Androgen sensitivity of the new human breast cancer cell line MFM-223

The mammary carcinoma cell line MFM-223 is characterized by high androgen and low estrogen and progesterone receptor levels. With the dextran charcoal method, androgen binding was determined at 160 fmol/mg protein corresponding to approximately 100,000 binding sites per cell in whole cell binding assays. The estrogen and progesterone receptor contents were between 8 and 18 fmol/mg protein. The proliferation of MFM-223 cells was significantly inhibited by doses greater than 0.01 nM dihydrotestosterone. The androgenic inhibition of cell proliferation was antagonized by the antiandrogens cyproterone acetate and hydroxyflutamide. In spite of the low estrogen receptor content, MFM-223 cell proliferation was slightly enhanced by 10 nM 17 beta-estradiol. Treatment with 17 beta-estradiol or dihydrotestosterone failed to provoke an increase of the progesterone receptor level. MFM-223 cells have characteristic patterns of isoenzyme polymorphism and of karyotype alterations revealing marker chromosomes and homogeneously staining regions. In the spectrum of human mammary carcinoma cell lines, MFM-223 cells offer a unique model to investigate molecular mechanisms of androgen receptor action.     

1,25-Dihydroxyvitamin D3 receptor measurement in primary renal cell carcinomas and autologous normal kidney tissue

Recently it was reported that 1-alpha,25-dihydroxyvitamin D3 [1,25-(OH)2D3] inhibited cell growth in a cell line derived from a metastasis from renal cell carcinoma. We have examined samples from 23 primary renal cell carcinomas for 1,25-(OH)2D3 receptor content, and compared it with the concentrations in autologous normal kidney tissue. Nineteen of 23 (83%) renal cell carcinomas had detectable (above 1 fmol/mg protein) 1,25-(OH)2D3 receptor levels, and 15 of 23 (65%) had levels above 5 fmol/mg protein. Mean value for the renal cell carcinomas was 8.2 fmol/mg protein (range, 0-28 fmol/mg protein), and the mean value for autologous normal kidney tissue was 23.1 fmol/mg protein (range, 6.6-53.7 fmol/mg protein). The 1,25-(OH)2D3 receptor levels in the renal cell carcinomas were significantly lower than in the autologous normal kidney tissue (P less than 0.001). The 1,25-(OH)2D3 receptor was characterized by sucrose gradient analysis and DNA-cellulose chromatography. The features found for renal cell carcinoma were similar to the 1,25-(OH)2D3 receptor in normal human tissue. No correlation of 1,25-(OH)2D3 receptor levels to clinical parameters was found. This study shows that carcinomas originating from the kidney, the major vitamin D regulating organ, usually contain the 1,25-(OH)2D3 receptor. The receptor may have a cellular function in the transformed cell.     

人胃癌NKM—45细胞株胞浆,胞核性激素受体含量测定及分析

作者采用葡聚糖包被活性炭法测定了人胃低分化腺癌ＮＫＭ－４５培养细胞中分离的胞浆及胞核ＫＣＩ抽提组分中的ＥＲ、ＰＲ和ＡＲ的含量。结果显示胃癌ＮＫＭ－４５细胞的胞浆及胞核抽提液中ＥＲ含量为２４．８ｆｍｏｌ／ｍｇ和２５．１ｆｍｏｌ／ｍｇ蛋白，而ＰＲ含量为１６．４ｆｍｏｌ／ｍｇ和１８．６ｆｍｏｌ／ｍｇ蛋白，ＡＲ均为阴性（＜１０ｆｍｏｌ／ｍｇ蛋白），说明ＮＫＭ－４５细胞为ＥＲ及ＰＲ阳性细胞，且ＥＲ和ＰＲ在该胃癌细胞的胞浆、胞核中均存在。作者认为胃癌可能是性激素依赖性肿瘤，适当的内分泌治疗可能对胃癌有效。     

Estrogen receptor and hormone responsiveness of medullary thyroid carcinoma cells in continuous culture

We have examined the estrogen responsiveness and estrogen receptor in medullary thyroid carcinoma using a model of an established human cell line, TT. TT cells bind [3H]estradiol with high affinity. Scatchard analysis reveals a single class of binding site with a concentration of 173 fmol/10(6) cells and a dissociation constant of 2.1 x 10(-9) M, values which are comparable to those of a well established model cell line for estrogen responsiveness, MCF-7 human breast cancer cell line. Estradiol in physiological concentrations moderately stimulated TT cell proliferation, whereas in pharmacological concentrations it markedly inhibited cell growth. [3H]Thymidine incorporation into acid-insoluble material was also stimulated following a 5-day treatment with 5 x 10(-9) M estradiol. Tamoxifen at a concentration of 1 microM reduced cell proliferation by 43-48% after 5-7 days of treatment. The growth suppression induced by tamoxifen was reversed by addition of 10 nM estradiol. This is the first report of estrogen growth stimulation and tamoxifen growth inhibition of a tumor cell line derived from human medullary thyroid carcinoma.     

