Zilkah, S., Section of Medical Oncology, the Evans Memorial Department of Clinical Research, the Department of Medicine, Boston, MA, United States, Division of Pediatric Hematology-Oncology, the Department of Pediatrics, Boston City Hospital, Boston, MA, United States
Osband, M., Section of Medical Oncology, the Evans Memorial Department of Clinical Research, the Department of Medicine, Boston, MA, United States, Division of Pediatric Hematology-Oncology, the Department of Pediatrics, Boston City Hospital, Boston, MA, United States, Departments of Medicine and Pediatrics, Boston University School of Medicine, Boston, MA, United States
McCaffrey, R., Section of Medical Oncology, the Evans Memorial Department of Clinical Research, the Department of Medicine, Boston, MA, United States, Division of Pediatric Hematology-Oncology, the Department of Pediatrics, Boston City Hospital, Boston, MA, United States
Shapiro, H., Laboratory of Cytokinetics, Sidney Farber Cancer Institute, Department of Pathology, Boston, MA, United States

Previously it was reported that the herbicide propachlor (α-chloro-N-isopropyl-acetanilide) has a strong inhibitory effect on the proliferation of L1210 mouse leukemia cells. It is now demonstrated that propachlor treatment causes L1210 cells to accumulate in the G1 phase as determined by flow cytometric analysis. This effect of propachlor is dose-dependent with more than 90% of G1 cells accumulating at 10μM. Kinetic experiments demonstrated that the accumulation of cells in G1 starts in about 10 hours, and increased for up to about 44 hours of incubation with 10μM propachlor. Treated cells can be revised to a normal DNA distribution by removing propachlor. © 1985.