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• W2183936028 abstract "addressed the problem of the dose of drugs used in treating patients with operable breast cancer. Before considering those trials in some detail, concepts must be put into perspective for the most appropriate interpretation of the findings. Any form of drug therapy must address the related concepts of how much (dose size), how long (duration of treatment, but also total delivered dose) and how (schedule) the drug(s) is given. This is especially true for drugs such as cytotoxic anticancer agents, for which the ratio between antitumor and toxic effects is narrow, meaning that the drugs are often used near the threshold value for antitumor activity. In the case of cytotoxic drugs, the problem has the additional complication of the interval between individual doses, which is always a compromise dictated by toxicity. The measure of dose per unit time is provided by dose intensity, a concept first proposed by Hryniuk and colleagues [2, 3], who showed in a retrospective analysis that a comparison of different trials according to normalized dose intensities clearly suggested a direct relationship between higher dose intensity and improved DFS and OS for patients undergoing adjuvant chemotherapy for breast cancer [2]. The hypothesis that an increase in dose per unit time would increase DFS and OS was based on experimental data showing a logarithmic increase in cytotoxicity with a linear increase in dose [4]. As later pointed out, this concept somewhat oversimplifies the complex relationship between patterns of tumor growth and cytotoxic effects of chemotherapy, especially in the case of microscopic dissemination as expected in women with operable breast cancer [5]. Based on a Gompertzian rather than logarithmic pattern of tumor growth, Norton predicted that shortening the interval between doses in what he termed a dose-dense approach would yield the best results [6, 7]. The different impact that the different variables associated with dose have on outcome of chemotherapy administration can be outlined looking at the main possible causes of inadequate results. The failure of chemotherapy to eradicate tumors depends on the persistence of sensitive tumor cells, hence insufficient treatment, and the presence or emergence of resistant tumor cells leading to ineffective treatment. As mentioned above, in considering these two patterns of failure, dose size and dose intensity are critical variables affecting treatment outcome. Dose-intensive therapy appears best suited to cause a larger effect on sensitive tumor cells than on preventing the development of resistant cells. In other words, dose-intensive therapy maximizes the chance of response, leading to higher response rates, but is unlikely to achieve an eradication of resistant clones, which will grow and void the likelihood of cure. High dose size is more effective in killing. It should therefore reduce the chance that resistant cell lines develop, and for this reason it should be ideal for maximizing the cure rate. Within this same conceptual frame, dose density, by reducing the interval for recovery of sublethally damaged tumor cells, should afford optimal chances for eradication of sensitive clones, and decrease the probability for acquired resistance." @default.
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• W2183936028 date "2004-10-01" @default.
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• W2183936028 title "Role of dose in the treatment of breast cancer" @default.
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• W2183936028 doi "https://doi.org/10.1093/annonc/mdh902" @default.
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