In rare cases, cancer treatments can cause serious long-term effects. These include so-called secondary leukemias. This form of blood cancer can develop when chemotherapy or radiotherapy damages the genetic material of healthy cells. A research team led by a scientist from Ulm has now discovered a molecular protective mechanism against such genomic damage: a peptide.

How do antimetabolite cancer drugs damage the genetic material of malignantly transformed cells and thereby destroy them? How might these drugs be used more precisely, particularly in the treatment of pediatric tumors? A new research group led by Dr. Christopher Carnie, a scientist at the Heidelberg Faculty of Medicine at Heidelberg University, will address these questions.

Cancer genomes are the result of diverse mutation processes. Scientists have analyzed the molecular evolution of tumors after exposure to mutagenic chemicals. DNA lesions that persists unrepaired over several cell generations lead to sequence variations at the site of damage. This enabled the researchers to distinguish the contribution of the triggering lesion from that of the subsequent repair in shaping the mutation pattern.

Genetic alterations that promote the development and spread of tumors are difficult to identify. This is especially true for mutations in the non-protein-coding regions of the genome, which include all important regulatory sequences. Scientists at the German Cancer Research Center have now published an algorithm that detects cancer drivers in both the protein-coding and non-coding regions of the genome.

Scientists from the German Cancer Research Center and Heidelberg University Hospital have for the first time been able to delay the development of hereditary colorectal cancer with a protective vaccination. Mice with a hereditary predisposition to colorectal cancer survived significantly longer after vaccination than unvaccinated animals. Combining the vaccination with an anti-inflammatory drug increased the protective effect.