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V Egilsson

Publications and source records attributed to V Egilsson.

46 records · Page 3Linked to original sources
PubMed1984

Isoenzyme pattern and subcellular localization of hexokinases in human breast cancer and nonpathological breast tissue.

Subcellular distribution of hexokinase (HK) isoenzymes in 22 human breast cancers (21 primary cancers and 1 axillary metastatic growth) and 7 non-pathological human mammary gland tissue samples was studied with starch gel electrophoresis on isolated cell fractions obtained by differential centrifugation. Fractions used were cytosol, mitochondria and microsomes. A comparison of two methods for detecting HK activity was made, yielding different results regarding HK II and HK III. A method based on the ability of NADPH to fluoresce in UV gave a constant pattern of HK isoenzymes. In non-pathological breast tissue, only HK I was seen, i.e. in the cytosol and the microsomal fractions. HK I was also seen in all fractions of the cancers, but another more anodal band of HK I, as well as HK II and HK III, consistently appeared in the cytosol fractions. The more commonly used staining technique with tetrazolium dye revealed HK II in 45% and HK III in 50% of the samples. The pattern of HK isoenzymes in the cancers was the same irrespective of estrogen and progesterone cytosolic receptor contents and the histology of the tumors. The fluorescence method is, therefore, much more sensitive than the tetrazolium technique for detecting HK activity after electrophoresis and could explain difference in results obtained by various laboratories.

Breast↗
PubMed1979

Toxic and mutagenic effects of carcinogens on the mitochondria of Saccharomyces cerevisiae.

Nineteen haploid yeast (Saccharomyces cerevisiae) strains were used to assess the relative growth inhibitory potencies on fermentable vs. non-fermentable media of a collection of carcinogenic and non-carcinogenic chemicals. The majority of carcinogens were distinctly more potent on the non-fermentable (glycerol) medium, where mitochrondrial function is required for growth, than on the fermentable medium, where it is not. The anti-mitochondrial selectivity indicated by these growth tests was much slighter for the non-carcinogens. Similarly most carcinogens induced the cytoplasmic petite mutation whereas the non-carcinogens did not. Five carcinogens which were tested impaired the development of cytochromes aa3 and b in glucose cultures. Six carcinogens, when tested, inhibited growth on three fermentable sugars, the utilisation of which requires mitochondrial function. Out of five carcinogens which were examined, four suppressed the surface-dependent phenomenon of fluocculence in a flocculating strain of yeast, at concentrations primarily affecting the mitochondrial system; the fifth had a similar but less pronounced effect.

Carcinogens↗
PubMedDate not supplied

Replication error in colorectal carcinoma: association with loss of heterozygosity at mismatch repair loci and clinicopathological variables.

Instability of microsatellite DNA or replication error (RER) is characteristic of tumours caused by mismatch repair (MMR) deficiency. Germline mutations in MMR genes are associated with Hereditary non-polyposis colorectal carcinoma (HNPCC) and somatic mutations in these genes are also found in a substantial fraction of colorectal cancers (CRC). In this study we concurrently screened colorectal tumours for the RER phenotype and loss of heterozygosity (LOH) at MMR gene loci. The RER phenotype was evident in 47/197 (24%) tumours. RER was more commonly detected in young patients (< 50 years) and in tumours located in the proximal colon. RER was positively associated with LOH at the hMSH2/hMSH6 loci on chromosome 2p, where LOH was observed in 46% of the RER+ tumours. LOH at hMLH1 and hPMS1 loci was more frequent in the younger patients (< 50 years). RER was not associated with clinicopathological parameters, such as Duke's stage and tumour differentiation (grade). The RER phenotype was associated with better overall survival, but there was a trend towards significance when multivariate analysis was used. This indicates that loss of MMR genes generate a less aggressive phenotype, and raises the question about RER being a useful indicator of prognosis for CRC patients.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

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. Patients were divided into two groups according to whether LOH was observed in their tumours or not, and tested for association with overall survival, the clinicopathological features: steroid receptor content, tumour size, node status, DNA ploidy and S-phase fraction, and LOH at other chromosomal regions. An association was found between 7q LOH and high S-phase fraction. An association was found between LOH at 7q and LOH at 1p, 3p, 9p, 13q and 17q. These results suggest the location of a putative tumour suppressor gene at chromosome 7q21-q35 that, in combination with other deletions, might enhance tumour growth.

Breast Neoplasms↗
PubMedDate not supplied

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. The marker D18S51 at the region 18q22 showed the highest LOH (42%). Tumors with and without LOH at 18q were tested for association with clinico-pathological features of the tumors, such as estrogen and progesterone receptor content, age at diagnosis, tumor size, node status, histological type, S-phase fraction, DNA ploidy and LOH at other chromosomal regions. A significant association was found between LOH at 18q and high S-phase fraction (99.9% confidence interval) and low progesterone receptor content (99% confidence interval). Furthermore, an association was found between LOH at 18q and LOH at 1p, 7q, 9p, 13q and 17q. We conclude that there are three separate LOH target regions at chromosome 18q, and that inactivation of one or more genes at these regions might be important for human breast carcinogenesis.

Breast Neoplasms↗
PubMedDate not supplied

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 (1.9%) of the cases at one or more chromosomal loci. The frequencies of type I and type II RER were similar. The majority of RER+ tumors showed ER+, PgR+, high S-phase fraction, tumor size >2 cm and LOH at 2p, 2q and 3p. All 8 RER+ tumors were of the ductal histotype. The breast cancer cases with RER are not part of an HNPCC syndrome and a family history of colorectal cancer growth is not detected in relatives, with the exception of one case. However, four of the RER+ cases are from individuals carrying the BRCA2, 999del5 mutation. We conclude that RER is a rare somatic event during human breast carcinogenesis and may be associated with progression of breast carcinomas.

Adult↗