Radiosensitivity of human prostate cancer and malignant melanoma cell lines

The relative radioresponsiveness of human prostate cancer compared to malignant melanoma is well known. The effects of beta-estradiol or testosterone on the X-irradiation survival of several human cell lines were studied, including: human prostate carcinoma cell lines PC3 and DU145 and human malignant melanoma cell lines A375 and A875. Lines PC3 and DU145 demonstrated 55-61 fmol per 10(6) cells of androgen receptor with no detectable estrogen or progesterone receptor. Cells were irradiated at 120 cGy/min dose rate. There was no detectable toxicity of up to 10(-4) M testosterone or beta-estradiol on PC3 or DU145 cells in the absence of X-irradiation. At plating efficiencies from 11-13%, and plating densities of 1 x 10(4) cells per 60 cm2 flask, cell lines PC3 and DU145 demonstrated a Do of 108.5 +/- 6.5, n 2.1 +/- 0.7 cGy, and Do of 143.5 +/- 1.5 cGy, n 2.4 +/- 0.5, respectively. The addition of testosterone or beta-estradiol at 10(-4) to 10(-10) M prior to or after, X-irradiation did not alter radiosensitivity. At the same dose rate of 120 cGy/min, malignant melanoma cell lines A375 and A875 had a Do of 125 +/- 2.5 cGy, n 1.56 +/- 0.8 SF2 0.65 +/- 0.03 and line A875 demonstrated a Do of 129 +/- 4.5 cGy, n 1.58 +/- 0.4 SF2 0.55 +/- 0.04, respectively. The radiosensitivity of melanoma cell lines did not decrease at low dose rate 5 cGy/min. Thus, the in vitro radiosensitivity of androgen receptor positive prostate cancer cell lines is not necessarily altered by the presence of androgen before or after irradiation. The data support the concept that all malignant melanoma cell lines do not show a broad-shouldered cell survival curve in vitro and intrinsic cellular radioresistance.     

Steroid hormone receptor status of colorectal cancers

Tumor samples of 26 consecutive colorectal carcinomas were studied for the presence of steroid hormone receptors for estrogen and progesterone. In all cases, the estradiol receptor binding capacity was below 2 fmol/mg cytosol protein. In 4 of 26 samples, progesterone receptor levels from 13 to 23 fmol/mg cytosol protein were observed. Because of the identification of steroid receptors in some cases and single reports in literature about tumor regression under hormone therapy of colorectal carcinoma, further investigations seem indicated to study the hormone sensitivity of colorectal carcinoma.     

Adrenocorticotropin production by a mammary carcinoma

A patient with clinical hypercortisolism and an infiltrating ductal carcinoma of the right mammary gland is presented. Provocative testing of adrenal function demonstrated the pattern of ectopic adrenocorticotropic hormone (ACTH) production. Ultrastructural analysis of the tumor revealed 150-200 nm electron-dense granules that when primarily fixed in OsO4 appeared as membrane-bound, centrally dense cored granules. ACTH was extracted from the tumor tissue and immunocytochemically localized in the tumor cell cytoplasm. A clinically significant level of estrogen receptor protein was present in the tumor tissue (120 fmol/mg protein). This case confirms the ability of mammary carcinoma to produce the ectopic ACTH syndrome.     

Estrogen and progesterone receptors in human breast cancer. Correlation with histologic subtype and degree of differentiation

