Current treatment regimes for many cancers are so successful that patients are surviving for much longer than initially envisaged. This presents a unique set of problems as the mutagenic effects of their chemotherapy can lead to the long-term development of a second malignancy, but the molecular interactions underlying these observations remain unclear. In February Cancer Cell, Asaf Hellman and colleagues from The Hebrew University, Jerusalem, Israel identify a mechanism by which some chemotherapy drugs create the conditions that can generate new cancerous growths.

Amplification of drug-selected genes in rodent cells is driven by recurrent breaks within chromosomal common fragile sites (CFSs), via the breakage-fusion-bridge (BFB) mechanism. Hellman et al. observed that the same mechanism is involved in the intrachromosomal amplification of the MET oncogene in a human gastric carcinoma. This suggested that in vivo induction of CFSs by chemotherapeutic drugs might play an important role in human...

Interested in reading more?

Become a Member of

Receive full access to more than 35 years of archives, as well as TS Digest, digital editions of The Scientist, feature stories, and much more!
Already a member?