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This Week in Cell: Oct 10, 2012

The skin cancer melanoma is characterized by a dip in 5-hydroxymethylation at cytosine nucleotides across the genome, according to a study in the September 14th issue of Cell. Researchers from the US, China, and Australia used several approaches to show that primary and metastatic melanoma samples have unusually low levels of 5-hmC methylation compared with normal melanocyte cells or benign skin growths. That drop in 5-hmC seems to stem from lower-than-usual activity by genes that code for related enzymes, the researchers report, particularly IDH2 and TET family genes. On the other hand, their experiments suggest that boosting the levels of such enzymes can staunch melanoma growth and invasion, both in animal models and cell lines.

The same issue of the journal features a pair of papers that use genomics to scrutinize two lung cancer subtypes. The first — from a Broad Institute, Harvard Medical School, and Dana Farber Cancer Institute-led team — focuses on lung adenocarcinoma. That group identified lung adenocarcinoma-related mutations through whole-exome and/or whole-genome sequencing on up to 183 tumor and matched normal samples. Meanwhile, Washington University Genome Institute Director Richard Wilson and colleagues report on mutations found in non-small cell lung cancer. Their analyses relied on whole-genome and transcriptome sequencing of tumors from a dozen smokers and five never-smokers. In addition to unearthing new mutations, both studies include comparisons of tumors from never-smokers and smokers, showing that the lung cancers in the latter group tend to have far more somatic mutations and/or distinct mutational profiles.

In the most recent issue of Cell, two studies explore the transcriptional consequences of having elevated levels of the transcription factor c-Myc — a situation that typifies some aggressive human cancers and which has been linked to poor patient outcomes. A Massachusetts-based team found that tumor cells with ramped up c-Myc levels tend to show amplified expression of genes that are already active in a given cell type. Likewise, based on experiments done in lymphocyte and embryonic stem cells, an independent group from the National Institutes of Health concludes that c-Myc turns up the expression of active genes "except for immediate early genes that are strongly induced before Myc." "This rule of Myc action explains the vast majority of Myc biology observed in the literature," authors of the latter study say.