Selective toxicity of diphtheria toxin for malignant cells

B. H. Iglewski, Marvin Rittenberg

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Purified diphtheria toxin has been shown to inhibit protein synthesis in Ehrlich-Lettre ascites carcinoma cells in vitro. Protein synthesis in Ehrlich-Lettre cells is at least 10,000 times more sensitive to toxin than protein synthesis in normal mouse spleen or thymus cells. This sensitivity correlates with the observation that Ehrlich-Lettre tumors regress in mice injected with (diphtheria toxin but not (diphtheria toxoid. Using the criterion of inhibition of protein synthesis in vitro, it was shown that other mouse malignancies (lymphoma and myeloma) are also more sensitive to diphtheria toxin than normal spleen or thymus. Metastatic human breast carcinoma cells from 2 individuals, cells from 2 melanoma nodules removed at different times from a third patient, and cells from melanoma nodules from 3 additional individuals are shown to be more sensitive to diphtheria toxin than some normal human cells. The toxin sensitivity of protein synthesis in some of the malignant cells tested was so much greater than that of normal cells and it is suggested that diphtheria toxin should be studied further since it might prove a useful anticancer agent in patients whose tumors are first shown to be highly sensitive to the toxin in vitro.

Original languageEnglish (US)
Pages (from-to)2707-2710
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume71
Issue number7
StatePublished - 1974

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Diphtheria Toxin
Proteins
Thymus Gland
Melanoma
Spleen
Diphtheria Toxoid
Neoplasms
Ascites
Antineoplastic Agents
Lymphoma
Breast Neoplasms
Carcinoma

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

Selective toxicity of diphtheria toxin for malignant cells. / Iglewski, B. H.; Rittenberg, Marvin.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 71, No. 7, 1974, p. 2707-2710.

Research output: Contribution to journalArticle

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