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Biomedical subjects

T E Davis

Publications and source records attributed to T E Davis.

At least 91 records · Page 5Linked to original sources
PubMed1979

Plasma triiodothyronine concentrations in breast cancer.

Plasma triiodothyronine (T3), thyroxine (T4) and thyroid-stimulating hormone (TSH) were measured in 44 early breast cancer patients, 48 with advanced breast cancer, 20 with cancer of the colon, and 56 healthy women of similar age. The plasma T3 concentrations were reduced significantly in both early and advanced breast cancer, but only in those colonic cancer patients with metastatic disease. The mean plasma TSH levels were higher in the breast cancer patients than in the other groups, but the increase was significant statistically only in the advanced disease. There was a negative correlation between plasma TSH and T3 in early breast cancer, but not in advanced breast cancer. All cancer groups had normal plasma T4 levels. It is concluded that a proportion of breast cancer patients are mildly hypothyroid, as judged by elevated plasma TSH and reduced T3 levels. In advanced cancer, other "nonspecific" factors also act to reduce the plasma T3.

Adult↗
PubMed1978

Plasma thyroid-stimulating hormone and thyroxine concentrations in breast cancer.

Plasma TSH and thyroxine levels were measured in 74 early breast cancer patients and 53 with advanced disease, 77 patients with cancer arising in other organs and 67 healthy women of similar age. The mean plasma TSH levels were higher in the breast cancer cases than the other two groups; the difference was statistically significant only in those with advanced disease. Twelve percent of the early breast cancer and 15% of the advanced breast cancer patients had elevated plasma TSH concentrations, compared with only 1% of the other cancer patients and 3% of the controls. Four breast cancer patients with plasma TSH levels above 85 microIU/ml had subnormal plasma thyroxine levels. Five of 29 (17%) early breast cancer patients had excessive plasma TSH responses to TRH.

Aged↗
PubMed1978

o,p'-DDD (mitotane) therapy of adrenal cortical carcinoma: observations on drug dosage, toxicity, and steroid replacement.

Four patients with adrenal cortical carcinoma were treated with standard doses of o,p'-DDD. Plasma levels of o,p'-DDD and its metabolites o,p'-DDA and o,p'-DDE were measured. o,p'-DDD was measurable for up to 8 months after stopping therapy, and trace levels of metabolites were detectable at 18 months. Although 2 of 3 patients with measurable disease had objective tumor response and one patient achieved a complete response, severe drug toxicity occurred in all patients and signs of adrenal insufficiency occurred in three. Low dose therapy with o,p'-DDD is suggested, together with full gluco and mineralocorticoid replacement. Measurement of o,p'-DDD and its metabolites in plasma may prove clinically useful in developing effective but less toxic dosage schedules.

Adrenal Cortex Neoplasms↗
PubMed1978

Drug treatment of breast cancer.

Breast cancer is the most common malignancy of women in the United States, affecting one out of every 13 women at some time in their lives. Although only 10% of patients have demonstrable distant metastases at the time of diagnosis, a majority will eventually die of disseminated disease. Chemotherapy was formerly considered to be the treatment of last resort in patients with breast cancer, reserved for those who had failed surgery, radiotherapy and hormonal manipulation. However, combination chemotherapy has now been shown to be highly effective. The most active drug combinations produce objective tumour regression in about 60% of patients with advanced disease. Parallel to the development of effective chemotherapy, there has been a renewal of interest in hormonal therapy. The ability to predict whether or not a patient will respond to hormonal therapy has been improved significantly by the clinical application of the oestrogen receptor assay. The selection of a specific treatment for the patients with advanced breast cancer must be individualised. It should take into account a number of prognostic variables, including: sites of metastatic involvement; total extent of disease; disease free interval; menopausal status; and the presence or absence of oestrogen receptor in tumour tissue. The final decision regarding treatment should then be based not only on the probability of response, but also on the anticipated degree of toxicity. Current efforts to improve the management of advanced breast cancer include the development of more effective drug regimens and the combination of chemotherapy with hormonal manipulation. For instance, it would appear that in premenopausal patients, the combination of chemotherapy with oophorectomy may yield results that are superior to those achieved with either treatment alone. The most promising development in the management of early breast cancer has been the use of chemotherapy as an adjuvant treatment in patients with operable disease.

Antineoplastic Agents↗
PubMed1977

Ovarian function in patients receiving adjuvant chemotherapy for breast cancer.

