26 research outputs found

    An Assessment of the Links Between International Diversification, Product Diversification, Performance and Risk Within Service Corporations

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    Services currently account for the dominant share of the workforce in all developed nations and are the fastest growing sector of employment in most developing nations. Services comprise approximately two-thirds of the GDP (gross domestic product) or total domestic output of final goods and services in highly industrialized nations from the OECD (Organization for Cooperation and Development). They make up almost half of the GDP in developing nations. All economic forecasts predict that services will continue to grow and account for the vast majority of future economic expansion throughout the world. Despite these facts, services have been studied infrequently among management scholars. This neglect stems from an historical lack of available data on services. However, recent advances in technology have made their study feasible. The major theories of the firm have been developed using manufacturing enterprises, and so may not be applicable to services. Similarly, most empirical work in the business literature uses manufacturing data. This dissertation attempts to fill this void in the literature. Much of the research in management has focused on finding variables that account for performance (Christensen and Montgomery, 1981; Hambrick and Mason, 1984; Hanson and Wernerfelt, 1989). Performance has been a popular topic because it is necessarily a consequence of strategy, and because performance typically is the key objective or goal that defines strategy. Therefore, academics have looked to strategies to account for performance. Among these are international diversification and product diversification. Many researchers have linked these terms, including Miller and Pras (1980), Grant, Jammine and Thomas (1988), Kim, Hwang and Burgers (1989) and Geringer, Beamish and daCosta (1989). However, no definitive relationships have been discovered. This work continues this stream of research while focusing on services. Specifically the relationships between international diversification, product diversification and performance observed among manufacturing firms by Hitt, Hoskisson and Kim (1997) are tested for U.S. service firms. The results show that the curvilinear line between international diversification and performance which is moderated by product diversification was not observed for services. This may be due to the differences between goods and services, which have been noted by a number of marketing scholars (Zeithaml, Parasuraman and Berry, 1990; Lovelock, 1983; Gronroos, 1990). To extend the analysis, the relationship between international diversification, product diversification and risk was also analyzed. Based on previous work a U-shaped curve was anticipated between international diversification and risk, which was moderated by product diversification. Interestingly, evidence of an inverted U-shaped curved line between international diversification and risk was found. The implications of these findings are given for managers and academics. Suggestions for future research are also provided

    Pilot trial of paclitaxel-trastuzumab adjuvant therapy for early stage breast cancer: a trial of the ECOG-ACRIN cancer research group (E2198)

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    BACKGROUND: Blockade of human epidermal growth factor receptor type 2 (HER2) has dramatically improved outcome for patients with HER2-positive breast cancer. Trastuzumab, an anti-HER2 monoclonal antibody, has previously demonstrated improvement in overall survival (OS) in patients with metastatic and early stage HER2-positive breast cancer. However, trastuzumab can cause congestive heart failure (CHF) with an increased frequency for patients who have also received an anthracycline. The current trial was designed to evaluate the impact of the duration of trastuzumab on CHF. METHODS: E2198 included 227 eligible women with histologically confirmed stage II or IIIA HER2-positive breast cancer. The patients were randomised to receive 12 weeks of paclitaxel and trastuzumab followed by four cycles of doxorubicin and cyclophosphamide (abbreviated Arm) or the aforementioned treatment with additional 1 year of trastuzumab (conventional Arm). The primary end point was to evaluate the safety of this variable duration of trastuzumab therapy, particularly cardiac toxicity defined as CHF or left ventricular ejection fraction decrease >10%. Secondary end points included disease-free survival (DFS) and OS. RESULTS: Compared with 12-week treatment with trastuzumab, 1 year of trastuzumab-based therapy did not increase the frequency or severity of cardiac toxicity: three patients on the abbreviated Arm and four on the conventional Arm experienced CHF. The 5-year DFS was 76% and 73% for the abbreviated and conventional Arms, respectively, with a hazard ratio (HR) of 1.3 (95% CI: 0.8-2.1; P=0.3). There was also no statistically significance difference in OS (HR, 1.4; P=0.3). CONCLUSIONS: Compared with 12 weeks of treatment, 1 year of treatment with trastuzumab did not significantly increase the risk of cardiac toxicity. Although not powered for efficacy comparisons, the longer duration of trastuzumab therapy did not demonstrate a signal for marked superiority

    Thinking About Museum Information

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    Effects of HIV Protease Inhibitor Ritonavir on Akt-Regulated Cell Proliferation in Breast Cancer

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    Purpose These studies were designed to determine whether ritonavir inhibits breast cancer in vitro and in vitro and, if so, how. Experimental Design Ritonavir effects on breast cancer cell growth were studied in the estrogen receptor (ER)-positive lines MCF7 and T47D and in the ER-negative lines MDA-MB-436 and MDA-MB-231. Effects of ritonavir on Rb-regulated and Akt-mediated cell proliferation were studied. Ritonavir was tested for inhibition of a mammary carcinoma xenograft. Results ER-positive estradiol-dependent lines (IC50, 12–24 µmol/L) and ER-negative (IC50, 45 µmol/L) lines exhibit ritonavir sensitivity. Ritonavir depletes ER-α levels notably in ER-positive lines. Ritonavir causes G1 arrest, depletes cyclin-dependent kinases 2, 4, and 6 and cyclin D1 but not cyclin E, and depletes phosphorylated Rb and Ser473 Akt. Ritonavir induces apoptosis independent of G1 arrest, inhibiting growth of cells that have passed the G1 checkpoint. Myristoyl-Akt, but not activated K-Ras, rescues ritonavir inhibition. Ritonavir inhibited a MDA-MB-231 xenograft and intratumoral Akt activity at a clinically attainable serum Cmax of 22 ± 8 µmol/L. Because heat shock protein 90 (Hsp90) substrates are depleted by ritonavir, ritonavir effects on Hsp90 were tested. Ritonavir binds Hsp90 (KD, 7.8 µmol/L) and partially inhibits its chaperone function. Ritonavir blocks association of Hsp90 with Akt and, with sustained exposure, notably depletes Hsp90. Stably expressed Hsp90α short hairpin RNA also depletes Hsp90, inhibiting proliferation and sensitizing breast cancer cells to low ritonavir concentrations. Conclusions Ritonavir inhibits breast cancer growth in part by inhibiting Hsp90 substrates, including Akt. Ritonavir may be of interest for breast cancer therapeutics and its efficacy may be increased by sustained exposure or Hsp90 RNA interference
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