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  • 2005-2009
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  • 1995-1999  (126)
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  • 1999  (126)
  • breast cancer  (126)
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  • 2000-2004
  • 1995-1999  (126)
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  • 101
    Electronic Resource
    Electronic Resource
    Differentially expressed genes associated with the metastatic phenotype in breast cancer (1999)
    Springer
    Breast cancer research and treatment 55 (1999), S. 125-134 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; differential display ; gene expression ; invasion ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that human breast carcinoma cells demonstrating an interconverted phenotype, where keratin (epithelial marker) and vimentin (mesenchymal marker) intermediate filaments are both expressed, have an increased ability to invade a basement membrane matrix in vitro. This increase in invasive potential has been demonstrated in MDA‐MB‐231 cells, which constitutively express keratins and vimentin, and in MCF‐7 cells transfected with the mouse vimentin gene (MoVi). However, vimentin expression alone is not sufficient to confer the complete metastatic phenotype in MoVi cells, as determined by orthotopic administration. Thus, in the present study, differential display analysis was utilized to identify genes that are associated with the invasive and/or metastatic phenotype of several human breast cancer cell lines. Forty‐four of 84 PCR fragments were differentially expressed as assessed by Northern hybridization analysis of RNA isolated from MCF‐7, MoVi, and MB‐231 cell lines. Polyadenylated RNA from a panel of poorly invasive, invasive/non‐metastatic, and invasive/metastatic breast carcinoma cell lines was used to differentiate between cell‐specific gene expression and genes associated with the invasive and/or metastatic phenotype(s). We observed that lysyl oxidase and a zinc finger transcription factor were expressed only in the invasive and/or metastatic cell line; whereas, a thiol‐specific antioxidant and a heterochromatin protein were down‐regulated in these cells. In contrast, tissue factor was expressed only in breast carcinoma cell lines having the highest invasive potential. These results suggest that specific genes involved in breast cancer invasion and metastasis can be separated by differential display methodology to elucidate the molecular basis of tumor cell progression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006188129423
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  • 102
    Electronic Resource
    Electronic Resource
    Reduced expression of p27Kip1 protein is associated with poor clinical outcome of breast cancer patients treated with systemic chemotherapy and is linked to cell proliferation and differentiation (1999)
    Springer
    Breast cancer research and treatment 55 (1999), S. 159-165 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; cell cycle ; cyclin‐dependent kinase inhibitor ; differentiation ; p27Kip1 ; prognosis ; proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cyclin‐dependent kinase inhibitor p27Kip1 is a negative regulator of cell proliferation. Its expression is known to be altered in a proteasome‐dependent manner without changes in DNA level. Reduced expression of p27Kip1 is associated with aggressive behavior in a variety of human cancers. We investigated expression of p27Kip1 protein in human breast cancer using immunohistochemistry to assess its biologic implication along with cell‐cycle analysis by flow cytometry. A total of 68 patients with invasive ductal cancer received adjuvant chemotherapy with cyclophosphamide, methotrexate, and 5‐FU every 3 weeks for six cycles. In epithelial cells of normal and benign breast disease, expression of p27Kip1 was well preserved while its expression markedly decreased in breast cancer (45 of 68). Expression of p27Kip1 is significantly reduced in poorly differentiated cancers and in the advanced stage of the disease. Levels of p27Kip1 expression correlated with cell populations in G0/G1 phase of the cell cycle. In survival analysis, p27Kip1 was useful to predict disease free survival but not overall survival of the patients after adjuvant chemotherapy. In summary, p27Kip1 seems to have a role in the cell proliferation and differentiation process during carcinogenesis of breast cancer. The results of the present study suggest that p27Kip1 can be used in predicting response to systemic chemotherapy in a subset of patients with breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006258222233
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  • 103
    Electronic Resource
    Electronic Resource
    G1‐S transition defects occur in most breast cancers and predict outcome (1999)
    Springer
    Breast cancer research and treatment 56 (1999), S. 103-110 
    Details
    ISSN: 1573-7217
    Keywords: cell cycle ; cyclins ; p16 ; p27 ; retinoblastoma protein ; breast cancer ; survival
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cell cycle deregulation is frequently observed in tumors and has moreover been proposed to be a requirement for tumor development. By analyzing the expression of p27 by immunohistochemistry in 100 primary breast tumors and combining the analyses with our earlier characterization of cyclin E, D1, p16, and the retinoblastoma protein (pRB), we have been able to cover the majority of potential G1–S transition defects and observed that 90% of the tumors had alterations in one or several cell cycle regulatory proteins. Considerable variations in protein levels were found among tumors, with low p16 expression as the most common alteration followed by cyclin E or cyclin D1 overexpression, low p27 expression or pRB inactivation in decreasing prevalence. Tumors were grouped according to observed combinations of defects and the proliferative capacity was determined for each group by analyzing Ki–67 labeling index. Low proliferation was observed in tumors with: low p16; high cyclin Dl with normal or high p16 expression; and in tumors without cell cycle defects. Tumors with high cyclin E/low p27 or pRB defects showed higher proliferation. The survival differed noticeably for patients with various combinations of cell cycle defects, and four distinctive clusters were identified showing significantly different breast cancer specific survival (p 〈 0.0001) for both node-positive (p=0.0006) and node-negative patients (p 〈 0.0001). In summary, we have shown that G1-S transition defects are nearly obligatory in breast tumors and that the specific type of cell cycle defect influences the clinical behavior of the tumor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006208419350
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  • 104
    Electronic Resource
    Electronic Resource
