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  • 1
    ISSN: 1573-7217
    Keywords: antiestrogens ; cytotoxic estrogens ; DNA-target for cytotoxicity ; estrogen receptor ; MCF-7 cells ; MDA-MB-231 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The estrogen receptor that is present in many breast tumors provides a mechanism for the concentration of estrogens. Hence, it should be possible to effect a selective, receptor-mediated killing of estrogen receptor-rich tumor cells with a suitable cytotoxic estrogen derivative. Because the dose per cell that can be delivered by a receptor-mediated process is limited by the capacity of the estrogen receptor system (ca. 1,000–10,000 molecules per cell), the cytotoxic moiety of these derivatives needs to be directed at a target where an effective cell kill can be achieved with this limited dose; DNA appears to be the most suitable target. The estrogen derivatives that contain DNA-alkylating and cross-linking groups and retain high affinity for the estrogen receptor should be carried selectively to the nucleus. There, it is hoped that they would react with DNA with reasonable efficiency. Definitive tests of receptor-mediated cytotoxicity in vitro could be performed in cultures of human breast tumor cells that are receptor positive (e.g., MCF-7) or receptor negative (e.g., MDA-MB-231). These tests would involve comparison of the potency of the cytotoxic estrogens with that of cytotoxic control compounds, both in the presence and absence of estradiol, in order to correct for possible differences in the sensitivity of the different cell lines to cytotoxic agents and to metabolic effects of estradiol. These agents would then be tested in experimental mammary tumor systems in the rat. Our current understanding of the characteristics of estrogen receptor binding, and the availability of suitable systems for studying these agents in vitro and in vivo, make a definitive test of selective cytotoxicity, mediated by the estrogen receptor, a timely and sensible endeavor.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7217
    Keywords: breast cancer ; clinical correlates ; prostaglandins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Determination of the levels of prostaglandin E2 (PGE2) and PGF2α were carried out using homogenized primary human breast tumors. Measurable levels of both prostaglandins were found in all but one tumor examined. In most samples, the absolute PGF2α level was higher than that of PGE2. Higher PGE2 levels are more often seen in postmenopausal women than in pre- or perimenopausal patients, though among postmenopausal women, PGE2 levels do not correlate with age. Thus, the ratio of PGF:PGE is higher in pre/perimenopausal women than in postmenopausal women. Differences in PGF2α do not appear to be associated with age or menopausal status. Tumors that are estrogen receptor positive (ER +) tend to have higher PGE2 levels than ER negative tumors. PGF2α is not associated with the presence of ER and neither prostaglandin is associated with the presence of progesterone receptor. Higher levels of both PGE2 and PGF2α are associated with less differentiated tumors, while tumor maximum diameter is negatively associated with PGE2 levels.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Breast cancer research and treatment 10 (1987), S. 131-131 
    ISSN: 1573-7217
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-7217
    Keywords: breast cancer ; chemotherapy ; drug accumulation ; endocrine therapy resistance ; glutathione ; multidrug resistance ; P-glycoprotein ; radiation therapy resistance ; resistance mechanisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Considerable insight into the problem of drug resistance has emerged in the past few years. An understanding of why tumors develop drug resistance is now at hand both from theoretical points of view and from experimental and clinical data. Experimental models of drug resistance, particularly related to the surface P-glycoprotein, have been remarkably successful in teaching us why tumor cells in culture develop resistance to common therapeutic agents. In this panel discussion, the clinical relevance of these and other proposed mechanisms will be examined, with the hope of providing an up-to-date overview on this exciting field.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-7217
    Keywords: familial breast cancer ; histological type ; tumor associations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A histological analysis was conducted in 138 female breast cancer patients, and the results were classified in accordance with “Histological Typing of Breast Tumours” (WHO, Geneva 1981). Since about half of these tumors showed more than one histological type of carcinoma, a simplified classification system with four groups was adopted. When patients were categorized according to the number and degree of kinship of their relatives with breast cancer, no specific association with the histological types was found. Familial tumors also encompassed a wide spectrum of histopathologic diagnoses. This suggests the absence of a histological marker in familial breast cancer. Pedigrees of all the patients were then analyzed, special emphasis being placed on relatives suffering from the same and other malignancies. It was found that 13.8% of the probands had at least one first-degree relative with breast cancer and that, compared with the tumor spectra in the male and female population, there was a significantly higher number of esophageal carcinomas in the fathers, of stomach cancers in the uncles and grandfathers, of brain tumors in the mothers, and of sarcomas in the brothers. An accumulation of the same tumors, especially stomach cancer and tumors related to the SBLA syndrome, was observed in families of index patients with tubular or medullary breast cancer. The SBLA syndrome is a complex familial cancer syndrome characterized by a proclivity toSarcomas,Breast cancers, brain tumors,Lung and laryngeal cancers, leukemia, andAdrenocortical carcinomas.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-7217
