Cancer Res July 15 2016 76 (14) 4023-4024;
These results reveal a mechanism that may help explain why obese cancer patients tend to have a poorer prognosis.
This study reveals a hitherto unknown generic mechanism for large-scale metabolic reprogramming in cancer cells, based on linear gene proximities between cancer-causing and -metabolic genes, with the identification of 119 genes likely to be involved in rewiring cancer cell metabolism.
This study significantly expands the repertoire of cancer genes that are regulated by RNA stability proteins and how these interactions impact the cancer patient survival.
A clinical ultrasound imaging system capable of predicting therapeutic responses to treatment with angiogenesis inhibitors may be valuable to predict patient outcomes.
These findings offer an initial guidepost toward the development of improved prognostic biomarkers or companion biomarkers for DCLK1-targeted therapies aimed at eradicating cancer stem-like cells in several GI malignancies.
While mTOR inhibitors can paradoxically induce protective T-cell immunity in renal cancer, prolonged treatment in this setting creates immunosuppressive effects that might be reversed by immune checkpoint blockade.
These findings offer a preclinical proof of concept for a readily translatable method to image different distribution patterns of transgenic T cells used in adoptive transfer therapies for cancer patients.
These results illuminate how a subset of cancer-associated fibroblasts can be programmed to contribute to an inflammatory tumor microenvironment, a feature of possible great importance in desmoplasia-associated cancers.
EGFR-driven tumor glycolysis is a major factor contributing to the lack of T-cell infiltration in squamous cell carcinoma, potentially contributing to immune escape.
These provocative results suggest a mechanistic explanation for the very early metastatic behavior of pancreatic cancers, with implications for early diagnosis and therapy in this aggressive disease.
These results reveal a complexity in cancer for miR-29b, which while ascribed a tumor suppressor role elsewhere, is found in this particular study of KRAS-mutant lung cancers to act as an oncogene that promotes apoptotic resistance.
These findings probe a metabolic Achilles' heel in a certain genetic subclass of liver cancer, providing a preclinical rationale for a new strategy to attack this deadly disease.
These findings offer a preclinical proof of concept for baicalein, a novel chemotherapeutic agent to treat up to 5% of colorectal tumors that are deficient for DNA mismatch repair.
This important study describes a novel mechanism for downregulation of the androgen receptor, which efficiently suppresses the growth of prostate cancer, regardless of its hormone sensitivity.
Missplicing of FGFR3 in hepatocellular carcinoma contributes significantly to its malignant character, with potential implications for therapeutic targeting.
These findings suggest the utility of little studied HPV strains in understanding tissue-specific mechanisms of carcinogenesis, which involve environmental risk factors.
Weight loss is associated with reduced circulating markers of angiogenesis, suggesting an incentive to reduce weight as a cancer prevention method in overweight and obese individuals.
These findings propose an E3 ligase-RhoGEF signaling axis as a candidate therapeutic target to block breast cancer metastasis, illustrating the possible selective benefits of therapies, which target Rho signaling in cancer cells.
This study shows how preventing the organization of abnormal architectures of collagen fiber in the extracellular matrix can effectively arrest the invasive behavior of malignant cells.
This important study offers a preclinical rationale to develop inhibitors of the glycolytic enzyme aldolase A as a generalized strategy to treat intractable hypoxic cancer cells, which are found in most human solid tumors.
These findings show how local activation of coagulation pathways in EMT-positive circulating tumor cells supports their metastatic colonization and spread, heightening the urgency for immediate clinical study of new anticoagulant drugs to prevent metastasis in cancer patients in remission after their initial treatment.
A proangiogenic factor that helps bypass anti-VEGF therapy appears to act at two levels in the tumor microenvironment to promote angiogenesis, by affecting both mesenchymal stromal cells and tumor-associated macrophages.
Manipulating the microRNA-mediated tumor suppressor pathway described in this study may offer a novel therapeutic approach to treat glioblastoma, the deadliest brain cancer.