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at all stages of the mitotic cycle, which are realized in a number of cell generations. He
called it “chain processes” in mutagenesis [10-12].
At the same time period staff of the laboratory under the direction of B. N. Sidorov
and N. N. Sokolov (Andreev V. S., Generalova M. V., Grinih L. I., Durymanova S.
E., Kagramanyan R. G., Protopopova E. M., Shevchenko V. V., and others) were con-
ducted extensive work on the induction of chromosomal damage, their localization
in the chromosomes, their association with the phases of the mitotic cycle and DNA
synthesis after treatment of seedlings by ethyleneimine, tio-TEF, radiation, and other
mutagens on the model object Crepis capillaris . They studied chromosome aberra-
tions in metaphase plates, which make it possible to take into account the polyploidy
of metaphases.
In the early 1960s, working at N. P. Dubinin, I investigated the cytogenetic ef-
fect of alkylating agent phosphemidum (lat. synonym phosphemid, phosphasin) di-
(ethyleneimid)-pyrimidyl-2-amido acid (Figure. 1).
FIGURE 1
Phosphemidum (syn. Phosphasin and phosphemid).
This compound is interesting because it consists of pyrimidine base and three
molecules of ethyleneimine. It was assumed that phosphemid will cause a lot of
damages in DNA synthesis and thereby would inhibit tumor growth. The drug was
synthesized in the laboratory of V. A. Chernov et al. [13], the All-Union Scien-
ti¿ c Research Chemical-Pharmaceutical Institute (now the Center for Chemistry of
Drugs), and was referred to N. P. Dubinin for cytogenetic studies. The drug is a
white crystalline powder, dissoluble in water and alcohol. Chernov et al. [13, 14]
have shown that phosphemid (named phosphasin) inhibits the growth of tumors in
rats, mice, rabbits, but at the same time it causes leukopenia, leukocytosis, and sup-
pressed erythropoiesis. But currently the drug used in medicine for the treatment of
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