Microscopic review of 490 consecutive human breast biopsy and mastectomy specimens were correlated with estrogen and progesterone receptor content of the tissue, by subtype and degree of differentiation. Of the 4 grades of differentiation, the less differentiated Grade III and IV tumors showed significantly lower levels of estrogen and progesterone receptors in infiltrating ductal and lobular carcinoma (P less than 0.001). In contrast, patients with medullary carcinoma had the lowest tissue levels of estrogen and progesterone receptors with approximately 80% of the cases with less than 10 fmol/mg protein. Patients with mucinous carcinoma had the highest percentages of positive estrogen and progesterone receptor levels (75% and 87%, respectively). Sixty-three percent of the patients with Grade IV infiltrating ductal carcinoma were younger than 53 years of age (P less than 0.001). Patients younger than 53 years of age with Grade II and III infiltrating ductal carcinoma also had significantly lower levels of estrogen receptors, but not of progesterone receptors, than those patients older than 53 years of age (P less than 0.001). Nineteen of 20 "normal" breast tissue specimens were negative (less than 3 fmol/mg protein) for estrogen and progesterone receptors. About 50% of 17 tissue specimens from benign breast lesions (fibroadenoma, fibrocystic disease, sclerosing adenosis) showed positive estrogen (greater than 10 fmol/mg protein) or progesterone receptor values. In two patients with gynecomastia, no estrogen or progesterone receptors were detectable.     

Androgen responsiveness of the new human endometrial cancer cell line MFE-296

MFE-296 endometrial cancer cells express androgen receptors in vitro. These cells, which are tumorigenic in nude mice, arc derived from a moderately differentiated human endometrial adenoeardnoma. They express vimentin and the cytokeratins 7, 8, 18, and 19. Karyotyping revealed near-tetraploidy for most of the cells. No marker chromosomes were observed. DNA analyses confirmed the genetic identity of the cell line and the patient from whom the cell line was derived. Proliferation of MFE-296 cells was inhibited by the progestin RS020 and the androgen dihydrotestosterone (DHT). The inhibition of proliferation by DHT was antagonized by the antiandrogen Casodex, demonstrating the involvement of the androgen receptor. Androgen binding was determined at 22,000 binding sites per cell using a whole-cell assay (K_D = 0.05 nM) and 30 fmol/mg protein with the dextran charcoal method; 7 fmol/mg protein of progesterone receptors were found, whereas estrogen receptors were below S fmol/mg protein. The androgen receptor was functionally intact, as demonstrated by transfection experiments with a reporter-gene construct, containing an androgen-responsive element. In MFE-296 cells the content of the androgen receptor was up-regulated by its own ligand. © Wiley-Liss, Inc.     

1,25-Dihydroxyvitamin D3 receptors in human carcinomas: a pilot study.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] receptor concentration was measured by an accurate immunoradiometric assay in primary tumors from 10 patients with colorectal carcinoma and 11 patients with non-small cell carcinoma of the lung. Measurements were also performed on a noncancerous sample of the same origin as the tumor from each patient. All of the tumors contained receptor with a mean concentration of 123.4 fmol/mg protein for colorectal and 75.1 fmol/mg protein for lung carcinoma. Compared to normal tissue from the same patient, 100% of the lung tumors and 70% of the colorectal tumors had significantly higher levels of the 1,25-dihydroxyvitamin D3 receptor. A correlation was found between well-differentiated colorectal tumors with no or few metastases and high levels of 1,25-dihydroxyvitamin D3 receptor. Receptor concentration was also assayed in metastatic lesions of malignant melanoma from 7 patients. 1,25-Dihydroxyvitamin D3 receptor was present in 85% of the metastases at a mean level of 26 fmol/mg protein. For these patients an inverse correlation was found between receptor level and age. The results obtained in this pilot study suggest that an alteration in 1,25-dihydroxyvitamin D3 receptor regulation may occur in vivo when a cell undergoes malignant transformation.     

Presence of steroid receptors in human soft tissue sarcomas of diverse histological origin

The incidence of cytosol receptors for androgen, estrogen, glucocorticoid, and progesterone was determined in a series of histologically diverse soft tissue sarcomas. Receptor binding was characterized in tumor specimens from 29 adult patients (14 female, 15 male) obtained during surgery. Nineteen (66%) tumor cytosols bound at least one steroid. Seven (24%) had more than one receptor. Ten of 23 (43%) cytosols assayed for androgen binding were positive (Kd 0.97 +/- 0.23 X 10(-9) M; 60.6 +/- 25.9 fmol/mg protein), 7 of 29 (24%) for estrogen (Kd 1.00 +/- 0.19 X 10(-9) M; 33.2 +/- 10.9 fmol/mg protein), 9 of 26 (35%) bound glucocorticoid (Kd 4.22 +/- 1.77 X 10(-9) M; 231.0 +/- 155.0 fmol/mg protein), and 1 of 28 (4%) bound progesterone (Kd 0.41 X 10(-9) M; 18.7 fmol/mg protein). Density gradient analysis suggested that androgen and estrogen binding was located predominantly in the 6S and 7 to 8S regions, respectively, whereas receptor for glucocorticoid sedimented at 8S. Steroid binding was not related to patient age. Estrogen-positive (71%) and glucocorticoid-positive (78%) cytosols appeared predominantly in tumors from female patients. Receptor distribution also appeared to be correlated to tumor histogenetic origin.     

