Cancer Res February 1 2017 77 (3) 591-592;
A mineable datasource places the DNA methylation levels for 17,559 genes into cell line signatures for easy comparison to molecular and pharmacological data.
The first global proteomic analysis of eIF4F-dependent translation in cancer provides a new perspective on the role of eIF4F in cancer and the use of selective eIF4F inhibitors for treating cancer.
A new fluorescent-labeling technique provides a quantitative, high-resolution map of tumor tissue in vivo.
These findings define an important axis controlling angiogenesis in metastatic liver cancers and a mechanistic foundation for rational drug development.
This seminal study suggests cautions in the development of autophagy-based strategies for cancer treatment, based on findings that blocking hypoxia-regulated autophagy can actually drive metastasis.
These results validate the importance of targeting both the tumor and its associated stroma in establishing the potency of a new combination therapy that can trigger efficacious allogeneic graft versus tumor effects.
Stromal cells respond to danger-associated factors secreted by pancreatic cancer cells, ultimately leading to profound stromal-mediated suppression of antitumor immunity.
Peritoneal mesothelial cells generate a tissue microenvironment favorable to cancer cell infiltration, with possible therapeutic implications for blocking progression.
A new mouse model of human metastatic neuroblastoma was exploited to identify novel genes, signaling pathways, candidate therapeutics, and a prognostic gene expression that could improve the treatment of this deadly pediatric disease.
This study addresses the long-standing question about why H-Ras and K-Ras oncogenes are associated with induction of different tumor types, which results here suggest that subtle differences in MAP kinase signaling in tumor cells may offer one explanation for functional nonequivalence.
These results offer a preclinical proof of concept for the use of nanoparticles to modify cancer-associated fibroblasts as a strategy to treat desmoplastic cancers.
These results provide a preclinical rationale to use a class of specific nuclear receptor antagonists to treat a particularly aggressive type of pediatric soft tissue tumors driven by the fusion gene PAX3-FOXO1A.
Chemotherapy-induced cognitive impairment—often informally referred to as “chemobrain”—is a widespread side-effect in cancer survivors who receive classical cytotoxic chemotherapy as part of their treatment.
These findings define a new kinase signaling pathway in mediating castration-resistant prostate cancer, the most aggressive form of the disease, with implications for the development of therapeutic agents needed for more effective control.
Expression of a little studied chromain modifier appears to mark a subset of colon cancer cells with selfrenewal properties, suggesting its use as a biomarker of early-stage colorectal cancers likely to have a poor prognosis.
These results suggest the existence of evolutionarily conserved pathways used by S100A4 to promote metastatic dissemination in the nervous system, which is not well understood but preferentially exploited by certain glandular tumors.
These findings reposition aspirin as a tool to treat breast cancer cell growth, supporting a rationale for its combination with PI3K inhibitors in therapy.
These findings propose that the cell of origin may have an important role for clinicopathological features of HGG such as malignancy and drug sensitivity.