tumorigenesis.

Loss of heterozygosity at chromosome 11 in breast cancer: association of prognostic factors with genetic alterations.

We examined DNA from 116 female and four male breast cancer patients for loss of heterozygosity (LOH). DNA was analysed by polymerase chain reaction using ten microsatellite markers on chromosome 11. Three distinct regions of LOH were identified: 11p15.

High frequency of allelic imbalance at chromosome region 16q22-23 in human breast cancer: correlation with high PgR and low S phase.

The loss of genetic material from a specific chromosome region in tumors suggests that presence of tumor-suppressor genes. Loss of heterozygosity (LOH) or allelic imbalance (AI) on the long arm of chromosome 16 is a known event in sporadic breast cancer. To locate the commonly deleted regions, and therefore (a) candidate tumor-suppressor gene(s), a deletion map of chromosome 16 was made, using 10 microsatellite markers on 150 sporadic breast tumors.