Biomedical subjects
Publications and source records attributed to V V Barinov.
The results of treatment of 443 patients with endometrial carcinoma (surgery--101 (22.8%), combined therapy--183 (41.3%) and complex therapy--159 (35.9%) are presented. The role of clinico-morphological factors, including steroid hormone receptor levels in tumor, is discussed with a view to combat tumor.
To study the early effects of steroid hormones on cells we investigated the influence of the sex steroids and tamoxifen on phospholipid turnover in endometrial carcinoma and breast cancer cells. Studies were performed on 19 human uterine adenocarcinomas and 29 breast cancer tumors. Progesterone in a final concentration of 10(-7) mol/l caused a twofold decrease of 32P incorporation into phospholipids (phosphatidylcholine and phosphoinositides) in 85% of the uterine adenocarcinomas where the progesterone receptor (PR) content was more than 100 nmol/kg and only in 30% of the tumors where the PR content was less than 100 nmol/kg. Treatment of the cells with 10(-8) mol/l 17 beta-estradiol or 10(-8) mol/l epidermal growth factor led to an increase in 32P incorporation into phospholipids. Analysis of the hormonal responsiveness of 29 human breast cancers showed that 17 beta-estradiol increased 32P incorporation into phospholipids in 47% of the tumors where the estradiol receptor (ER) content was more than 10 nmol/kg and in 21% of the receptor-negative tumors (ER < 10 nmol/kg) The results show that phospholipid turnover in uterine and breast cells can be regulated by sex steroids. Treatment of the breast cancer cells with the antiestrogen tamoxifen (10(-6) mol/l) led to an increase of 32P incorporation into phosphoinositides and a decrease of 32P incorporation into phosphatidylcholine. Addition of an activator of protein kinase C, i.e. 2 x 10(-7) mol/l 12-0-tetradecanoylphorbol-13-acetate, weakened the inhibitory effect of tamoxifen on phosphatidylcholine turnover. These findings suggest that tamoxifen action can be mediated via an alteration of the growth signal transducing system.
The cycle of phospholipid turnover has been found to be under the negative control of hormonal cytostatics (progesterone) and under the positive control of proliferation stimulants (17 beta-estradiol, epidermal growth factor). Specific changes in the synthesis of phospholipids are shown when tamoxiphen, an antiestrogen and an inhibitor of protein kinase C, was used. The findings suggest that changes in the turnover rate of phospholipids are one of the key stages of steroid action on target cells and may be regarded as an additional criterion of tumor genetic sensibility.
A rare observation of an unilateral ovarian tumour in a 62-year-old patient is presented. According to the clinical data and the results of the ultrasound examination the tumour was considered as a carcinoma. Hysterectomy with appendages and large omentum resection were performed. A tumour of the right ovary, 13 x 10 x 10 cm was found: cyst with a grey-brown soft node was observed in the cut surface. Histologically, the struma remnants were observed in the cyst wall and structures corresponding to the follicular carcinoma of the thyroid, the central parts of which had a structure of the C-cell thyroid carcinoma. Ultrastructural examination confirmed a light microscopic diagnosis of the malignant monodermal ovarian teratoma developing from the struma with areas of follicular solid C-cell carcinoma.
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