Contrasting actions of tamoxifen on endometrial and breast tumor growth in the athymic mouse

The effects of the antiestrogen tamoxifen (TAM) on the growth of two hormone-sensitive human tumors have been examined in athymic mice. The endometrial tumor, EnCa101, was stimulated to grow by TAM either alone or when combined with estradiol. This contrasted with the nonstimulation of the breast tumor, MCF-7, by TAM alone and the antagonist action of TAM on estradiol-stimulated growth of MCF-7 tumors. The individual tumor responses were observed even when the two tumor types were implanted on opposite sides of the same animal. This suggests that host metabolism of TAM does not dictate tissue response. The conclusion is supported by the finding of very similar patterns of metabolites in the two tumors after administration of [ring-3H]TAM. Tissue metabolism therefore is unlikely to be involved. Progesterone receptor levels were higher in estradiol (376 +/- 35 fmol/mg cytosol protein)- or TAM (317 +/- 37 fmol/mg cytosol protein)-stimulated EnCa101 tumors than control (42 +/- 5 fmol/mg cytosol protein) and increased further with combined treatment (485 +/- 75 fmol/mg cytosol protein). Estrogen receptor levels, however, were lower in estradiol (45 +/- 11 fmol/mg cytosol protein)-treated tumors than control (92 +/- 13 fmol/mg cytosol protein) but higher than control in TAM (200 +/- 15 fmol/mg cytosol protein)-treated tumors. Tumors grown with estradiol and TAM had lower estrogen receptor levels (130 +/- 7 fmol/mg cytosol protein) than tumors grown with TAM alone. Estrogen receptor levels indicate that TAM may not be acting exactly as estradiol in the EnCa101 tumor. Overall, these findings suggest that the disparate pharmacology of TAM is a tissue-specific phenomenon.     

Female sex steroid receptor status in primary and metastatic breast carcinoma and its relationship to serum steroid peptide hormone levels

In order to obtain more information on the interrelationships between cytosol estrogen (ER) and progestin (PR) receptors in breast carcinoma, and their distribution according to age, menopausal status and endocrine parameters of the patients, these receptors were measured in 605 primary and 150 metastatic lesions, and correlated with serum levels of estradiol, progesterone, FSH, LH and prolactin in some of these patients. Measurable estrogen receptor (> 3 fmol/mg cytosol protein) was found in 78.0% and progestin receptor (> 10 fmol/mg cytosol protein) in 60.5% of all the samples studied. The receptors were simultaneously present in 57.2%, estrogen receptor only in 20.8%, progestin receptor only in 3.3%, while both receptors were absent in 18.7% of the whole material. In samples from 253 premenopausal patients, measurable ER was found less frequently (71.1% of cases) and its concentration was lower (39.9 ± 5.1 fmol/mg cytosol protein, mean ± SEM) than in 502 postmenopausal patients (82%; 148.2 ± 11.6 fmol/mg). The frequencies of ER-positive samples and ER concentration were rather similar in primary and metastatic lesions, whereas PR was more often present (64 versus 47%) and its concentrations significantly higher (151.2 ± 12.5 versus 102.6 ± 21.1 fmol/mg) in primary than in metastatic tumors. When present simultaneously, there was a significant correlation between ER and PR concentrations in both primary and metastatic lesions independent of the menopausal status of the patient. ER concentration correlated significantly with age in both pre- and postmenopausal patients, while PR concentration correlated with age only in postmenopausal patients. The group with the highest ER values (above 100 fmol/mg cytosol protein) had a significantly lower serum estradiol concentration that the other patients. Serum estradiol values had a significantly positive correlation with cytosol PR content in the samples with a measurable PR. Serum progesterone, FSH, LH and prolactin did not correlate with tumor ER or PR concentrations. We conclude that concomitant assays of ER and PR from a breast carcinoma specimen provide a correct picture of the endocrine characteristics of the tumor independently of the serum concentrations of estradiol, progesterone, FSH, LH and prolactin.     

