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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol and other estrogens are not classified as genotoxic carcinogens, but rather as tumor promoters in the multistage process of carcinogenesis. This study is a reexamination of the carcinogenic status of estradiol and the catecholestradiols (2-OHE2 and 4-OHE2) with the recently developed bacterial assays for genotoxic carcinogens, the Chromotest. The bacterial kits revealed estradiol and catecholestradiols as biphasic and potential genotoxic carcinogens with the following SOS inducing potency values: E2 43,265 (SD 8,300); 2-OHE2 30,153 (SD 2,500), and 4-OHE2 68,939 (SD 4,500). The differences between these values are statistically highly significant (p less than 0.0005). These results were confirmed by studies on Escherichia coli, which showed an increase in cell number and a stimulation of DNA content in the presence of the estrogens. It is therefore concluded that estradiol and the catecholestradiols are possible genotoxic carcinogens which probably act as tumor inducers rather than tumor promoters.
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PMID:Estradiol and catecholestradiols as possible genotoxic carcinogens. 254 8

The possibility to detect the antibody to hepatitis C virus (HCV) has allowed to estimate the prevalence of this virus in patients with hepatic disease, mostly in those with hepatitis considered non-A non-B. Literature shows that HCV causes about 75% of cases of cryptogenic hepatitis and more than the 90% of post-transfusional hepatitis. Circumstantial evidence suggests the existence of a relationship between parenterally-transmitted non-A non-B hepatitis (PTH) and primary liver cancer (PLC). With the advent of anti-HCV, it is now possible to assess directly whether or not there is a relationship between PTH and PLC. So anti-HCV was looked for in the sera of 365 patients with cirrhosis prospectively followed-up for early detection the development of PLC, using an enzymatic immunoassay (ELISA Ortho DS). At baseline anti-HCV was detected in 221 patients (60%). During 5-39 month 53 patients developed PLC and anti-HCV was detected in 68% of them. The univariate analysis demonstrated that alcohol abuse, anti-HBs and anti-HBc were the only covariates that were significantly associated with an increase risk of developing PLC. When these factors were introduced in the step wise regression analysis, age and alcohol were found to be the only independent risk factors. The high prevalence of anti-HCV found in patients with cirrhosis and PLC suggests that HCV might play a role in this tumor; the frequent co-occurrence of HCV and HBV markers suggests that HCV-HBV coinfection might be pathogenically important; alcohol was the most important non-viral risk factor for PLC.
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PMID:[Primary carcinoma of the liver and hepatitis C virus in Italy. A prospective study in patients with cirrhosis]. 256 1

The steroid receptor-positive human ovarian cancer (BG-1) was evaluated to determine its usefulness as a tumor model. This tumor grows in intact male and female nude mice without hormone supplements. Moreover, its growth was significantly accelerated in ovariectomized mice, and the increased growth rate could be reversed by estradiol administration. Evaluation of tumor growth following endocrine therapy revealed that, while antiandrogens did not affect the tumor growth, both an aromatase inhibitor and a luteinizing hormone-releasing hormone agonist significantly impaired growth of this human ovarian tumor. Estradiol was also shown to up-regulate both estrogen and progesterone receptors in tumors grown in ovariectomized mice. Therefore, the BG-1 human ovarian carcinoma grows without hormonal supplements and yet responds to specific forms of endocrine therapy. Moreover, the steroid receptors present in this tumor respond to exogenous steroids. In conclusion, this tumor may serve as an ideal model for the study of hormonal regulation of ovarian tumor growth.
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PMID:Endocrine characterization of a human ovarian carcinoma (BG-1) established in nude mice. 260 60