    Overexpression of basic fibroblast growth factor (FGF–2) downregulates Bcl–2 and promotes apoptosis in MCF–7 human breast cancer cells (1999)
    Springer
    Breast cancer research and treatment 56 (1999), S. 151-165 
    Details
    ISSN: 1573-7217
    Keywords: apoptosis ; basic FGF ; Bax ; Bcl–2 ; breast cancer ; MCF–7 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Basic fibroblast growth factor (bFGF, FGF–2), a classical transforming factor, mitogen, and survival factor in multiple cell types, and has a paradoxic role in mammary epithelial cell transformation and proliferation. We have also demonstrated that recombinant FGF–2 uncharacteristically promotes cell death in MCF–7 human breast cancer cells. In this study, we investigated the effects of FGF–2 overexpression on survival in the same MCF–7 cells. In eight breast cancer cell lines and two nontransformed mammary epithelial cell lines, we demonstrated that high levels of Bcl–2 are only expressed in cells with undetectable levels of FGF–2 on western blot. In retrovirally transduced MCF–7 cells expressing both cytoplasm– and nucleus–localizing FGF–2 species and ones expressing only cytoplasm–localizing FGF–2 species, Bcl–2 levels were strongly decreased at both the mRNA and protein levels. Immunoprecipitation of Bax demonstrated a decreased association of Bax with Bcl–2 in these cells. Levels of Bax did not correlate with expression of FGF–2 in the 10 cell lines or in MCF–7 cells. The clonogenic potential of MCF–7 cells in tissue culture was decreased by the expression of FGF–2 and was additively suppressed by the chemotherapeutic agents etoposide and 5–fluorouracil in a dose and time dependent manner. MCF–7 cells overexpressing FGF–2 had a greater rate of programmed cell death at baseline and in response to etoposide and 5–fluorouracil in a TUNEL assay by immunofluorescent microphotography and by flow cytometric quantitation. The pro–apoptotic effect of FGF–2 overexpression on the chemosensitivity of these cells was confirmed by quantitative morphologic determination. These data demonstrate that the expression of FGF–2 downregulates Bcl–2 and promotes programmed cell death in MCF–7 human breast cancer cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006258510381
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  • 105
    Electronic Resource
    Electronic Resource
    Cisplatin–epirubicin–paclitaxel weekly administration in advanced breast cancer: A phase I study of the Southern Italy Cooperative Oncology Group (1999)
    Springer
    Breast cancer research and treatment 56 (1999), S. 237-250 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; cisplatin ; epirubicin ; paclitaxel ; weekly administration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: Both cisplatin and epirubicin have been shown to enhance the antitumor activity of paclitaxel in vitro. Weekly administration could result in a substantial improvement in the therapeutic index of cisplatin and paclitaxel. This study was aimed at determining the MTDs of epirubicin and paclitaxel given weekly with a fixed dose of cisplatin. Patientsandmethods: Sixty–three breast cancer patients with advanced disease (24 locally advanced and 39 metastatic), who had not received prior chemotherapy (except adjuvant), received weekly cisplatin (CDDP) doses of 30 mg/m2 together with escalating doses of paclitaxel (PTX) and epirubicin (EPI) for a minimum of six cycles. The dose escalation was stopped if DLT occurred during the first six treatment cycles in 〉33% of patients of a given cohort. Results: Nine different dose levels were tested, for a total of 506 weekly cycles delivered. G–CSF support on days 3–5 of each week was also given in the last four cohorts (24 patients). An overall 11 patients showed DLT in the first six cycles. EPI and PTX doses up to 40 and 85 mg/m2/week, respectively, were safely delivered without G–CSF support. However, the actually delivered mean dose intensity was only 64 in this cohort. Therefore, the dose escalation continued with the addition of filgrastim from day 3 to day 5 each week. Doses of EPI and PTX up to 50 and 120 mg/m2/week were administered without observing DLT in the first six cycles in more than one third of the patients enrolled. No toxic deaths were observed. Only two patients had to be hospitalized because of sepsis. Grade 3–4 neutropenia, thrombocytopenia, and anemia occurred in 25, 9, and 16 patients, respectively. Alopecia was almost universal. Other nonhematologic toxicities were generally mild, being of grade 3–4 in only eight patients (fatigue and loss of appetite in two cases, diarrhoea in four cases, peripheral neuropathy and mucositis in one case).abstract
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006263226099
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  • 106
    Electronic Resource
    Electronic Resource
    Effective treatment of advanced estrogen–independent MXT mouse mammary cancers with targeted cytotoxic LH–RH analogs (1999)
    Springer
    Breast cancer research and treatment 56 (1999), S. 265-274 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; cell death ; cell proliferation ; doxorubicin ; LH–RH analogs ; targeted chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cytotoxic agents linked to hormonal carriers provide new approaches to tumor therapy, and LH–RH receptors expressed by breast cancers can be used for targeting chemotherapeutic compounds. In the present study, large, advanced estrogen–independent MXT mouse mammary cancers were treated with cytotoxic LH–RH analog AN–152 containing doxorubicin (DOX) or AN–207 incorporating superactive derivative 2–pyrrolino–DOX (AN–201). These cytotoxic hybrid molecules were administered once i.v., close to their maximum tolerated doses, at various time intervals after transplantation of tumors. The cytotoxic LH–RH analogs and the radicals alone, given at earlier stages of tumor development, inhibited growth of MXT cancers. Cytotoxic LH–RH conjugate AN–207 had significantly stronger effect than its respective cytotoxic radical, particularly when larger tumors were treated, causing 95, 89, 100 and 96 tumor growth reduction when administered on days 1, 7, 10 or 14, respectively. AN–152, AN–201, and DOX, given on day 14, were virtually ineffective. Histological characteristics of tumor cell proliferation and cell death were analyzed in large MXT cancers 1–4 days after treatment with AN–207 and AN–201. AgNOR scores were decreased and apoptotic indices increased after treatment of tumors with AN–207 or AN–201, but enhanced apoptosis and decreased AgNOR numbers persisted longer in the case of AN–207. In contrast to AN–201, AN–207 also increased the extent of necrosis in tumors. In conclusion, on the basis of its powerful inhibitory effect on the aggressive MXT mouse mammary tumor, the cytotoxic LH–RH analog AN–207 could be considered for treatment of advanced human mammary carcinomas that express LH–RH receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006267327007
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  • 107