    Keywords: advanced breast cancer ; sequential chemotherapy ; cyclophosphamide plus Adriamycin ; high-dose methotrexate plus cisplatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The results of two empirically designed and potentially non-cross-resistant combinations administered sequentially in advanced breast cancer with the intent of achieving a high rate of durable complete remissions were analyzed. The two drug combinations consisted of cyclophosphamide plus Adriamycin and high-dose methotrexate plus cisplatin given for a total of three cycles; twenty evaluable patients, not previously treated with chemotherapy, were entered into the study. Ten patients were allocated to receive cyclophosphamide and Adriamycin first followed by high-dose methotrexate and cisplatin, while the remaining patients received the opposite sequence. The overall response rate for the entire group was 85% (17 of 20). However, only three of 20 (15%) patients achieved complete remission. One additional complete response was observed when treatment was prolonged for an additional complete cycle. The overall median duration of response was 13 months (range, 5–20+ months). Responses were similarly distributed among different sites of lesions. Myelosuppression and gastrointestinal toxicity were mild and transient. Reversible acute renal failure was observed after methotrexate administration in three cases. Present results indicate that overall this sequential treatment appears effective in patients with advanced breast cancer. However, the lack of an increased complete remission rate over conventional regimens coupled with a potential risk of renal toxicity prevents further studies with this multiple drug combination.
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  • 7
    ISSN: 1573-7217
    Keywords: aminoglutethimide ; apoproteins ; cholesterol ; lipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Plasma lipids, apolipoproteins, and gamma-glutamyl-transpeptidase (GGT) were measured in 28 patients receiving aminoglutethimide (500 mg) and hydrocortisone (30 or 40 mg) for advanced breast cancer. A rise in cholesterol (CHOL), LDL-CHOL, apoprotein B, apoprotein CIII, and GGT was observed after 45 days. When the patients were divided in two groups according to lipid basal plasma levels, those with high CHOL and triglyceride did not experience any modification of lipid parameters (only GGT were elevated). Conversely normolipidaemic patients experienced an increase in CHOL, triglycerides, LDL-CHOL, apoproteins B and CIII, and GGT.
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Breast cancer research and treatment 10 (1987), S. 205-205 
    ISSN: 1573-7217
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Breast cancer research and treatment 10 (1987), S. 215-215 
    ISSN: 1573-7217
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-7217
    Keywords: alpha-fetoprotein ; breast cancer cytosol ; AFP-binding protein ; estrogen receptor ; proliferative capacity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Direct evidence was obtained for the existence of a specific high affinity alpha-fetoprotein (AFP)-binding protein in the cytosol of both MCF-7 human breast cancer cultured cells and primary breast cancer tissue from postmenopausal women using a nitrocellulose blotting assay. Scatchard analysis of the binding data for MCF-7 cells at 37° C revealed the presence of a single class of AFP binding sites with an apparent Kd of 4.5 × 10−8 M, and 75,000 binding sites per cell. All 9 primary breast cancer cytosols obtained from postmenopausal women also contained measureable levels of this specific AFP-binding protein. The number of AFP molecules specifically bound varied considerably between patients and ranged from 29–250 fmol per mg cytosol protein. Levels of AFP-binding protein levels and estrogen receptor measured in these same breast cancer cytosols showed a positive statistical correlation (r = 0.85). Taken together, the present evidence for the existence of a specific cytoplasmic AFP-binding protein in MCF-7 cells and previously reported evidence forde novo synthesis of free immunoreactive and bound nonimmunoreactive forms of cytoplasmic AFP by MCF-7 cells is consistent with the conclusion that most of the endogenous AFP synthesized in breast cancer cells is rapidly bound to specific cytoplasmic AFP-receptors, and that binding of AFP to these receptors masks its immunoreactivity. The association of AFP synthesis with rapidly growing fetal liver and adult regenerating liver, germ-cell tumors, immature uterus, and breast cancer cells suggests that a positive correlation exists between cytoplasmic AFP-receptor levels and the proliferative capacity of malignant breast tumors, and therefore such measurements may provide useful therapeutic and/or prognostic information in individual patients.
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