Effect of the Inhibition of Nucleic Acids and Protein Synthesis upon the Development of Melanotic Tumors in <i>Drosophila</i>

Abstract

Ethidium bromide and chloramphenicol which inhibit the synthesis of DNA and of proteins in mitochondria, respectively, are devoid of any important effect on the development of melanotic tumors in Drosophila. Mitomycin C, added to the food of larvae carrying the tu^48amutant gene, increases the number and the size of tumors. It is effective only if the treatment is begun long before the appearance of the tumors and acts probably by weakening the defence reactions of the host. Actinomycin D, an inhibitor of RNA synthesis, increases the number of tumors most effectively if administered at the time of tumor gene activity. Cycloheximide, which is known to inhibit protein synthesis on cytoplasmic ribosomes, is effective during the entire larval life and increases the number of tumors. The results suggest that the melanotic tumor development in Drosophila is linked to the loss of cellular functions rather than to the acquisition of new ones.

The natural history of a family of transplantable melanomas in hamsters

“…Since then, metastases have been found in 48% of Ab-tumor bearing (35--46) 32 (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26) In parentheses: first and last passage in a given year.…”

“…3) Other induced melanotic tumors; a) induced with chemical carcinogens in the skin of hamsters, gerbils, mice, and guinea pigs [16,17]; b) virally induced cutaneous [18] and uveal [19] melanomas in cats. 4) Spontaneous hereditary melanomas occurring with high frequency in graying horses [20], Sinclair miniature swine [21], xiphophorine fish [22], and the fruit fly Drosophila [23].…”