Search PubMed⌕ Search

Biomedical subjects

D M Radford

Publications and source records attributed to D M Radford.

23 records · Page 2Linked to original sources
PubMed1992

Pathology and treatment of impalpable breast lesions.

With the increasing use of mammography, more needle-localized breast biopsies (NLBB) are being done. The purpose of this study was to analyze the pathology of impalpable breast lesions and the impact of NLBB on treatment strategies. From 1985 to 1990, 1,605 NLBB were performed, of which 321 (20%) were malignant. Twenty-five percent of malignant biopsies demonstrated in situ disease only. The average size of all lesions detected was 16 mm, and, for invasive cancer, 12 mm. Eighteen percent of invasive cancers had metastasized to the axillary lymph nodes. Surgical management consisted of mastectomy in 74% of patients and breast conservation treatment (BCT) in 26%. No significant difference in surgical management for women 50 years of age or younger compared with those older than 50 years of age was noted. Although the use of BCT for eligible women is recommended by the National Institutes of Health, it is not widely practiced, possibly reflecting less physician acceptance of BCT. These observations suggest that the detection of smaller, impalpable breast cancers has had no impact on treatment strategies.

Adult↗
PubMed1991

Sarcomatous change in a teratoma after treatment of testicular carcinoma.

Treatment can transform the metastases of nonseminomatous germ cell carcinoma into histologically mature teratoma. These lesions typically have a benign clinical course. The authors present a case of leiomyosarcoma occurring within such a lesion. It arose 18 years after therapy for metastatic embryonal carcinoma of the testis and appears to have been radiation induced.

Adult↗
PubMed1990

Loss of heterozygosity of markers on chromosome 11 in tumors from patients with multiple endocrine neoplasia syndrome type 1.

Multiple endocrine neoplasia type 1 is an autosomal dominant condition characterized by the development of parathyroid hyperplasia, pituitary adenomas, and pancreatic islet cell tumors. Recently the gene for multiple endocrine neoplasia type 1 was mapped to the long arm of chromosome 11 between the loci PGA and INT2. We tested the hypothesis that tumor development is the result of a somatic deletion that unmasks a constitutional mutation. By investigating DNA isolated from tumors and somatic tissues in 12 patients from 4 different families with multiple endocrine neoplasia type 1, we found loss of heterozygous markers mapped to 11q13 in 9 (82%) of 11 informative tumors. In contrast, we were unable to identify allelic loss from other chromosomes using a variety of informative probes. This high incidence of chromosomal deletion of 11q13 suggests that this region is important in the oncogenesis of this disorder.

Chromosome Deletion↗
PubMed1990

Two chromosomal locations for human ornithine decarboxylase gene sequences and elevated expression in colorectal neoplasia.

The polyamines are known to be essential for cellular proliferation. Ornithine decarboxylase (ODC) is a rate-limiting enzyme in the synthesis of these amines, and activity is elevated in colorectal tumors and polyps. Two ODC genes (designated ODC1 and ODC2) were localized by somatic cell hybridization and in situ techniques to 2p25 and 7q31-qter, respectively. Investigation of the expression of ODC in colorectal neoplasia reveals a consistent increase in mRNA expression compared with normal adjacent mucosa and control mucosa, ranging from 1.3- to 12.2-fold. No amplification of the loci was seen. Comparison of ODC mRNA expression with ODC activity from the same samples revealed no direct correlation, suggesting that regulation of ODC in this system occurs at the posttranscriptional level.

Chromosome Mapping↗