    Electronic Resource
    Electronic Resource
    Biomarkers for local recurrence after breast‐conservation — a nested case‐control study (1999)
    Springer
    Breast cancer research and treatment 57 (1999), S. 245-259 
    Details
    ISSN: 1573-7217
    Keywords: biological markers ; breast cancer ; ipsilateral breast tumor recurrences ; prognosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: A previous cohort study of 759 women with invasive T1‐T2 breast cancer operated on with breast‐conserving surgery in Stockholm between 1976 and 1986 indicated that age 〈50 years, no postoperative irradiation, and nodal involvement were independent risk factors for ipsilateral breast tumor recurrences (IBTR). The aim of the current study was to analyse if selected biological markers assayed in tumor specimens from these patients could add prognostic information, thereby helping to identify groups of patients at high versus low risk of IBTR. Methods: The study was designed as a case‐control study ‘nested’ within the cohort. The cohort was stratified according to nodal status and the use of postoperative irradiation. In these four strata, the cases were those 80 women who developed IBTR between 1977 and 1994. In each stratum, women without IBTR were randomly selected as controls (n=159). Median time at risk was 12 (8–18) years. The following factors were analysed: histopathological tumor grade according to Elston–Ellis, DNA ploidy, immunohistochemical staining for apoptosis, angiogenesis, Ki‐67 (MIB‐1), c‐erbB‐2, p‐53, waf‐1, and bcl‐2. The prognostic role of each factor was assessed using linear logistic regression methods. Results: In univariate analyses only age 〈50 years was identified as a significant risk factor for IBTR, whereas none of the studied biomarkers yielded statistically significant information. However, in a multivariate model, age, MIB-1-index, and tumor grade significantly influenced the risk for IBTR: the odds-ratio (OR) for age ≥50 years was 0.4, 95% confidence interval (CI) = 0.2–0.9; for medium or high grade tumors it was 0.4 (CI = 09–0.9); and for MIB-1-index 〉30%, 2.1 (CI = 1.0–4.4). In women ≥50 years, MIB-1-index 〉30% was associated with an OR of 3.5 (CI = 1.4–8.8) compared to those who were younger. Patients ≥50 years with MIB-1-index ≤30% were thus identified as a low-risk group with an OR of 0.2 (CI = 0.1–0.5). A possible high-risk group was patients 〈50 years with tumors showing a combination of c-erbB-2 and waf-1 immunoreactivity, with an OR of 6.7 (CI = 1.3–34.7). Conclusion: Women ≥50 years with MIB-1-index ≤30% constituted a subgroup with a low risk of IBTR. This observation raises the issue whether this group of patients might be spared postoperative irradiation following breast-conserving surgery. However, due to the methodology of the study, including the large number of comparisions, the presented results warrant cautious interpretation and should be regarded as tentative.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006281718793
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  • 108
    Electronic Resource
    Electronic Resource
    Antimetastatic effect of desmopressin in a mouse mammary tumor model (1999)
    Springer
    Breast cancer research and treatment 57 (1999), S. 271-275 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; desmopressin ; metastasis ; tumor cell aggregation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have investigated the effects of desmopressin (DDAVP), a synthetic analog of the natural hormone vasopressin, on experimental lung colonization of mammary tumor cells using a syngeneic BALB/c mouse model. Coinjection of DDAVP (1–2 μg/kg body weight) at the time of i.v. inoculation of F3II carcinoma cells or LM3 adenocarcinoma cells significantly inhibited the formation of experimental lung metastases. In both cases, the number of pulmonary nodules was reduced about 70%. Inhibition of metastasis was also obtained with i.v. administration of DDAVP 24 h after tumor cell inoculation. Interestingly, the inhibition of lung metastasis was not due to direct cytotoxic effects of DDAVP on mammary tumor cells. The in vitro formation of multicellular aggregates in the presence of citrated plasma from control and DDAVP‐treated mice was also examined. Control plasma rapidly induced a significant tumor cell aggregation. In contrast, in the presence of plasma from DDAVP‐treated mice, tumor cells remained as a single cell suspension. DDAVP may help to dissolve the protective fibrin shield of circulating tumor cells. Our data suggest, for the first time, that adjuvant DDAVP therapy may impair successful implantation of circulating mammary tumor cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006291607871
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  • 109
    Electronic Resource
    Electronic Resource
    Tamoxifen and fenretinide in women with metastatic breast cancer (1999)
    Springer
    Breast cancer research and treatment 57 (1999), S. 277-283 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; dark adaptation ; fenretinide ; lipids ; tamoxifen ; transforming growth factor‐β
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Tamoxifen and fenretinide combination therapy has been shown to be an active treatment regimen in metastatic breast cancer patients. This pilot study sought to determine whether the addition of fenretinide to tamoxifen would be associated with antitumor activity in metastatic breast cancer patients who had been previously treated with tamoxifen or who had hormone receptor negative disease. The effect of this therapy on circulating plasma transforming growth factor‐beta (TGF‐β) levels and serum lipids was also examined. Patientsand Methods: Thirty‐one patients were treated with tamoxifen (20mg po daily), and fenretinide (400mg po daily with a 3‐day drug holiday each month). Plasma TGF‐β testing was performed using isoform specific sandwich ELISA. Results: Twenty four of the 31 patients were evaluable for an antitumor response including 14 estrogen receptor (ER) positive patients who had failed prior tamoxifen therapy, seven ER‐negative patients, and three hormone therapy naive ER‐positive patients. There were no objective antitumor responses; three patients had stable disease for 8, 8, and 24 months. Five patients (16%) discontinued therapy for toxicity (one for grade 3 skin rash and four for abnormal dark adaptation). There was a statistically significant decrease in total cholesterol (median change per patient of −13.5 mg/dl; p=0.049, a 6.5% decrease), and an increase in HDL levels (median change per patient of +18 mg/dl, p=0.0001, a 35% increase) with tamoxifen and fenretinide therapy. TGF-β1 plasma levels were normal in 26 of 28 patients, and no changes in these levels post-treatment were demonstrated. Conclusions: Tamoxifen and fenretinide therapy is not an active combination in ER negative metastatic breast cancer or in patients whose disease has progressed on tamoxifen. This combination had a beneficial effect on total serum cholesterol and HDL levels with no associated rise in serum triglyceride levels. The 400 mg dose of fenretinide was associated with symptomatic nyctalopia in one-third of patients making it an unsuitable dose for use in breast cancer prevention studies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006216409688
