In PLOS One, researchers with Chronix Biomedical and other centers in Göttingen, Germany, report on a method used to track down canine cancer markers and later detect them in circulating, cell-free DNA in the dogs' blood. The group identified and verified copy number shifts and structural glitches in five mammary carcinoma tumors from three subtypes using sequencing and digital droplet PCR, respectively. In four of the tumors they found a deletion affecting a tumor suppressor gene called PFDN5 — a deletion that ultimately turned up in half of the 20 mammary tumors tested for the study. By profiling breakpoints in four tumors, the team found markers that ultimately made it possible to detect metastatic disease in cell-free DNA circulating in the blood of one dog with cancer more than a year after surgery.
For more on the study, check out a news story from our sister publication GenomeWeb Daily News.
Primary infection by the bovine leukemia virus, or BLV, involves interplay between proviral insertion within gene or promoter sequences and negative selection from the host that weeds out clones that carry proviruses in sequences near transcribed sequences, according to a study appearing in PLOS Pathogens. Belgian and Argentinean researchers relied on high-throughput sequencing to see proviral insertion sites in bovine cells infected by BLV as part of their effort to follow the factors influencing early infection and subsequent clonal expansion processes. The study's authors found that viral integration in and around genes and gene promoters during primary BLV infection, coupled with host selection, both contribute to the composition of clonal populations at play in later stages of infection.
A genome-wide association study in PLOS Genetics is linking alterations in a methyltransferase gene to a skin disorder in Labrador retrievers. A University of Bern-led team genotyped 13 labs with an inherited condition called hereditary nasal parakeratosis, or HNPK, which causes crusty and cracked dog noses. When they compared these patterns to those found in 23 unaffected control dogs, the researchers saw a chromosome 2 site that seemed to coincide with HNPK. Through a series of follow-up sequencing and genotyping experiments, they determined that the HNPK culprit appears to be a missense change to a histone 3 lysine 9 methyltransferase-coding gene called SUV39H2 that slows terminal keratinocyte differentiation in affected pooches.