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  • 1
    Electronic Resource
    Electronic Resource
    TGFβ Independently Regulates Invasiveness, Chemotaxis, and Proliferation of Human Breast Cancer Cells (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 593 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb16146.x
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  • 2
    Electronic Resource
    Electronic Resource
    Production and characterization of mammary-derived growth factor 1 in mammary epithelial cell lines (1992)
    s.l. : American Chemical Society
    Biochemistry 31 (1992), S. 610-616 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00117a044
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  • 3
    Electronic Resource
    Electronic Resource
    Purification and characterization of a novel growth factor from human breast cancer cells (1992)
    s.l. : American Chemical Society
    Biochemistry 31 (1992), S. 7330-7340 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00147a018
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Molecular biology of breast carcinoma (1994)
    Springer
    World journal of surgery 18 (1994), S. 12-20 
    Details
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Pendant ces dernières années, la recherche fondamentale a permis d'identifier les chemins qu'empruntent les signaux de transduction aidant ainsi à comprendre les mécanismes de contrôle de la croissance des cellules cancéreuses du sein. Beaucoup de ces facteurs sont des produits de proto-oncogènes on des gènes represseurs. Cette revue décrit le rôle de certains de ces facteurs dans le développement du cancer du sein, dans leur évolution et leur diffusion métastatique. Les implications de l'avenir sont discutées.
    Abstract: Resumen En los últimos años la investigación básica ha permitido identificar muchos de los factores involucrados en las vías celulares y moleculares de transducción de señales, lo cual nos da una mejor comprensión de los mecanismos de control del crecimiento de las células del cáncer mamario. Muchos de los factores promotores son los productos de proto-oncogenes y de genes supresores. La presente revisión describe el papel de algunos de estos factores en el desarrollo del cáncer mamario, de su progresión y de la aparición de metástasis, y discute las implicaciones para futuras directrices de manejo.
    Notes: Abstract During the last several years basic research has resulted in the identification of many of the factors involved in signal transduction pathways, leading us to a greater understanding of the mechanisms of growth control in breast cancer cells. Many of these factors are the products of proto-oncogenes or suppressor genes. This review describes the role of some of these factors in breast cancer development, progression, and metastasis and discusses implications for future directions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00348187
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  • 5
    Electronic Resource
    Electronic Resource
    Psychosocial factors in the development and progression of breast cancer (1994)
    Springer
    Breast cancer research and treatment 29 (1994), S. 141-160 
    Details
    ISSN: 1573-7217
    Keywords: psychosocial factors ; dietary fat ; alcohol ; prevention ; survival
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The factors responsible for the genesis of breast cancer remain unclear. Emerging, although controversial, evidence suggests that factors related to life-style, such as dietary fat or alcohol intake, or exposure to various forms of stressors, are associated with mammary tumorigenesis. The possible role of life-style factors in breast cancer is important in light of the fact that mortality to this disease is increasing in most countries and that development of curative therapies for breast cancer has not been forthcoming. Thus, determining the role of life-style factors in the onset and progression of breast cancer, particularly among individuals genetically vulnerable to breast cancer or women with breast cancer in remission, is critical to prevent this disease. We will review the three main hypotheses which have been suggested to link psychosocial factors to the etiology of cancer, emphasizing data obtained through animal models. Interpretation of the existing data suggests that the number of stressful life-events does not predict vulnerability to develop breast cancer or survival from it; a certain level of stress appears to protect from malignancies. The crucial factor affecting tumor growth is the interaction among stress, an individual's personality, and available psychosocial support, and the effect of this interaction on an individual's ability to cope with stress. In addition, other risk factors for breast cancer known to be closely associated with psychosocial factors, namely dietary fat and alcohol consumption, may interact with the effects of psychosocial factors on breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00665676
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  • 6
    Electronic Resource
    Electronic Resource
    Comparison of pain, motion, and edema after modified radical mastectomy vs. local excision with axillary dissection and radiation (1992)
    Springer
    Breast cancer research and treatment 21 (1992), S. 139-145 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; conservation treatment ; local excision ; mastectomy ; radiotherapy ; rehabilitation ; surgery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent data suggest that prognosis is similar for women with primary breast cancer whether they receive modified radical mastectomy (MRM) or local excision and axillary dissection with radiation (XRT). The effects of either of these treatments on arm mobility, pain, or edema have not been compared. To assess the impact of MRM or XRT on mobility, pain, or edema, we evaluated patients treated in a prospective randomized trial designed to assess prognosis following MRM or XRT. All were provided a standardized physical therapy program including arm mobilization, shoulder strengthening, prevention and treatment of upper extremity edema, and education about arm function. Patients were evaluated for chest wall pain, arm motion, muscle strength, and edema as determined by circumferential measurements at the wrist, forearm, and arm. Evaluations were performed preoperatively and at yearly anniversaries of their surgery. Women receiving XRT had more chest wall tenderness at 1 and 2 years after surgery than those receiving MRM (p2〈0.0001 and p2=0.0007 respectively). Those receiving MRM were slower to reach their preoperative range of motion (ROM) (p2=0.043). Incidence of muscle weakness was similar in both groups. The few patients with local recurrence of tumor had more upper extremity edema than those who did not recur (p2=0.085) at 1 year and (p2=0.02) at 2 years. In patients who did not develop local recurrence, those who had received XRT had greater but nonsignificant increases in upper extremity circumferential measures compared with those receiving MRM at any anniversary evaluation. Patients receiving MRM and XRT are likely to have some differences in functional outcome. These differences may be important to individuals and be significant in helping them choose between MRM and XRT based upon individual functional needs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01836960
