Clinical Cancer Chemotherapy Aimed at Potential Cell Regulators

Frances E. Knock, PhD, MD; Raymond M. Gait, MD; Oliver V. Renaud, MD; Y. Thomas Oester, MD, PhD
Arch Surg. 1970;100(2):167-172. doi:10.1001/archsurg.1970.01340200055013.
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Marked toxicity to wound healing and bone marrow has plagued clinical cancer chemotherapy, with drugs like mechlorethamine hydrochloride (nitrogen mustard) and fluorouracil (5-fluorouracil) attacking nucleic acids or blocking their synthesis. For adjuvant chemotherapy following cancer surgery, anticancer drugs must attack cancer preferentially, to permit normal wound healing while regressing cancer. The search for cancerocidal drugs that can be used immediately after major cancer surgery has led to clinical use of selected drugs attacking potential cellular regulators.1-3 These drugs have regressed a variety of human cancers without injury to wound healing and with minimal injury to hematologic status, or even improvement in some patients.

Cellular regulators are generally believed to be proteins. For attack at potential regulatory proteins of chromosomes, cytoplasm, cell membranes, and steroid receptors, sulfhydryl (SH) groups on protein appear to be the most reactive and vulnerable, and the most essential for maintaining proper architecture of the proteins


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