Genome-wide association studies have linked Forkhead Box F1 (FOXF1) to Barrett’s esophagus (BE) but functional data are lacking. Using in vitro models and human material, the authors found that FOXF1 promotes columnar phenotype and cell motility in esophageal squamous epithelial cells, which may have a critical role in BE development.

Patient-derived xenograft (PDX) models are valuable platforms to assess preclinical and clinical trials for cancer therapy including lung cancer. The authors clarified that enriched expression of immune system-associated genes such as CD19 and CD23 are the most critical factors to obstacle the PDX generation, particularly in lung squamous cell carcinoma.

The authors report the successful assessment of LD-RT-PCR, a cheap, fast, sensitive, specific, and easily upgradable assay for routine detection of theranostic gene translocations and MET exon 14 skipping in thoracic oncology. It appears to be an excellent cost-effective alternative to FISH and to more expensive and complex assays such as RNA-seq.

PLODs play important roles in cancer progression. In silico analysis of PLOD expression in ovarian cancer was performed. PLOD-enriched pathways and related genes were validated by immunohistochemistry in OvCa tissue blocks and in vivo xenograft murine models. PLODs are generally overexpressed in OvCa and each PLOD may be functionally non-redundant.

Real-time lipid patterns can identify liver tumors and their inter-tumor and intra-tumor heterogeneity. Ceramides and related sphingolipids are a common feature of necrotic tumors and can characterize the tumor phenotype based on metabolic shifts relevant for cell death pathways. Lipid patterns have the potential to improve clinical decision-making in the near future.

Using approaches involving chimeric mice and macrophage-adipocyte cocultures, the authors demonstrate that PFKFB3 disruption only in hematopoietic cells exacerbates the severity of diet-induced adipose tissue inflammation and systemic insulin resistance. Mechanistically, macrophage factors generated in response to PFKFB3 disruption act to enhance adipocyte proinflammatory responses and impair adipocyte insulin signaling.