Plasma oestradiol-plus-oestron (E2 + E1), follicle-stimulating hormone (F.S.H.), luteinising hormone (L.H.), androstenedione (A2), and dehydroepiandrosterone sulphate (D.S.) were measured in 33 breast-cancer patients before and after adjuvant chemotherapy. Before treatment the plasma E2 + E1, A2, and D.S. levels were significantly higher and the L.H. and F.S.H. lower in the 16 premenopausal patients than in the 17 postmenopausal patients. After 6 mo of adjuvant chemotherapy the premenopausal patients, 11 of whom had become amenorrhoeic, showed striking reductions in plasma E2 + E1 and A2 and elevations in plasma L.H. and F.S.H. Further changes were evident after 12 mo of treatment. Plasma-A2 fell after chemotherapy in the postmenopausal group; the other hormones were unchanged. The beneficial effects of adjuvant chemotherapy for breast cancer may result, in part, from suppression of ovarian function.

Adult↗
PubMed1977

Cell wall studies of Histoplasma capsulatum and Blastomyces dermatitidis using autologous and heterologous enzymes.

Enzymes capable of hydrolyzing cell walls of Blastomyces dermatitidis and chemotypes I and II of Histoplasma capsulatum were prepared in the laboratory or obtained from commercial sources. They included chitinases, beta-1,3-glucanases, beta-1,6-glucanase, and Pronase. Monosaccharides and disaccharides of glucose released from the cell walls by the enzymes were determined qualitatively by paper and gas-liquid chromatography, and monosaccharides were quantitated by the latter technique as well. An enzyme system isolated from Streptomyces sp. containing both chitinase and glucanase released maximum amounts of glucose and N-acetylglucosamine from the cell walls of H. capsulatum chemotype I. A chitinase preparation, free of glucanase, from Serratia marcescens released only chitobiose and N-acetylglucosamine from chemotype I cell walls, but the total quantity of N-acetylglucosamine released was about 60% less than that released by the Streptomyces system. A beta-1,3-glucanase from Bacillus circulans hydrolyzed the cell walls of H. capsulatum chemotype I, but a beta-1,6-glucanase failed to release glucose from the same walls. Autolytic enzymes, viz., beta-1,3-glucanases and several glycosidases were detected as constitutive enzymes in both yeast and mycelial phases of B. dermatitidis and H. capsulatum chemotypes I and II. No difference in the amount of activity was found between cell sap and culture filtrate preparations. The beta-glucanases prepared from the Histoplasma and Blastomyces strains were active on the cell walls of the yeast phases of H. capsulatum chemotypes I and II, releasing laminaribiose and glucose, but were essentially inactive on the cell walls of B. dermatitidis. Chitinase, beta-1,6-glucanase, alpha-glucanase, and alpha-glucosidase activities were absent from these fungal enzyme preparations.

Acetylglucosamine↗
PubMed1976

Further clinical studies with megestrol acetate in advanced breast cancer.

A previous study showed activity of megestrol acetate in advanced breast cancer; as a result the study was expanded. Of 101 patients treated with this compound, 26 (26%) met our criteria of improvement. The drug was well tolerated and produced no toxicity and, as opposed to androgens and estrogens, no endocrine effects were observed. Prior hormonal or cytotoxic compounds, including alkylating agents, did not appear to reduce the subsequent responsiveness to this potent progestational compound. We now include it, often as the initial hormonal trial in postmenopausal patients, in our sequential treatment of disseminated breast cancer because of its favorable therapeutic ratio.

Breast Neoplasms↗
PubMed1975

Further clinical studies with intrahepatic arterial infusion with 5-fluorouracil.

A total of 419 patients with progressive liver disease, in nearly all cases metastatic from gastrointestinal primaries, were treated by intrahepatic arterial infusion with 5-FU. Three-fourths of these patients had had prior trials with intravenous 5-FU for 1 or 2 months to several years and had been switched to the infusion upon the development of progression. Catheters were placed percutaneously and the patients infused with 5-FU at a dose of 20 to 30 mg/kg/day X 4, then 15 mg/kg/day X 17, at which point the catheter was removed and the patient sent home on weekly i.v. doses at 15 mg/kg. Toxicity, morbidity, and mortality were minimal with the intrahepatic arterial infusion treatment and the rigid criteria of improvement were met by 55% of the study cases. The survival rate of those patients who responded to the treatment was greater than the survival rate of those who failed to respond.

Fluorouracil↗