Researchers from Israel and the US explore the potential presence of parainflammation in human cancers. There was evidence that this subtle, low-grade form of inflammation might contribute to tumorigenesis in mice missing the tumor suppressor p53, they say. Using a 40-gene signature gleaned from mouse models of parainflammation and from an inflammatory response gene database, the team scoured data from hundreds of cancer cell lines and thousands of primary tumors. The search suggested parainflammation does occur in some human cancers, particularly tumors marked by p53 mutations and those associated with poor survival outcomes.
Blood lipids seem to influence DNA methylation features in circulating immune cells, according to investigators at Leiden University Medical Center and elsewhere. The team analyzed methylation and transcriptome profiles in blood samples from more than 2,000 individuals, focusing on potential ties between triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels. In the process, the group found half a dozen cytosine methylation marks influenced by blood lipids — epigenetic changes that coincided with expression shifts at several lipid metabolism-related genes.
A University of Oxford team describes recurrent copy number gains, amplifications, or expression increases in metabolic genes it detected in a pan-cancer analysis involving tumors from 10 cancer types. By analyzing more than 2,700 metabolic genes in 6,538 paired tumor-normal samples profiled for the Cancer Genome Atlas, the International Cancer Genome Consortium, or Metabric, the researchers highlighted 44 metabolic genes that were affected by copy number gains, amplifications, and/or expression shifts in at least 20 percent of the cases considered, especially in tumors with low oxygen-associated features. They subsequently picked up the signature in additional breast, kidney, and colorectal cancers and delved into specific metabolic features associated with cancer cell survival during hypoxia.