DCC法检测食管鳞癌组织中雌,孕激素胞浆,胞核受体

对３０例原发食管鳞癌组织及１６例正常食管组织中雌、孕激素受体在胞浆和胞核（ＥＲｃ、ＥＲｎ、ＰｇＲｃ、ＰｇＲｎ）中分布进行分析，结果显示：正常食管组织中ＥＲｃ、ＥＲｎ、ＰｇＲｃ和ＰｇＲｎ均未检出；癌组织中上述受体含量分别为０～８４．６ｆｍｏｌ／ｍｇ蛋白、０～８７．７ｆｍｏｌ／ｍｇＤＮＡ、０～６８．０ｆｍｏｌ／ｍｇ蛋白和０～６９．４ｆｍｏｌ／ｍｇＤＮＡ，阳性率分别为３６．７％、３３．３％、３０％和３０％，受体含量及阳性率均明显高于正常食管组织（Ｐ＜０．０５）。上述受体阳性率随癌组织学分级增加而明显下降，且女性高于男性（Ｐ＜０．０５）。     

Small cell carcinoma cell lines contain opioid peptides and receptors

Two human small cell carcinoma cell lines were assayed for total opioid and beta-endorphin-like immunoreactivity. Small cell carcinoma cell line NCI-H146 contained approximately 1.1 pmol/mg protein of total opioid immunoreactivity. This material was similar in size and immunoreactive determinants to C-terminally modified beta-endorphin. Small cell carcinoma cell line NCI-H187 contained approximately 0.2 pmol/mg protein total opioid immunoreactivity, which was of low molecular weight. NCI-H187 also contained approximately 1.2 pmol/mg protein of material similar in size and immunoreactive determinants to beta-lipotropin. The two small cell carcinoma cell lines were also examined for opioid receptors with the use of [3H]-etorphine as ligand. Both cell lines contained between 50 and 100 fmol/mg protein of specific, saturable, high-affinity opioid receptor binding sites. Together, these findings suggest a possible autocrine role for opioids in small cell carcinoma of the lung.     

Decrease in estradiol-stimulated progesterone receptor production in MCF-7 cells by epidermal growth factor and possible clinical implication for paracrine-regulated breast cancer growth

These studies have evaluated the modulation by epidermal growth factor (EGF) of estrogen receptor (ER) levels and estradiol-stimulated progesterone receptor (PgR) synthesis. Short-term culture of MCF-7 cells in an "estrogen (phenol red indicator)-free" environment caused a rise in ER concentration that is inhibited by EGF at 10(-8) M and 10(-7) M. Estradiol at 10(-10) M induced a 5-fold increase of PgR over a 5-day assay period. However, the rise in PgR was diminished or prevented by increasing concentrations of EGF (10(-9) M to 10(-7) M). Similarly, the concentration-related rise in PgR caused by estradiol (10(-13) M to 10(-9) M) was abolished after a 7-day pretreatment with EGF (10(-7) M). For both the ER and PgR receptor, EGF treatment caused a decrease in receptor number without an apparent change in receptor affinity. Thus, EGF appears to down regulate the ER by approximately 50% and to diminish the ability of estradiol to induce PgR. In addition, a survey of ER+PgR+ and ER+PgR- values of primary breast tumors from women between the ages of 55 and 70 demonstrated significantly less (50%) (85 to 39 fmol/mg of cytosol protein) ER in ER+PgR- tumors (P = 0.0005). The median PgR values for the PgR-positive tumors were 139 fmol/mg of cytosol protein. We propose that ER+ breast cancer that has changed to a paracrine growth factor-driven system (from stromal cells or ER- breast cancer cells) is less responsive to gonadal steroids. The loss of PgR in these ER+ carcinomas may be an indicator of this type of hormone independence.     

The value of estrogen and progesterone receptor determinations in advanced breast cancer. Estrogen receptor level but not progesterone receptor level correlates with response to tamoxifen.

Four hundred fifteen patients with metastatic breast cancer with known hormone receptor status received primary treatment with tamoxifen. Measured values for the estrogen receptor (ER, i.e., with estrogen binding) followed a continuous distribution (range, 3 to 1000 fmol/mg of protein). These values correlated positively with age. The response to treatment with tamoxifen correlated with the ER level, with response rates of approximately 80% when the ER level was greater than 30.1 fmol/mg of protein. Two hundred eighteen (218 of 415, 52%) patients had progesterone receptor (PR) values greater than 10 fmol/mg. The PR positivity correlated with the ER level. Patients with PR levels greater than 10 fmol/mg of protein (124 of 226, 55%) had a significantly higher response rate than those with values less than 10 fmol/mg of protein (45 of 189, 24%). However, in a multivariate analysis including both receptor levels, age, site, and number of metastases, only the ER level was significant in predicting the response to treatment with tamoxifen. A quantitative estimation of the ER level thus is the best predictor of response to hormonal treatment with tamoxifen for advanced breast cancer.     