Mammary carcinomas have been induced by 3.5 Gy whole-body gamma radiation administered at age 40 to 50 days to virgin female Sprague-Dawley rats. In 142 irradiated controls carcinoma incidence averaged 7.8% in survivors observed less than 300 days and 38.3% of those surviving longer (P less than 0.001 by t test). Mammary cancer promotion was inhibited by two methods: estriol (E3) 638 micrograms/month (2.2 microns/mo) subcutaneously for natural life span begun 2 weeks after exposure reduced cancer incidence from 76% in controls to 48% after 331 to 449 mean days observation until neoplasia was palpable (P less than 0.02 by chi-square analysis). Uterine weights were similar in control and treated groups, and were 15% to 18% greater than uteri of nonirradiated controls from other simultaneous experiments. Six monthly 638-micrograms doses of 17 alpha ethinyl estriol (EE3) reduced tumors from 88% in controls to 64% (P less than 0.05 by chi-square analysis) and delayed cancer onset (P less than 0.01-0.04 by life table analysis). Ethinyl estradiol (EE2) after 6 months' treatment similarly delayed mammary tumor development reducing incidence to 75% (NS), with a six-fold increase in nonmammary epithelial malignant tumors. Estriol administration begun between 3 days before to 5 days after radiation did not alter mammary cancer incidence in six experiments. Monthly implantation of 2.5 mg tamoxifen (4.44 microns/mo) started 2 weeks after radiation reduced mammary cancer incidence from 83% to 14% after 307 to 314 days' observation (P less than 0.001 by chi-square analysis). Treated rats had atrophic ovaries and uteri consistent with blockade of endogenous estradiol activity. Short-term parenteral E3 or EE3 therapy using 10 to 30 micrograms/kg/day (35-100 microns/kg/day) rapidly differentiated virgin rat mammary glands without impairment of subsequent estrus cycles and offers an alternative to castration or life-long antiestrogen therapy for reduction of risk of radiogenic mammary carcinoma.
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PMID:Inhibition of radiogenic mammary carcinoma in rats by estriol or tamoxifen. 270 80

A new cell line, designated as HOC-I, was established from a recurrent region of ovarian endometrioid carcinoma. HOC-I was subcultivated more than 55 times. 1) The monolayer culture cells showed a pavement like arrangement with polygonal cells and had a tendency to pile up. PAS positive substance could be seen in the cytoplasm. Desmosomes, microvilli and well developed cell organelles could be found by electron microscopy. 2) The population doubling time was about 75 hours. The chromosomal number showed pseudodiploidy of which the mode was 46. 3) By heterotransplantation to the nude athymic mouse, the tumor easily developed. 4) The effects of estradiol and progesterone on the cellular growth were assessed by the 3H-TdR uptake test. Estradiol increased 3H-TdR uptake of HOC-I but progesterone decreased it. These data suggested that HOC-I had sex-steroid hormone dependency. 5) Estrogen receptor was not detected in HOC-I by the ER-EIA method or the ER-ICA method. 6) The HOC-I cells produced CA125 and TPA in culture media.
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PMID:[Establishment and characterization of human ovarian endometrioid carcinoma cell line]. 272 84

Antineoplastic drugs (methotrexate, 5-fluorouracil, adriamycin) arrest the proliferation of Ehrlich ascites tumor cells in mice but have no influence on L-leucine uptake in vitro. Tamoxifen does not influence either process. Estradiol increases both the cellular proliferation and the amino acid uptake. The absence of estrogen receptors in the cells indicates that the hormone acts on cellular proliferation through mechanisms other than activation of DNA replication, such as stimulation of amino acid transport.
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PMID:Effect of antineoplastic drugs and estradiol on leucine uptake and proliferation of Ehrlich tumor cells. 277 58

The prognostic value of progesterone (P), androstenedione (A), Estradiol, Testosterone, 20 alpha-hydroxy-progesterone, sex hormone binding globulin, and albumin (Alb) was investigated in 51 women with ovarian carcinoma. All patients had observation periods greater than 5 years. The plasma concentrations of P, A, and Alb and the P/Alb and A/Alb ratios showed a significant correlation with the observation time of the patients. P, P/Alb, Alb, and A/Alb separately or in combination showed the highest prognostic specificity and sensitivity. The patients with a plasma concentration above an optimal limit or above mean + 2 SD of a control group of 20 postmenopausal women were grouped together. The groups with P/Alb, A, A/Alb, and Alb above the limit showed an equal survival rate as patients in FIGO stage IV. Patients with a high A/Alb ratio and a high testosterone concentration showed an even poorer prognosis than FIGO stage IV patients. Among the patients in stage IV the A/Alb ratio and sex hormone binding globulin gave additional prognostic information on the stage. The steroid concentration is not only related to tumor volume, as shown earlier, but also reflects the prognosis of the disease.
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PMID:Significance of initial plasma steroid concentrations in the prognosis of 'nonendocrine' malignant ovarian tumors. 277 33

