Latest issue of Genome Biology

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Following on from Naomi’s blog on the highlights of 2012 in Genome Biology, I’m going to expand on her mention of our cancer articles. We published four cancer-related articles in December: two Research, and two Methods.

Jinghui Zhang and colleagues from the St Jude Hospital in Memphis, together with collaborators from Washington University, St Louis and the Memorial Sloan-Kettering Cancer Center in New York, have assessed the telomere content of a large panel of pediatric cancers. Telomeres are the specialized structures at the ends of chromosomes that, in normal cells, shorten with every cell division. Once they have shortened to reach a critical length threshold, the cells are unable to divide further. Since cancer is a disease of unrestricted cell division, tumors somehow need to overcome this telomere shortening in order to proliferate. In the study published in Genome Biology, the researchers sequenced 235 childhood cancer samples from a variety of cancer types in order to assess the telomere content. They found telomere gain was very rare in brain or blood cancers, but occurred in about a third of solid tumors. There were associations between the extent of telomere gain with the frequency of other mutations in the tumors, leading to the possibility that malignant progression could be monitored by assessing telomere content.

Gastric cancer is the fourth most common cancer globally, but its high mortality rate means it is the second most common cause of cancer death after lung cancer. It is particularly prevalent in East Asia. Yijun Ruan and colleagues in Singapore have sequenced two gastric tumors with contrasting mutational profiles in order to discover mutations that may have contributed to the cancers. This was followed up by further targeted sequencing in 134 other tumors, which confirmed a suite of recurrently mutated genes in this type of cancer.

Identifying recurrently mutated genes in a specific cancer type does not necessarily mean you have identified the mutations that cause that cancer type. Because tumors generally have a high mutation rate, genes can be mutated even if those mutations are not contributing to the tumorigenesis. Differentiating the so-called driver mutations from passenger mutations is not an easy task. Sohrab Shah and colleagues at British Columbia present DriverNet, a method for identifying driver mutations based on the premise that the mutations that contribute to tumorigenesis are likely to have large impacts on transcription within the tumor.

Because cancer-causing mutations will often alter transcription within a tumor, and different mutations will have different effects on transcription, identifying the differences in transcription between different cancers can provide valuable information about the tumors. In particular, transcriptional signatures can give important clues to prognosis. Guanming Wu and Lincoln Stein from Ontario have published a method that can identify gene expression markers associated with patient survival.

It wasn’t all cancer, though. We finished a great year for Genome Biology with another strong month of publications, encompassing Research and Methods, covering microbiology and mRNA, nucleosomes and networks, flies and flowers (well, Arabidopsis anyway). Look out for more exciting publications this year.