Overexpression of cholecystokinin receptors in azaserine-induced neoplasms of the rat pancreas.

Cholecystokinin (CCK) is a growth factor for normal pancreas. Numerous studies also suggest that CCK promotes pancreatic carcinogenesis in the rat. Our previous studies suggested that growth of preneoplastic pancreatic foci was stimulated by CCK more than that of normal pancreas. We hypothesized that such differential growth might be due to increased numbers of CCK receptors in neoplastic tissue. Azaserine-induced pancreatic carcinoma (DSL6) had an increased high-affinity CCK receptor binding capacity of 122 +/- 23 (SD) fmol/mg protein compared to 12 +/- 2 fmol/mg protein in normal pancreas (P less than 0.001). The Kd of the high-affinity site was 0.33 +/- 0.04 nM for carcinoma and 0.46 +/- 0.08 nM for normal pancreas (P less than 0.01). The amount of cholecystokinin octapeptide (CCK-8) bound to high-affinity receptor was 8.6 +/- 1.9 fmol/mg protein for DSL6 compared to 0.6 +/- 0.2 fmol/mg protein in normal pancreas (P less than 0.001). Azaserine-induced premalignant nodules were compared to remaining internodular pancreas. Nodules demonstrated a mean high-affinity CCK receptor binding capacity of 38 +/- 9 fmol/mg protein compared to 6 +/- 3 fmol/mg protein in internodular pancreas (P less than 0.001). The amount of CCK-8 bound to high-affinity receptor was 3.1 +/- 0.8 fmol/mg protein in nodules compared to 0.6 +/- 0.3 fmol/mg protein in internodular pancreas (P less than 0.001). Overexpression of high-affinity CCK-8 receptor in premalignant and malignant azaserine-induced tumors may result in a growth advantage relative to normal pancreas.     

Regulation of growth and epidermal growth factor receptor levels of LNCaP prostate tumor cells by different steroids

The growth of LNCaP cells, derived from a lymph-node carcinoma of the human prostate, was stimulated by different hormones. Optimal growth (3- to 4-fold increase in DNA content per culture versus controls) was observed at 0.1 nM R1881 (a synthetic androgen), 1 nM progesterone or 10 nM estradiol. Triamcinolone acetonide had no effect. Dihydrotestosterone maximally stimulated cell growth at 10 nM. When the culture medium was changed 4 times in 6 days instead of twice, optimal growth was observed at 1 nM dihydrotestosterone. This indicates that a rapid metabolism of dihydrotestosterone influenced growth response. LNCaP cells contained considerable amounts of androgen receptors (920 fmol/mg cytosol protein) while progestagen, estrogen and glucocorticoid receptors were absent. The affinity of steroids for the androgen receptor decreased in the order of: R1881 (relative binding affinity: 100.0) greater than dihydrotestosterone (67.7) greater than progesterone (29.4) greater than testosterone (23.8) greater than estradiol (4.3) greater than triamcinolone acetonide (less than 0.1). Effects on cell growth of these steroids paralleled their affinity for the androgen receptor. The number of EGF receptors per cell increased in a dose-dependent manner upon treatment with various hormones. Again the amount of steroid needed for maximal effects reflected the affinity of the steroid for the androgen receptor. An approximately 2-fold increase in EGF receptor number was observed within 24 hr and before an increase in growth could be detected. Actinomycin-D and cycloheximide inhibited the hormonally induced increase in EGF receptor numbers.     

人胃癌SGC-7901细胞胞浆胞核性激素受体测定

 作者采用葡聚糖包被活性碳饱和分析法(DCC法)分别测定了培养的人胃低分化腺癌SGC-7901细胞的胞浆及胞核KCL抽提液中的雌激素受体(ER)、孕激素受体(PR)和雄激素受体(AR)的含量。 结果证明胃癌SGC-7901细胞的胞浆及胞核抽提液中ER含量为30.2和35.7fmol/mg蛋白，而PR的含量为20.3和22.7fmol/ng蛋白, 但AR均为阴性(<10fmol/mg蛋白), 这说明SGC-7901细胞为ER及PR阳性细胞, 其ER和PR在胞浆、胞核中均有分布。 提示胃癌可能为性激素依赖性肿瘤, 有内分泌治疗的可能。