Purpose: Before October 2000, physicians in our institution handwrote chemotherapy orders on blank order sheets. There was no standard to which the physician could include variables that were crucial to the completeness of a chemotherapy order. For this reason, chemotherapy orders were frequently incomplete and had to be adjusted by the pharmacist after discussing the missing variables with the ordering physician. As a part of our goal to minimize errors, standard chemotherapy forms were initiated at our institution in October 2000. Methods:The first standard form implemented was a written order form that constituted a standard of the ideal variables necessary to accurately complete chemotherapy orders. These variables were the diagnosis, regimen, height, weight, body surface area (BSA), route, frequency, duration and chemotherapy dose and calculation based upon BSA. The next updated form was an electronic version similar to the original, and was implemented in April 2002.
592 Background: Statin drugs, which enzymatically inhibit HMG CoA reductase, are used in the treatment of hypercholesterolemia. In vitro, statins have been shown to induce apoptosis and inhibit growth in breast cancer cell lines. Although controversial, recent clinical data has indicated that statins may have a chemopreventive effect against breast cancer. Our objective was to determine whether the long-term intake of statins (at least four years) demonstrates a protective effect against breast cancer as a primary endpoint. Methods: We conducted a retrospective, case-control study of female patients from a community-based hospital and medical center located in southeastern Michigan. Cases included patients diagnosed with invasive breast carcinoma between 1995–2005, as identified through the tumor registry. Controls were family practice patients (age > 35 years) randomly selected from a database generated for this same time-period. Patients completed a mailed questionnaire with information pertaining to their use of statins and other medications, as well as other breast cancer risk factors. Subjects (N = 521) and controls (N = 521) were case matched by age, race, and body mass index (BMI). Results: The mean age of patients was 62.9 (range 35–101 yrs.) with an average BMI of 27.5. Reported usage of statins for four or more years prior to diagnosis was 5.5% in breast cancer subjects and 6.9% in case-matched controls. Compared to nonusers, women who had been on statin therapy for four or more years prior to diagnosis were not found to have a decreased risk of breast cancer (odds ratio 0.78: 95% CI 0.47 - 1.31). Similarly, there was no difference in risk for nonusers versus those taking statins for <1 yr., 1–4 yrs., or ≥ 4 yrs. However, nulliparity, positive family history, report of any benign breast biopsy, and ≥ 5-year use of oral contraceptives (before age 30) were significantly associated with the occurrence of breast cancer (p < 0.002, Chi-square test). Conclusion: Although statins have been shown to inhibit growth in breast cancer cell lines in vitro, its effect in vivo has remained inconclusive. Our study did not demonstrate a significant protective effect against breast carcinoma in women who had ever taken statins, or those who had taken the drug for a minimum of four years. No significant financial relationships to disclose.
2546 Background: Trastuzumab, a recombinant humanized anti-HER2 monoclonal antibody, has been found to have potent antiproliferative effects in HER2 overexpressing human breast tumors. Lovastatin, an HMG-CoA reductase inhibitor suppresses growth, and induces apoptosis in breast cancer cells. Both agents induce a G0/G1 arrest of cell cycle progression. The purpose of this study was to evaluate the antiproliferative effect of the novel combination of lovastatin and trastuzumab in human breast cancer cell lines. Methods: Increasing doses of lovastatin (0.16-40 μM) and trastuzumab (0.039-1 μg/ml) were tested alone and in combination. Three breast carcinoma cell lines were studied: two HER2 overexpressing lines (BT474 and SKBR3) and one cell line that expresses low levels of the receptor (MCF7). Inhibition of growth was assessed after 7 days of treatment by the MTT colorimetric assay, while apoptosis was detected using an in situ DNA Fragmentation Detection kit. Results: A dose-dependent growth inhibition was demonstrated in all three cell lines tested with lovastatin, while trastuzumab was only effective in the HER2 overexpressing cells. Trastuzumab (0.06 μg/ml) inhibited cell growth by 29.3% and 40.1%, while lovastatin (2.5 μM) caused an inhibition of 19.1% and 43% in the BT474 and SKBR3 cell lines, respectively. The combination of trastuzumab and lovastatin, at these doses, significantly inhibited growth in BT474 and SKBR3 cells by 45.4% and 68.9% (P < 0.001, oneway ANOVA) compared to either agent alone. Conclusions: Lovastatin plus trastuzumab treatment led to increased growth inhibition in HER2 positive breast cancer cell lines. Further studies in an animal model are warranted. This combination may also have important clinical therapeutic implications. No significant financial relationships to disclose.
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