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  • 7
    Electronic Resource
    Electronic Resource
    Editor-in-chief's page (1992)
    Springer
    Breast cancer research and treatment 23 (1992), S. 3-3 
    Details
    ISSN: 1573-7217
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01831469
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  • 8
    Electronic Resource
    Electronic Resource
    The role of erbB2 signal transduction pathways in human breast cancer (1993)
    Springer
    Breast cancer research and treatment 27 (1993), S. 83-93 
    Details
    ISSN: 1573-7217
    Keywords: erbB2 signal transduction ; erbB2 ligand ; estrogen receptor ; gp30 ; breast cancer progression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The erbB2 receptor is expressed at very high levels in nearly 30% of human breast cancer patients and plays an important role in the transformation and the prognosis of breast cancer. While evidence accumulates to support the relationship between erbB2 overexpression and poor overall survival in human breast cancer, understanding of the biological consequence(s) of erbB2 overexpression remains elusive. Our recent discovery, cloning, sequencing, and expression of the erbB2 ligand (gp30) has allowed us to identify a number of related but distinct biological endpoints which appear responsive to signal transduction through the erbB2 receptor. These endpoints of growth, invasiveness, and differentiation have clear implications for the emergence, maintenance, and/or control of malignancy, and represent established endpoints in the assessment of malignant progression in breast cancer. Studiesin vitro have shown that gp30 induces a biphasic growth effect (induction of growth at low concentrations and inhibition of growth at high concentrations) on cells with erbB2 over-expression. Strikingly, we have recently observed that the erbB2 signalling pathway can be modulated by estrogen acting through the estrogen receptor (ER). Conversely, we observed that down regulation of erbB2 by estrogen can be blocked by gp30 acting through the erbB2 receptor. Clearly, mechanistic aspects of the erbB2/ligand interaction need to be understood from a therapeutic standpoint, and may furthermore provide additional insights into treatment synergy for particular patients. We think that these studies will facilitate the emergence of erbB2-targeted therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00683195
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  • 9
    Electronic Resource
    Electronic Resource
    Perinatal factors increase breast cancer risk (1994)
    Springer
    Breast cancer research and treatment 31 (1994), S. 273-284 
    Details
    ISSN: 1573-7217
    Keywords: estrogen ; perinatal environment ; risk behaviors ; dietary fat ; stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Emerging evidence suggests that breast cancer may originate during early life. In particular, offspring of mothers who during pregnancy exhibited behaviors that are associated with increased incidence of breast cancer, may be at risk. These behaviors include intake of high fat diet or alcohol, or stressful life style. We have found that neonatal exposure to handling that leads to improved ability to cope with stress, reduces 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors in rats. Further, our results indicate that maternal exposure to high fat diet increases the incidence of DMBA-induced mammary tumors in female offspring. High fat diet also increases serum 17β-estradiol (E2) levels in pregnant animals. These results support the hypothesis thatin utero concentrations of estrogens play a critical role in the vulnerability to develop breast cancer. The mechanism of estrogen action might be related to its effect on the induction of epithelial hyperplasia and altered breast differentiation. These events then increase the rate of genetic/epigenetic changes that increase the possibility of neoplastic transformation. Increased pregnancy estrogens may also lead to behavioral alterations in the offspring. This could explain the proposed association between certain behavioral patterns and increased tumorigenity. Our results in transgenic mice overexpressing transforming growth factor α (TGFα) are in accordance with this interpretation. The male TGFα mice exhibit elevated serum E2 levels, impaired ability to cope with stress, increased voluntary alcohol intake and high incidence of spontaneous hepatocellular tumors. These findings indicate that animal models offer a unique opportunity to investigate the role of timing of risk behaviors on breast cancer. They are also useful in the attempts to understand the mechanism of early estrogen action on mammary tumorigenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00666160
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  • 10
    Electronic Resource
    Electronic Resource
    Antiestrogen resistance in ER positive breast cancer cells (1994)
    Springer
    Breast cancer research and treatment 31 (1994), S. 301-307 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; tamoxifen ; estrogen receptor ; antiestrogen resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acquisition of the antiestrogen resistance by breast cancer cellsin vivo may result from a variety of mechanisms. The main pathway appears to involve loss of estrogen receptor (ER) expression or selection for ER negative cells among heterogenous population of tumor cells. However, clinical data suggest that, in about 30% of the cases, antiestrogen resistance arises even in the presence of estrogen receptors. Postulated mechanisms leading to the latter phenotype include selection for variant receptor forms during treatment, development of novel metabolic pathways for the drug, loss of nuclear co-factors, or activation of signal transduction pathway that cross activate ER signals. We have used anin vitro experimental system utilizing LY-2 cell line, an ER positive and antiestrogen resistant MCF-7 cell variant, to study the mechanism of antiestrogen resistance in the presence of functional ER. Result from a complementation experiment suggests that LY-2 phenotype is a recessive trait. Cloning of the genetic defect in the LY-2 cells would provide further insight for the mechanism of antiestrogen resistance in ER positive breast cancer cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00666162
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