In Clinical Cancer Research this week, researchers at the Johns Hopkins Medical Institutions report on microRNA alterations that arise during the early development of pancreatic cancer. The team determined the levels of 735 miRNAs in 34 pancreatic intraepithelial neoplasias and 15 normal pancreatic duct samples. They identified 107 aberrantly expressed miRNAs in pancreatic intraepithelial neoplasias compared to normal pancreatic tissue. "These differentially expressed miRNAs included those that have been previously identified as differentially expressed in pancreatic ductal adenocarcinomas as well as miRNAs not previously described as differentially expressed in these lesions," the authors write. "The miRNAs, such as miR-196b, whose expression is limited to PanIN-3 lesions or pancreatic cancers could be useful as diagnostic markers."
Also in Clinical Cancer Research this week, researchers in Germany analyze changes in keratin expression during the metastatic progression of breast cancer and its impact on the detection of circulating tumor cells. The team assessed the protein expression of a variety of keratins in 11 breast cancer cell lines and 50 primary breast carcinomas and their lymph node metastases. "Breast cancer cells show a complex pattern of keratin expression with potential biologic relevance," the authors write. "Individual keratin antibodies recognizing only a limited set of keratins inherit the risk to miss biologically relevant CTCs in cancer patients, and antibody cocktails including these keratins are therefore recommended."
Finally in Clinical Cancer Research this week, researchers in Canada and the UK report that PTEN deletion in prostate cancer cells doesn't associate with loss of RAD51 function. Further, they analyze the implications of this for the treatment of prostate cancer. The team studied prostate cancer cell lines and xenografts with known PTEN status, and examined primary prostate cancers with known PTEN status for RAD51 expression. "PTEN status is not associated with reduced RAD51 mRNA or protein expression in primary prostate cancers. Decreased PTEN expression did not reduce RAD51 expression or clonogenic survival following PARP [inhibition] among prostate cancer cells that vary in TP53 and PTEN," the authors write. "These data suggest that the relationship between PTEN status and survival following DNA damage is indirect and complex. It is unlikely that PTEN status will be a direct biomarker for [homologous recombination] status or PARPi response in prostate cancer clinical trials."