Skip to main content
Premium Trial:

Request an Annual Quote

Cell Studies Explore Microbiome Genes, Tumor Influence, More

A Stanford University-led team presents a collection of previously unappreciated small proteins found using a reference-free comparative genomic analysis involving nearly 1,800 microbial metagenome sequences generated from four human body sites in 263 healthy volunteers. Using the gene prediction tool MetaProdigal and other computational approaches, the researchers focused in on more than 4,500 conserved small protein families, including many not found in the past. In a series of follow-up experiments, they took a closer look at the expression of the small protein-coding genes in available metatranscriptome data, while analyzing the function and distribution of small proteins across microbial taxa and microbiome sites. GenomeWeb has more on the study, here.

Researchers from the University of Texas MD Anderson Cancer Center and elsewhere propose a potential role for tumor microbes in pancreatic cancer survival, based on findings from their own microbiome study. That team relied on targeted 16S ribosomal RNA gene sequencing to identify microbial community members in tumors from dozens of pancreatic ductal adenocarcinoma (PDAC) patients with longer-than-usual survival times (beyond 10 years, on average). Compared to PDAC patients with more typical, poor survival outcomes, the long-term had more diverse tumor microbiomes and improved immune infiltration, the authors report, prompting a subsequent search for prognostic tumor microbial signatures and fecal microbial transplant experiments in mouse models of the disease. GenomeWeb also covers this, here.

Members of the Genetic Modifiers of Huntington's Disease Consortium suggest that Huntington's disease onset is influenced by CAG trinucleotide repeat sequences in HTT, independent from the gene's polyglutamine segment length. Starting with clues gleaned from a prior genome-wide association study, the researchers re-imputed genotypes for almost 9,100 participants to search for signals tied to age of onset. While HTT expression, expression quantitative trait loci, and polyglutamine length were not significantly linked to age of onset, the team's analysis led to the CAG repeat region, as well as variants in DNA maintenance genes. "These findings have profound implications for the pathogenesis of [Huntington's disease] and other repeat diseases," they write, "and question the fundamental premise that polyglutamine length determines the rate of pathogenesis in the 'polyglutamine disorders.'