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  • 110
    Electronic Resource
    Electronic Resource
    p73 mutations are not detected in sporadic and hereditary breast cancer (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 25-29 
    Details
    ISSN: 1573-7217
    Keywords: p73 ; mutation ; breast cancer ; sporadic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recently, a novel tumor suppressor gene, p73, was isolated and mapped to chromosome 1p36, a region commonly associated with loss of heterozygosity in neuroblastoma and other human malignancies, including breast cancer. The p73 gene shares considerable homology with the common tumor suppressor gene p53, both in composition and function. This study examines the potential participation of p73 in the pathogenesis of sporadic and hereditary breast cancers. Mutation analysis of 29 hereditary breast cancer cases revealed five independent silent mutations in the hereditary cases that are unlikely to play a role in tumor development. Mutation analysis of 48 sporadic breast tumors did not identify any unique variants. Eleven common polymorphisms scattered throughout the gene were also detected. Thus, mutations in the p73 gene appear to play little if any role in hereditary or sporadic breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006237031070
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  • 111
    Electronic Resource
    Electronic Resource
    The pure antiestrogen ICI 182780 is more effective in the induction of apoptosis and down regulation of BCL‐2 than tamoxifen in MCF‐7 cells (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 87-97 
    Details
    ISSN: 1573-7217
    Keywords: antiestrogens ; apoptosis ; BCL‐2 ; breast cancer ; MCF‐7 ; tamoxifen ; ZM 182780
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is increasing evidence that induction of apoptosis by antihormones is an important mechanism in regard to their growth inhibitory action on hormone dependent tumors. In this report we have compared the efficiency of tamoxifen (Tam) and the pure antiestrogen ICI 182780 (ZM) to induce apoptosis in the estrogen dependent breast cancer cell line MCF‐7. Clear evidence for induction of apoptosis could be demonstrated after treatment with both antiestrogens. Application of the pure antiestrogen ZM led to a significantly higher induction of apoptosis compared to the partial agonistic compound Tam. The ability of the two compounds to induce apoptosis correlated with their growth inhibitory action. On the molecular level administration of ZM led to a time dependent steady decrease of BCL‐2 mRNA and protein. Administration of Tam also initially decreased the expression of BCL‐2. In contrast to ZM treatment, BCL‐2 expression increased again after 8 h of incubation with Tam. After 96 h Tam treated cells expressed BCL‐2 levels nearly as high as untreated cells. In general, ZM decreased BCL‐2 levels more effectively than Tam. Our results demonstrate that ZM and Tam possess quantitative and qualitative differences in their ability to down regulate BCL‐2 expression. The higher ability of the pure antiestrogen to down regulate BCL‐2 expression may explain the superiority of the pure antiestrogen to induce apoptosis and to inhibit the growth of MCF‐7 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006338123126
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  • 112
    Electronic Resource
    Electronic Resource
    Bone marrow micrometastases in breast cancer patients (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 123-130 
    Details
    ISSN: 1573-7217
    Keywords: bone marrow ; breast cancer ; micrometastases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The presence of epithelial cells in bone marrow may be a prognostic factor in breast cancer, and so we evaluated their evolution in treated and untreated patients. A first bone marrow aspirate was obtained from 125 stage I/II breast cancer patients at diagnosis and repeated every 6–8 months; the samples were processed for leukocyte separation, used to prepare cytospin slides, stained with a pool of monoclonal antibodies (MoAb) recognising epithelial antigens, and immunocytochemically processed. The median follow-up was 48 months (range 15–82); 23 patients relapsed, and 14 died. MoAb positive cells were observed in 31.2% of first, 24.3% of second, and 27.8% of third aspirates. In 68/100 pairs of successive aspirates, bone marrow status remained unchanged; in 20 it became negative, and in 12 positive (not statistically significant even after adjusting for adjuvant therapy). An analysis based on Mantel and Byar's approach to time-dependent covariates using all 225 aspirates found no statistically significant prognostic difference between the patients with negative and positive bone marrow. Bone marrow status changed over time in about 1/3 of the patients; adjuvant therapy did not affect the probability of its becoming negative or positive. No significant association was found between bone marrow evolution and relapse or death, but the relatively high probability of a change in status over time cannot exclude the possibility that a positive aspirate during the course of breast cancer may be a negative prognostic factor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006336100142
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  • 113
    Electronic Resource
    Electronic Resource
    Static disease on anastrozole provides similar benefit as objective response in patients with advanced breast cancer (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 157-162 
    Details
    ISSN: 1573-7217
    Keywords: anastrozole ; breast cancer ; static disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. This paper reports on the clinical relevance of durable static disease (SD) (≥24 weeks) in breast cancer patients treated with the aromatase inhibitor anastrozole. Patients and methods. All patients were part of two prospective, randomised, multicentre studies in postmenopausal women with advanced disease in which megestrol acetate was compared with anastrozole 1 mg. Survival from initiation of treatment was analysed by the response type, i.e., complete response (CR)/partial response (PR), static disease (SD) (≥24 weeks), or progressive disease (PD), achieved on therapy. Results. Median survival with anastrozole 1 mg was similar between patients who obtained CR/PR and SD (≥24 weeks). Similarly, no difference in survival was observed in patients treated with megestrol acetate who achieved CR/PR and SD. With both treatments patients with CR/PR and SD had improved survival over those patients with PD within 24 weeks. There was no difference between treatment arms for patients showing PD within 24 weeks. Conclusions. These data confirm that durable SD (≥24 weeks) is a clinically useful remission criterion in postmenopausal women with advanced breast cancer with predictive value for overall survival. It also confirms the value of this endpoint with anastrozole, a new generation aromatase inhibitor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006391902868
