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D M Eccles

Publications and source records attributed to D M Eccles.

43 records · Page 3Linked to original sources
PubMed1991

Mitozantrone and prednimustine in the treatment of advanced breast cancer--a toxic regimen with low activity.

The combination of mitozantrone and prednimustine has been reported to elicit response rates of around 50% in patients with advanced breast cancer. In the present trial, either three or nine courses of this combination were given to previously untreated patients with advanced breast cancer. Mitozantrone was given at 12 mg/m2 on day 1 and prednimustine was given orally at 130 mg/m2 on days 1-5; treatment was repeated every 4 weeks. A total of 34 patients were treated; the performance status was 0-1 in 29 subjects and 2 in 5 cases. Locoregional disease only was present in 13 patients; 9 showed lung involvement; 8, liver; 3, bone; and 1, stomach involvement. A total of 10 subjects had received no prior hormone therapy. The median disease-free interval from the time of initial diagnosis was 24 months (range, 0-144 months). In all 14/23 patients exhibited an oestrogen receptor level of greater than 20 fmol. Grade 1 nausea and vomiting occurred in 16 patients and that of grade 2-3, in 11 subjects; nausea was prolonged for greater than 10 days in 7 cases. Grade 4 neutropenia occurred in 2 patients. The response rate was 21% (95% confidence interval, 8%-38%). The combination of mitozantrone and oral prednimustine is toxic and displays low activity.

Adult↗
PubMed1990

Allele losses on chromosome 17 in human epithelial ovarian carcinoma.

16 epithelial ovarian carcinomas (12 serous, 2 mucinous and 2 endometrioid) and 2 benign ovarian adenomas were studied using recombinant DNA technology to compare loci on chromosome 17 in germ-line and tumour DNA. Four polymorphic probes mapping to 17p and one mapping to 17q were used. There was a high frequency of allele loss on 17q/(77%) and a slightly lower frequency on 17p (69%). These findings probably indicate loss of tumour suppressor genes which are of fundamental importance in the genesis or progression of epithelial ovarian carcinomas.

Adenoma↗
PubMed1989

Cervical intraepithelial neoplasia in lymphoma patients: a cytological and colposcopic study.

Twenty-seven patients with Hodgkin's (n = 19) and non-Hodgkin's (n = 8) lymphomas underwent cytological and colposcopic screening of the uterine cervix. Colposcopically directed cervical punch biopsies were taken from all patients in whom a colposcopic abnormality was detected. Lymphoma patients were compared with 79 controls with normal cervical cytology and no known haematological abnormality. Colposcopically directed punch biopsies were taken from the cervical transformation zone of all controls. Significantly more lymphoma patients (19%) than controls (3%) had CIN II or III (P less than 0.01) and cervical human papillomavirus infection, as judged by the presence of koilocytes (52% of lymphoma patients; 27% of controls; P less than 0.02). All six lymphoma patients with CIN had Hodgkin's disease (HD), and five had received combination chemotherapy. Half of the cases of CIN in lymphoma patients and all the cases of CIN in control patients were not detected by cervical cytology. This study suggests that female patients with HD are at increased risk of CIN, and that cervical cytology alone may be an inadequate form of screening for these patients.

Adult↗
PubMedDate not supplied

Prediction of genetic risks from segregation analyses of morbid risks.

Segregation analysis provides a genetic model of disease based upon morbid risks in age-specific classes, from which the model derives genotype-specific morbid risks. In the absence of disease-specific mortality each morbid risk is a cumulative incidence (age-specific penetrance). If disease-specific mortality reduces the number of affected in the older classes, the morbid risk is less than the corresponding penetrance. When counselling individuals with a family history of disease, their genetic risk is a function of penetrances, which can be calculated from morbid risks. We have applied this method to breast, ovarian and colorectal cancer.

Genetic Diseases, Inborn↗
PubMedDate not supplied

Allele loss on chromosome 11p is associated with poor survival in ovarian cancer.

RFLP (restriction fragment length polymorphism) analysis in 46 ovarian tumour and paired blood samples shows that 33 per cent (5/15) of informative carcinomas had loss of heterozygosity (LOH) at 11p15.4 (Calcitonin locus) and 18% (4/22) had LOH at 11p15.5 (Ha-ras). No LOH was detected in five borderline and four benign ovarian tumours. Analysis of survival in the carcinoma group (37 patients) showed a significantly poorer survival in patients whose tumours showed LOH at either or both of these 11p loci (chi 2 = 7.771, p = 0.005). This suggests the presence of a tumour suppressor gene (tsg) on the short arm of chromosome 11 whose loss is associated with particularly aggressive disease.

Alleles↗