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The promise of chemotherapeutic control in the field of oncology seemed, in the beginning, no less bright than it had proven in the field of bacterial disease, and, therefore, its failures were felt all the more. Despite the serendipitous discoveries and inspired insights which tantalized us with striking remissions, or the rare tumors which proved to be fully susceptible to a given agent, in the main, there has been either total failure or a painfully slow acquisition of an armamentarium against a limited number of malignancies. To expect more, however, was the result of ignorance of the malignant cell, for, as has been described in the previous volumes of this series, the exploitable differences between malignant and normal cells are few or undiscovered. "Differences" is the "numerator" in this formula, but "exploitable" is the operational term, for, although a great number of differences beteen normal and malignant cells have been described, rarely are these differences observed in a vital metabolic pathway or a crucial macromolecu lar structure. Essentially, the basic metabolic pathways and nutritional require ments for :lOrmal and malignant cells are the same, resulting in the fact that no chemotherapeutic agent can successfully inhibit a function in the majority of malignant cells without adversely affecting a similar function in the normal cell. It was, therefore, naive to expect a "magic bullet" which would select the malignant cell and destroy it.
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