Open AccessDifferential effects of nitrogen mustard in vivo on the cancer and host cells in MCa‐11 tumours
Author(s) -
Bose K. K.,
Zahurak M. L.,
Allison D. C.
Publication year - 1995
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.1995.tb00081.x
Subject(s) - nitrogen mustard , host (biology) , in vivo , biology , differential effects , differential (mechanical device) , genetics , chemotherapy , endocrinology , cyclophosphamide , engineering , aerospace engineering
We analysed the effects of nitrogen mustard (HN 2 ) on the growth, cell cycle distributions, and ratios of tumour cells to host cells for MCa‐11 tumours grown in vivo. Treatment of tumour‐bearing BALB/c mice with 3 mg/kg of HN 2 produced a significant slowing of MCa‐11 tumour growth. Seventy‐two hours after treatment in vivo with either 3 or 4 mg/kg of HN 2 , the host cells in the treated tumours showed a significantly decreased G 0 /G 1 peak and an increased G 2 /M peak ( P < 0.01), whereas the cancer cells in the treated tumours showed significant increases in the G 0 /G 1 peak coupled with relatively decreased proportions of S and G 2 /M tumour cells ( P < 0.001). The ratio of the total number of cancer cells to the total number of host cells in the tumours was significantly increased 72 h after HN 2 administration ( P <0.01). Thirty‐two days after treatment with HN 2 , the cell cycle distributions of the host and tumour cells in the treatment and control tumours had returned to being identical, but the ratio of the total number of cancer cells to the total number of host cells remained increased in the treated tumours ( P <0.01). These results show that the administration in vivo of HN 2 can lead to entirely different cell cycle effects for the host and cancer cells in the same tumour, and that the partial growth arrest of MCa‐11 tumours from HN 2 treatment may be due in part to the preferential destruction of host cells rather than solely to a direct cytotoxic effect on the cancer cells.