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  • 114
    Electronic Resource
    Electronic Resource
    Changes associated with delay of mammary cancer by retinoid analogues in transgenic mice bearing c-neu oncogene (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 239-252 
    Details
    ISSN: 1573-7217
    Keywords: N-(4-hydroxyphenyl) retinamide ; arotinoid Ro 40-8757 ; breast cancer ; erbB2 expression ; IGF-1 levels ; toxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Breast cancer is one of the common cancers and is a leading cause of cancer mortality in women. The TG.NK transgenic mouse line on FVB strain background expresses the c-neu oncogene under the control of a MMTV promoter in mammary tissue and appears to be a useful animal model for evaluation of strategies to delay or prevent mammary cancer. Fiber-rich nonpurified diet (NTP-2000) and some retinoid analogues have delayed mammary cancer in the TG.NK model. Four week old hemizygous TG.NK female mice with MMTV/c-neu (erbB2) activated oncogene were fed NTP-2000 diet containing the retinoid analogue 4-hydroxyphenylretinamide (4-HPR) at 7 mmol/kg or the arotinoid Ro 40-8757 at 1.5 and 2.5 mmol/kg for 26 weeks. The 4-HPR at 7 mmol/kg diet delayed the development of palpable tumors up to 24 weeks, but by 26 weeks, the incidence markedly increased and was closer to the NTP-2000 diet control group. However, the 4-HPR diet markedly decreased the average weight of the tumors at 26 weeks with no decrease in multiplicity. The 4-HPR also caused significant increase in liver weights without an effect on body weight. Arotinoid Ro 40-8757 caused marked decrease in the number and branching of mammary ducts, and inhibited mammary tumor development with significant decrease in the incidence, multiplicity, and tumor weights compared to the NTP-2000 diet control. Arotinoid also caused a significant dose-related increase in liver weights without a significant effect on body weights. At the doses tested, the arotinoid but not 4-HPR decreased the circulating levels of IGF-1. However, there was no association between the IGF-1 levels and the size, incidence, or absence of tumors when evaluated for any treatment group or for all mice in the study irrespective of treatment. The oncogene erbB2 (c-neu) and the growth factor EGF expression were more prominent in the small tumors of the mice treated with arotinoid than in the larger tumors of the control group. PCNA staining was observed in areas where there was high erbB2 and EGF staining. The delay in onset of mammary tumors by the above retinoid analogues may be related to the delay in development of mammary glands.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006315716713
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  • 115
    Electronic Resource
    Electronic Resource
    MMP-2 positivity and age less than 40 years increases the risk for recurrence in premenopausal patients with node-positive breast carcinoma (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 285-291 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; gelatinase A ; hematogenous metastasis ; prognostic factors ; 72 kDa type IV collagenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Node-positive breast carcinoma is associated with a poor prognosis. Some patients benefit from adjuvant chemotherapy but new treatment modalities should still be developed in order to further increase the cure rate in this patient group. Prognostic factors are needed to define patients for such studies. Here, the prognostic value of matrix metalloproteinase-2 (MMP-2) and age was evaluated in 108 premenopausal, node-positive breast carcinoma patients treated with an adjuvant chemotherapy. Expression of MMP-2 protein was studied in paraffin-embedded tissue sections from primary tumors by using specific MMP-2 monoclonal antibody in an immunohistochemical staining. Age less than 40 years predicted 5-year recurrence free survival (RFS) as unfavorable, being 74% in patients 41–49 years of age and 54% in those under age 40 (p=0.02). The 5-year RFS rate was 85% in patients with an MMP-2 negative primary tumor while it was 65% in the MMP-2 positive patient group. This difference was not, however, statistically significant (p=0.07). Correlation between hematogenous metastasis and MMP-2 positivity in breast carcinoma was demonstrated for the first time (p=0.03). A risk group for a relapse was identified using MMP-2 immunohistochemistry and age. The RFS rate in patients less than 40 years with an MMP-2 positive primary tumor was only 50% while it was 74% in other premenopausal patients (p=0.007). Young age and MMP-2 positivity may, thus, associate with early relapse in node-positive breast carcinoma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006326513176
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  • 116
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    Electronic Resource
    A novel orthotopic model of breast cancer metastasis to bone (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 163-170 
    Details
    ISSN: 1573-7276
    Keywords: bone metastasis ; breast cancer ; model ; PTHrP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Breast cancer affects approximately one woman in twelve and kills more women than any other cancer. If detected early, patients have a five year survival rate of 66%, but once metastatic disease has developed, there is no effective treatment. About 70% of patients with metastatic disease have bone involvement, while lungs and liver are the other common targets. Bone metastases cause severe pain, pathological fractures and hypercalcaemia and thus are a significant clinical problem. The development of new therapies for metastatic breast carcinoma depends on a better understanding of the mechanism of homing of the tumour cells to bone, liver and lungs and the factors required for their growth in these organs. Research on mechanisms of breast cancer metastasis, particularly to bone, has relied on in vitro studies or on tumour models in which the inoculation route is designed to promote delivery of tumour cells to a specific organ. Metastases in bone are achieved by inoculation into the right ventricle of the heart. To our knowledge there has been no report of a model of metastatic spread from the mammary gland to distant sites which reliably includes bone. In this paper, we describe our recent development of a novel murine model of metastatic breast carcinoma. The new model is unique in that the pattern of metastatic spread closely resembles that observed