Biomedical subjects

M T Travers

Publications and source records attributed to M T Travers.

40 records · Page 3Linked to original sources

PubMed1988

Growth factor expression in normal, benign, and malignant breast tissue.

Several oncogenes seem to encode certain growth factors that may play a part in regulating cell growth in tumours. To assess whether such factors are synthesised endogenously by tumour cells the amounts of messenger RNA for several growth factors known to be synthesised by cancer cells of the breast in vitro were examined in biopsy specimens from 52 malignant and 15 non-malignant tumours of the breast and four samples of normal breast. Transforming growth factor beta messenger RNA was significantly more abundant in breast cancers (32 of 42 (76%) having appreciable amounts) than non-malignant breast tissue (five of 13 (38%) having similar amounts). Transcripts for both transforming growth factor alpha and its receptor, epidermal growth factor receptor, were found more commonly in carcinomas that were negative for oestrogen receptor (64% and 87%, respectively) than in those that were positive (27% and 30%, respectively). Insulin-like growth factor II messenger RNA was present in all 15 samples of non-malignant tissue but was found (in considerably lower amounts) in only 11 of 21 (52%) carcinomas. Epidermal growth factor receptor was also found in all non-malignant breast tissues, compared with 19 of 45 (42%) carcinomas. Platelet derived growth factor A and B chain transcripts coexisted in all normal and benign tissue and most carcinomas. This differing pattern of expression growth factors in tissue from malignant tumours compared with benign tumours and normal breast tissue suggests that some growth factors, particularly transforming growth factors alpha and beta, may have an important role in controlling growth of human breast cancers, particularly those that are hormone independent.

Breast↗

PubMed1988

The isolation of recombinant RNA species responsive to oestrogen and tamoxifen in rat uterus and MCF-7 cells.

We have previously shown that oestrogen elicits profound effects on the mRNA population of the immature rat uterus. In order to follow these responses in a more precise manner, we have prepared a cDNA library to uterine mRNA and screened this for sequences most responsive to the hormone. The stimulatory effect of oestrogen and tamoxifen on the levels of selected uterine mRNA species has been compared with the effect of the hormone and its agonist on total uterine poly(A)+ RNA levels. Two of the selected recombinant species were also expressed in the MCF-7 breast carcinoma cell line where their relative levels were again stimulated by oestrogen. Tamoxifen greatly reduced the poly(A)+ RNA levels of MCF-7 cells.

Animals↗

PubMed1987

Characterization of estrogen receptor messenger RNA in human breast cancer.

The importance of estrogen receptor (ER) determination in breast cancer is well established. Approximately 70% of ER-positive tumors are hormone responsive compared to 5-10% of ER-negative tumors. However, one-third of ER-positive tumors fail to respond, and the reasons for this are unclear. To further investigate these relationships we have determined levels of ER protein and mRNA in a number of human breast cancer biopsies. ER protein was estimated by the dextran-coated charcoal steroid binding method and by an ER immunocytochemical assay using a specific monoclonal antibody. A complimentary DNA clone (lambda OR3) encoding part of the human ER was used to determine mRNA levels. Dot blot analysis of twenty-seven tumors revealed a close agreement between ER mRNA and the dextran-coated charcoal assay (rs = 0.9; P less than 0.001). ER immunocytochemical assay staining also correlated with ER mRNA in twenty-five cases (rs = 0.75; P less than 0.001). Tumors from postmenopausal patients contained much higher levels of ER mRNA and ER protein than their premenopausal counterparts. ER-negative tumors produced no measurable ER mRNA. Northern blot analysis revealed a 6.4- and 3.7-kilobase species in ER-positive tumors and also in the human breast cancer cell line MCF-7. No differences in transcript sizes were found in tumors from hormone-responsive patients compared to nonresponding patients. We have also demonstrated, in tissue sections of normal and malignant breast, localization of ER mRNA by in situ hybridization to the same population of cells which exhibit immunoreactive ER.

Breast Neoplasms↗

PubMed1987

Oestrogen-induced expression of oncogenes in the immature rat uterus.

4 h after a single precocious administration of oestrogen there was a considerable but short-lived surge in the uterine levels of myc-encoded polyadenylated mRNA. This was followed by a further peak 28 h after hormone administration. The expression of rasHa showed a totally different time course with a build up of hybridizable message that peaked 8 h after oestrogen administration.

Animals↗