text: A common myth holds that Goodman and Gilman were prompted to study nitrogen mustards as a potential treatment for cancer following a 1943 incident in Bari, Italy, where survivors exposed to mustard gas became leukopenic. In fact, animal and human trials had begun the previous year, Gilman makes no mention of such an episode in his recounting of the early trials of nitrogen mustards, and the marrow-suppressing effects of mustard gas had been known since the close of World War I.
  Agents acting nonspecifically
  Some alkylating agents are active under conditions present in cells; and the same mechanism that makes them toxic allows them to be used as anti-cancer drugs. They stop tumor growth by crosslinking guanine nucleobases in DNA double-helix strands, directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. These drugs act nonspecifically. Electrophilic alkylating agents such as nitrogen mustards, methanesulfonates, and cisplatins tend to act in this manner to produce a variety of DNA damage products such as mono- and dialkylation, inter- and intrastrand crosslinks, and DNA-protein crosslinks.
  Agents requiring activation
  Some of the substances require conversion into active substances in vivo (e.g., cyclophosphamide).
  Cyclophosphamide is one of the most potent immunosuppressive substances. In small dosages, it is very efficient in the therapy of systemic lupus erythematosus, autoimmune hemolytic anemia, granulomatosis with polyangiitis, and other autoimmune diseases. High dosages cause pancytopenia and hemorrhagic cystitis.
  Dialkylating agents, limpet attachment, and monoalkylating agents