Steroid receptor levels were determined in 196 samples of endometrial adenocarcinoma: cytosol estradiol receptors (ERc) were measured in 171 samples, cytosol progesterone receptors (PRc) in all samples; nuclear estradiol receptors (ERn) and nuclear progesterone receptors (PRn) in 68 samples; total estradiol receptors (ERt = ERc plus ERn) and total progesterone receptors (PRt = PRc plus PRn) were measured in 68 samples. The ERc levels were 88.2 +/- 8.9 (mean +/- SEM) and ERn were 94.4 +/- 15.6 fmol/mg protein; PRc levels were 197.9 +/- 25.9 and PRn 178.3 +/- 55.9 fmol/mg protein. The ERt levels were 162.6 +/- 23.2 and PRt 249.8 +/- 75.7 fmol/mg protein. The presence of PRc was related to the ERc levels according to the cut-off used. Estradiol receptors (ER) and progesterone receptors (PR) were present in the cytoplasmic and nuclear fractions in 60.2% and 36.8% of cases, respectively. The simultaneous presence of both ERt and PRt was observed only in 27.9% of cases. In the normal endometrium ERc and PRc were negatively correlated (r = -0.525, P less than 0.005), whereas in endometrial adenocarcinoma the correlation was positive (r = 0.491, P less than 0.001). In contrast with the normal endometrium the correlation between ERc and ERn was positive (r = 0.582, P less than 0.001) in tumor tissue. In neoplastic tissue Scatchard analysis showed a single class of specific ERc sites with a dissociation constant (Kd) of 1.39 +/- 0.8 X 10(-9) mol/l, one tenth of that found in the normal premenopausal endometrium. Qualitative and quantitative analysis of the receptor status showed that in 30% to 40% of cases studied the behavior of the neoplastic cell was similar to that found in the normal endometrial cell. In a 4-year follow-up of patients affected by endometrial adenocarcinoma there is better survival in the groups of patients with a simultaneous presence of ERt and PRt than in the group with their absence.
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PMID:Hormone receptor status in human endometrial adenocarcinoma. 281 66

The case history of a 26 year old woman describes the occurrence of a primary cholangiocarcinoma in the woman's liver during her 1st pregnancy with no signs of skeletal metastasis. During the previous 8 years, she had taken oral contraceptives (Microgynon 50). The case was successfully treated with chemotherapy (treatment with APD) and surgical removal of the tumor. It was considered highly unusual since malignant tumors of the liver occur seldom in the West, and very seldom among young people. Most patients are over 50; the illness strikes nearly twice as often in men as women. A tumor occurs in a cirrhotic liver in about 75% of cases; and, indications reveal that persistent hepatitis B plays a role in the development of hepatocellular carcinomas. The patient did not fit into any of the those categories. The patient's initial complaints occurred during her pregnancy. Previous medical literature has described patients with a malignant tumor of the liver during pregnany, and since 1970, many articles have shown a relationship between hepatic dysfunctions in women and the use of oral contraceptives. The benign dysfunctions usually involved liver cell edema and focalized nodular hyperplasia. Malignant liver tumors in such patients have been less frequently described in the literature; thus, their relationship with the use of oral contraceptives is less certain. Artlcles have appeared, however, indicating a connection between liver malignancy and the use of sex hormones. There are also indications that humoral hypercalcemia is a frequent finding in primary liver cancer.
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PMID:[A young woman with a liver tumor and hypercalcemia]. 302 Apr 47

Nine granulosa-theca cell tumors (four pure theca cell tumors, one granulosa cell tumors, two granulosa-theca tumors and two juvenile granulosa-theca tumors) were studied endocrinologically and clinico-pathologically. The cases of juvenile granulosa-theca tumors developed precocious pseudopuberty. Three of seven other cases were re-feminized and four cases showed no hormonal manifestation clinically. The peripheral vein serum values of estradiol, progesterone, testosterone and prolactin were elevated in six of eight cases, three of four cases, four of six cases, and two of three cases, respectively. The concentration ratios between tumor harboring ovarian vein samples and peripheral vein (or opposite normal ovarian vein) samples was 2.7 to 16.9 for estrone, 8.8 to 28.6 for estradiol, 3.6 to 4.7 for progesterone, 1.6 to 6.6 for testosterone and 0.6 to 1.0 for prolactin. Estradiol was localized in both granulosa cells and theca cells, and testosterone was localized in granulosa cells in half of the cases and in theca cells in 60% of the cases. Also, testosterone was localized in all three cases in which luteinized theca cells were present. There were no cases with positive prolactin localization. These results are compatible with the concept that in granulosa-theca cell tumor, both granulosa and theca cells can produce a wide range of steroid hormones.
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PMID:[Endocrinological and clinico-pathologic study of granulosa-theca cell tumors of the ovary]. 302 12


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