in human breast cancer. In particular, these murine breast tumours metastasise to bone from the primary breast site and cause hypercalcaemia, characteristics not normally found in murine tumours, but common in human disease. Furthermore, in a preliminary characterisation of this model, we show that secretion of parathyroid hormone-related protein, a role for which has been implicated in breast cancer spread to bone, correlates with metastasis to bone. This model therefore provides an excellent experimental system in which to investigate the factors that control metastatic spread of breast cancer to specific sites, particularly bone. The special advantage of this system is that it involves the whole metastasis process, beginning from the primary site. Existing models consider mechanisms that pertain to growth of tumour once the site has been reached. An understanding of the regulation of these factors by potential therapeutic agents could lead to improvement in therapies designed to combat metastatic disease. For the first time, this development will allow exploration of the molecular basis of site-specific metastasis of breast cancer to bone in a clinically relevant model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006689719505
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  • 117
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    Electronic Resource
    ERK signalling in metastatic human MDA-MB-231 breast carcinoma cells is adapted to obtain high urokinase expression and rapid cell proliferation (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 649-654 
    Details
    ISSN: 1573-7276
    Keywords: u-PA ; cyclin D1 ; breast cancer ; ERK
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Increased urokinase plasminogen activator (u-PA) production is associated with tumor invasion and metastasis in several malignancies, including breast cancer. The mechanisms underlying constitutive u-PA expression are not well understood. We examined the relationship between the signal strength of the ERK pathway and the level of u-PA expression in the metastatic human breast cancer cell line MDA-MB-231. Treatment with the MEK1 inhibitor PD98059 resulted in decreased ERK1/2 phosphorylation and decreased u-PA mRNA and protein expression. Inhibition of ERK1/2 activity also led to decreased cell proliferation and to decreased cyclin D1 expression. Less than 5% of total ERK1/2 was phosphorylated in exponentially growing MDA-MB-231 cells, and ERK1/2 activity could be stimulated by okadaic acid. Okadaic acid did not stimulate u-PA expression, but induced strong expression of the cdk-inhibitor p21Cip1. These findings suggest that ERK1/2 signaling is tuned to a level which results in high u-PA expression and rapid cell proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006741228402
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  • 118
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    Electronic Resource
    Increased levels of α6 integrins are associated with the metastatic phenotype of human breast cancer cells (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 323-330 
    Details
    ISSN: 1573-7276
    Keywords: breast cancer ; integrins ; metastasis ; progression ; xenograft model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Integrins play an important role in interactions between cells and the extracellular matrix, and thus have a potential role in metastasis. Expression levels of α6, β1 and β4 integrin sub-units were measured in a panel of human breast cancer cell lines by RT/PCR, immunoprecipitation and flow cytometry. All the lines expressed α6, with the highest levels in the MDA-MB-231 and MDA-MB-435 cells. These grew the most aggressively and were metastastic in nude mice. Low levels of α6 protein were measured in breast cancer cells that were poorly tumorigenic and non-metastatic in nude mice, and there was an inverse relationship between ER and α6 expression. RT/PCR revealed that all lines expressed the 2 isoforms of α6, with the α6A isoform generally more abundant than α6B isoform. Clones of MDA-MB-435 were isolated by sterile sorting for cells with high or low α6 expression, and two variants established from metastases in nude mice were found to differ in α6 expression. When injected into nude mice, the α6-high variants produced significantly more lung metastases than the α6-low variants. β1 was abundant in all lines, while β4 was not detected in MDA-MB-134 cells, and in the MDA-MB-435 cells an alternately spliced variant of β4 was identified. Sequencing of the alternate variant revealed a novel sequence from a splicing event in the cytoplasmic tail of β4. None of the cells with this variant mRNA expressed detectable levels of β4 protein. Our results suggest that high α6 expression in human breast cancer cells is associated with tumorigenicity and metastatic potential.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006659230585
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  • 119
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    Electronic Resource
    Chemokines induce the cellular migration of MCF-7 human breast carcinoma cells: Subpopulations of tumour cells display positive and negative chemotaxis and differential in vivo growth potentials (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 389-396 
    Details
    ISSN: 1573-7276
    Keywords: breast cancer ; chemokine ; integrin ; metastasis ; migration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We previously reported that chemotactic cytokines (chemokines) induce the directional migration of cells derived from the breast carcinoma cell line MCF-7 in vitro, however it was apparent that only a small percentage of cells displayed the ability to migrate upon stimulation. In the present study three sub-lines derived from the parental MCF-7 cell line were selected for their ability to migrate in response to MIP-1α, MIP-1β or RANTES across Transwell filters of 8 μm pore size. The first round selection of migratory cells resulted in sub-populations which demonstrated an increased chemotactic response compared with parental cells. Cells migrating to MIP-1β were subjected to four further rounds of positive or negative selection, resulting in two sub-lines, MCF-7L4 and MCF-7U4 which displayed an increased and decreased chemotactic response respectively to MIP-1α MIP-1β and RANTES. No difference in chemokine receptor RNA message expression between these sub-lines and the parental MCF-7 line were detected, although increased levels of α3, α6 and αv integrin sub-units were shown for MCF-7L4 (positively selected sub-line) compared with MCF-7U4 cells. Moreover, the in vivo growth of cells derived from the two MCF-7 sub-lines was inversely correlated with their chemotactic response. The results of this study depict further the inherent heterogeneity in cancer, suggesting that the chemotactic response may influence the migratory traits of sub-populations within the tumour and potentially contribute to their in vivo behavior, growth and survival.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006657109866
