Bloom syndrome B-lymphoblastoid cells are hypersensitive towards carcinogen and tumor promoter-induced chromosomal alterations and growth in agar.

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Abstract
The effects of the carcinogens (4NQO, 4‐nitroquinoline‐N‐oxide; MNNG, N‐methyl‐N'‐nitro‐N‐nitrosoguanidine; AFLG1, aflatoxin G1; AFLB1, aflatoxin B1; BNU, butylnitrosourea; MNU, methylnitrosourea) and the tumor promoter (TPA, 12‐O‐tetradecanoylphorbol‐13‐acetate) on sister chromatid exchanges (SCE), chromosome aberrations and colony formation (CF) were examined in three types of Bloom syndrome (BS) B‐lymphoblastoid cell lines (B‐LCLs); type I with normal SCE and normal karyotype; type II with high SCE and normal karyotypes; type III with high SCE and abnormal karyotypes. BS type I cells had the same SCE and CF response as normal cells to these carcinogens and TPA. In BS type II and III cells treated with carcinogens the SCE frequency increased to 140/cell from a baseline of 70/cell versus an increase of only 10/cell in normal cells. Colony formation occurred at the concentrations that caused the highest SCE. TPA caused a significant SCE increase and highly enhanced CF with dose dependency only in type III cells, suggesting that type III cells may be already in a pre‐malignant state; type II cells appear to be one step behind those of type III in the process of becoming malignant. BS type II and III cells may be usable to establish a sensitive system to detect SCE‐inducing agents.

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