An anticancer agent that acts by induction of DNA strand breaks.
Description :
An anticancer agent that acts by induction of DNA strand breaks; also inhibits incorporation of thymidine into DNA strands; a hybrid peptide-polyketide natural product.
Pancreatic Cancer
Bleomycin (BLM) is chosen as the best-studied micronucleus (MN) inducers in human lymphocytes with different mechanisms of genotoxicity. The most frequent Bleomycin-induced DNA lesions are single and double strand breaks and single apuinic/apyrimidinic sites. At the same time Bleomycin is true radiomimetic compound, resembling almost completely the genetic effect of ionizing radiation[1]. The IC50 value of Bleomycin sulfate for UT-SCC-19A cell line is 4.0±1.3 nM. UT-SCC-12A and UT-SCC-12B are both more resistant to Bleomycin (BLM); IC50 values are 14.2±2.8 nM and 13.0±1.1 nM, respectively[2]. Bleomycin (BLM) induces a significant increase in the percentage of aberrant cells (i.e., cells showing at least one aberration) and in the frequency of chromosomal aberrations per cell compare with control cultures 18 h after treatment (p<0.05)[3].
A short-range beta-emitting radionuclide combined to Bleomycin (In-111-BLMC) is a tumor-targeting agent in SCCs. Within 35 days the weight of nude mice increases 2.8±0.6g. At 25 and 35 days after tumor inoculations the tumor volumes are 111±51 mm3 and 874±577 mm3, respectively. The calculated doubling time is 3.86±0.76 days. SCC cell lines demonstrate different sensitivity to Bleomycin. Our SCC tumor xenograft model shows a rapid growth proper for radiochemotherapeutic studies using In-111-BLMC. The uptake of In-111-BLMC in vivo has been directly proportional to proliferation activity, and the tumors with high binding capacity could be predicted from animal model dose calculations[2].