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  • 120
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    Electronic Resource
    N-linked oligosaccharides and metastatic propensity in in vivo selected mouse mammary adenocarcinoma cells (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 437-444 
    Details
    ISSN: 1573-7276
    Keywords: breast cancer ; carbohydrate ; glycosylation ; invasion ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Studies using metastatic variant selected in vivo from a cloned parental cell line demonstrate that the expression of β1-6 branched, N-linked carbohydrates and sialic acid were positively associated with in vitro invasiveness and inversely associated with metastatic potential, adherence, and in vivo growth rate. These results suggest that at least within one tumor model, a negative association occurs between metastatic potential and β1-6 branched oligosaccharide expression. In these studies two metastatic variants, Cl-66M1 and Cl-66M2, were selected following serial in vivo passage of Cl-66, a clonal cell line obtained from a mouse mammary adenocarcinoma cell line. The parent cell line and the two metastatic variants were approximately equal in their adherence to fibronectin, laminin, and collagen type IV coated plastic. In contrast, both Cl-66M1 and Cl-66M2 had a significantly increased ability to invade through matrigel invasion chambers and expressed significantly increased levels of β1-6 branched, N-linked carbohydrates, and sialic acid compared to the clonal parental cell line, Cl-66. Furthermore, the in vivo tumor growth rates of these selected variants were decreased compared to Cl-66 with the longest tumor volume doubling time observed with Cl-66M2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006629119030
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  • 121
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    Electronic Resource
    Is the Fischer 344/CRJ rat a protein-knock-out model for dipeptidyl peptidase IV-mediated lung metastasis of breast cancer? (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 609-615 
    Details
    ISSN: 1573-7276
    Keywords: breast cancer ; Fischer 344/CRJ rats ; metastasis ; mutant DPP IV (G633R)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fischer 344/CRJ rats harbor a G633R substitution in dipeptidyl peptidase IV (DPP IV) that leads to retention and degradation of the mutant protein in the endoplasmic reticulum (Tsuji E, Misumi Y, Fujiwara T et al. Biochemistry 1992; 31 (47): 11921–7 [1]). However, when these rats were used as a ‘protein knock-out’ model in further evaluating the previously established role of DPP IV in metastasis, lung colonization of the highly metastatic MTF7 rat breast cancer cell line was reduced by only 33% relative to normal Fischer 344 rats. To examine whether lung endothelia leak expression of mutant DPP IV and whether mutant DPP IV exhibits the same adhesion qualities as wild type DPP IV, detailed immunohistochemical, biochemical, transfection, and FACS analyses were performed to assess the surface expression of mutant DPP IV on lung endothelia and transfected HEK293 cells and adhesion assay to compare the adhesion qualities of wild-type and mutant DPP IV. Both endothelial and transfected HEK293 cells expressed mutant, enzymatically inactive DPP IV on their surfaces, albeit at greatly reduced levels when compared to expression of wild type DPP IV. Purified mutant DPP IV had identical adhesion qualities for lung-metastatic MTF7 cells as wild type DPP IV, and competitive inhibition of MTF7 lung colonization by truncated DPP IV confirmed involvement of mutant DPP IV in lung metastasis of Fischer 344/CRJ rats. Although metastasis appears to be mediated by several, often parallel mechanisms involving multiple tumor and host factors, these data indicate that altered expression of a single component can drastically change the outcome of metastatic disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006757525190
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  • 122
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    Electronic Resource
    Mycoplasma-Mediated Uptake of the Exogenous Human BRCA1 Gene by Hatching Blastocysts (1999)
    Springer
    Journal of assisted reproduction and genetics 16 (1999), S. 546-550 
    Details
    ISSN: 1573-7330
    Keywords: breast cancer ; mycoplasma ; Ureaplasma urealyticum ; foreign DNA ; gene transfer ; transgenic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: Biological vectors for cell transfection are mainly viral in origin, with inherent shortcomings. Mycoplasmas are ubiquitous organisms that traverse cells easily. The objective was to determine if Ureaplasma urealyticum (T-mycoplasma) would vector exogenous BRCA1 DNA into blastocysts. Methods: Hatching mouse blastocysts (N = 70) were incubated in the presence of either viable or dead Ureaplasma urealyticum at 37°C for 1 hr. The blastocysts were exposed to human BRCA1 DNA lacking homology in the mouse genome for 2 hr, followed by DNase-I treatment and wash. Polymerase chain reaction and agarose gel electrophoresis analysis of amplified products were performed. Results: The BRCA1 gene was detected in the blastocysts only when viable Ureaplasma was present. PCR analyses of control Ureaplasma and untreated blastocysts were negative. Conclusion: Viable Ureaplasma organisms were shown to mediate the uptake of DNA fragments into blastocysts, resulting in transgenic mouse blastocysts with a normal human BRCA1 exon 11 gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020553322073
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  • 123
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    Electronic Resource
    Clinical Relevance of Minimal Residual Cancer in Patients with Solid Malignancies (1999)
    Springer
    Cancer and metastasis reviews 18 (1999), S. 91-100 
    Details
    ISSN: 1573-7233
    Keywords: micrometastases ; immunohistochemistry ; minimal residual cancer ; marrow disease ; lymph node metastases ; breast cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract With the advent of new therapeutic modalities, the treatment options for oncologists can vary greatly depending upon the aggressiveness of the patient's cancer. Patients may receive no therapy, adjuvant therapy, aggressive adjuvant therapy (taxane based), monoclonal antibody therapy (e.g. Herceptin) or bone marrow transplantation. It is now mandatory to determine accurate prognostic patient profiles at diagnosis and during therapy to determine who would benefit most from a particular therapeutic regimen or to determine who should be shifted into more aggressive therapy. We now have ultra-sensitive methods of tumor cell detection that can determine the presence of minimal residual cancer (MRC) in marrow, stem cell product (SCP) and lymph node to help create these prognostic profiles. The author has conducted a critical review of the literature regarding the type of testing used to detect MRC, the incidence of MRC in marrow, SCP, and lymph node, and the clinical significance of MRC at diagnosis and during therapy. To date it is now clear that immunohistochemistry is a very useful diagnostic tool with adequate sensitivity to detect MRC. The presence of MRC at diagnosis in marrow and/or lymph node is associated with a poor prognosis for a number of disorders including breast cancer, neuroblastoma, gastrointestinal tumors, and lung cancer. In addition, the presence of MRC during therapy in marrow and/or SCP is associated with a very poor prognosis for patients with breast cancer. The use of testing for MRC in the patient provides prognostic information that may be of use to the oncologist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006264420822
