In Cancer Research this week, researchers at the University of California, San Francisco, and elsewhere examine common structural and epigenetic changes in the genome of castration-resistant prostate cancer. The team defined and validated 495 genes that showed significant copy-number changes in CRPC. "Significant copy-number differences existed between tumors with or without AR [androgen receptor] gene amplification, including a common loss of AR repressors in AR-unamplified tumors," the authors write. "Simultaneous gene methylation and allelic deletion occurred frequently in RB1 and HSD17B2, the latter of which is involved in testosterone metabolism." The team adds that genomic DNA from CRPC samples was hyper-methylated compared with that from benign prostate tissue.
Also in Cancer Research this week, a team led by researchers at Harvard Medical School reports its method for classifying human brain tumors using lipid imaging with mass spectrometry. Using desorption electrospray ionization-mass spectrometry, DESI-MS, the team imaged 36 human glioma samples. The researchers found gray and white matter readily distinguishable from one another, and that "detailed diagnostic information" could be obtained. In addition, "classifiers for subtype, grade, and concentration features generated with lipidomic data showed high recognition capability with more than 97 [percent] cross-validation," the team says. "Together, our findings offer proof of concept that intraoperative examination and classification of brain tissue by mass spectrometry can provide surgeons, pathologists, and oncologists with critical and previously unavailable information to rapidly guide surgical resections that can improve management of patients with malignant brain tumors," the authors write.
Finally in Cancer Research this week, researchers in China and Texas report a novel FoxM1-caveolin signaling pathway that they say promotes pancreatic cancer invasion and metastasis. In examining preclinical models of pancreatic cancer and human tissue samples, the team found that Cav-1 expression levels correlated with metastatic potential and epithelial–mesenchymal transition of pancreatic cancer cells. "Elevated levels in cells promoted EMT, migration, invasion, and metastasis in animal models, whereas RNA interference-mediated knockdown inhibited these processes," the authors write. "We determined that levels of Cav-1 and the Forkhead transcription factor FoxM1 correlated directly in pancreatic cancer cells and tumor tissues. Enforced expression of FoxM1 increased Cav-1 levels, whereas RNAi-mediated knockdown of FoxM1 had the opposite effect."