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  • 124
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    Electronic Resource
    Infusion Reactions Associated with the Therapeutic Use of Monoclonal Antibodies in the Treatment of Malignancy (1999)
    Springer
    Cancer and metastasis reviews 18 (1999), S. 465-471 
    Details
    ISSN: 1573-7233
    Keywords: monoclonal antibodies ; side effects ; toxicity ; lymphoma ; breast cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract With the FDA approval of Rituximab in 1998 for the treatment of lymphoma, and Trastuzumab in 1999 for the treatment of breast cancer, monoclonal antibodies were officially added to the therapeutic armamentarium against malignancy. Most of the side effects associated with these agents are due to antigen-antibody interactions on specific cells and tissues. One of the most predictable side effects of these products is a constellation of various systemic effects including flu-like syumptoms such as headache, fever, sweats, skin rash, shortness of breath, hypotension, nausea, and asthenia that occurs with the first infusion of such products. Rarely severe hypotension, bronchospasm, and hypoxia and even death have occurred. The pathophysiology of these reactions appears to be secondary to the release of cytokines as the antibodies bind do circulating antigen-expressing cells that are then removed in the reticuloendothelial system of the lungs, spleen and liver. In patients with large numbers of antigen-dense cells that have a high mitotic index, such as prolymphocytic leukemia, mantle cell lymphoma, or lymphosarcoma cell leukemia, there is a risk of true tumor lysis syndrome. One should be particularly cautious when treating patients with high numbers of circulating antigen-expressing cells in the setting of underlying cardiovascular or respiratory disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006341717398
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  • 125
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    Electronic Resource
    Antiestrogens – Tamoxifen, SERMs and Beyond (1999)
    Springer
    Investigational new drugs 17 (1999), S. 285-311 
    Details
    ISSN: 1573-0646
    Keywords: breast cancer ; estrogen-related diseases ; estrogen receptor ; ERβ ; chemoprevention
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Estrogens play a central role in reproductive physiology. The cellular effects of estrogens are mediated by binding to nuclear receptors (ER) which activate transcription of genes involved in cellular growth control. At least two such receptors, designated ERα and ERβ, mediate these effects in conjunction with a number of coactivators. These receptors can directly interact with other members of the steroid receptor superfamily. A complex cross-talk exists between the estrogen-signaling pathways and the downstream signaling events initiated by growth factors, such as epidermal growth factor and insulin-like growth factors. Estrogens are also a causative factor in the pathogenesis of a variety of neoplastic and non-neoplastic diseases, including breast cancer, endometrial cancer, endometriosis, and uterine fibroids, among others. Antiestrogens, such as tamoxifen, are widely used for the treatment of breast cancer. Tamoxifen produces objective tumor shrinkage in advanced breast cancer, reduces the risk of relapse in women treated for invasive breast cancer, and prevents breast cancer in high-risk women. Although, initially developed as an antiestrogen, tamoxifen can also prevent postmenopausal osteoporosis as well as reduce cholesterol, due to its estrogen-agonist effects. Its estrogen-agonist activity, however, can lead to significant side-effects such as endometrial cancer and thromboembolic phenomena. This has led to the concept of “ideal” selective estrogen receptor modulators (SERMs), drugs that would have the desired, tissue selective, estrogen-agonist or -antagonist effects. Raloxifene is a SERM which has the desirable mixed agonist/antagonist effects of tamoxifen but does not cause uterine stimulation. “Pure” antiestrogens may provide very potent estrogen-antagonist drugs, but are likely to be devoid of beneficial effects on bone and lipids. Future drug development efforts should focus on developing superior SERMs that have a greater efficacy against ER-positive tumors and do not cause hot flashes or thromboembolism, and explore combination strategies to simultaneously target hormone-dependent as well as hormone-independent breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006348907994
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  • 126
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    Electronic Resource
    The Prophylactic Mastectomy Dilemma: A Support Group for Women at High Genetic Risk for Breast Cancer (1999)
    Springer
    Journal of genetic counseling 8 (1999), S. 163-173 
    Details
    ISSN: 1573-3599
    Keywords: prophylactic mastectomy ; breast cancer ; women at high genetic risk for breast cancer ; psychiatric evaluation ; psychosocial support ; support group ; genetic counseling ; education and health promotion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Psychology
    Notes: Abstract The goal of this pilot study was to test the usefulness of a six session psychoeducational support group for women at high genetic risk for breast cancer who were considering prophylactic mastectomy. The themes of the group sessions included overestimation of and anxiety about risk; desire for “hard data”; the emotional impact of watching a mother die of breast cancer; concerns about spouse reactions; self- and body image; the decision-making process; and confusion over whom to trust in decision making. Both the participants and the multidisciplinary leaders concluded that as a supplement to individual counseling, a support group is a beneficial and cost-effective treatment modality. Recommendations for the optimal format for such a group are described.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1022834706495
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